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109 publications mentioning rno-mir-29c-2 (showing top 100)

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-29c-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 265
Conversely, inhibition of mTORC1 signaling resulted in up-regulation of miR-29 expression and suppressed MCL-1 expression in cardiomyocytes. [score:12]
Moreover, since DM is associated with either insulin deficiency or a lack of insulin signaling, we also posited that insulin would suppress the expression of the miR-29 family in cardiomyocytes and up-regulate MCL-1 expression. [score:10]
Data presented here shows that insulin down-regulates the expression of diabetic marker miR-29 family miRNAs in mouse cardiomyocytes and preserves the expression of cardioprotective MCL-1. Consistent with this insulin effect, 11-week old hyperinsulinemic ZDF rats only had a mild loss of MCL-1 expression and did not show any damage in myocardium. [score:10]
Conversely, inhibition of mTORC1 signaling by Rap or inhibitors of mTORC1 substrates significantly increased expression of miR-29 family miRNAs and suppressed cardioprotective MCL-1 in mouse cardiomyocytes. [score:9]
Since MCL-1 is a target of miR-29 family miRNAs, and Rap treatment increases miR-29 expression, we investigated whether a miR-29 inhibitor cocktail (inhibitors of miR-29a, b and c) would improve MCL-1 expression in Rap treated HL-1 cells. [score:9]
Since miR-29 suppresses MCL-1 and the miR-29 family miRNAs are elevated in DM we hypothesized that one of the mechanisms by which DM promotes heart disease is by causing dysregulation of the miR-29-MCL-1 axis and suppressing MCL-1 levels in cardiomyocytes that can lead to cardiomyocyte disorganization. [score:8]
B) Expression of miR-29 family miRNAs (miR-29a, b and c) in mouse cardiomyocyte HL-1 cells is suppressed by treatment with INS (100 nM; 12 h) and up-regulated by treatment with Rap (10 nM; 12 h). [score:8]
Transfection of HL-1 cells with miR-29 inhibitor cocktail reversed Rap -mediated suppression of MCL-1 expression. [score:7]
analysis using anti-MCL-1 antibody showed that Rap treatment substantially suppressed MCL-1 expression in HL-1 cells transfected with Allstars negative control siRNA, but not in HL-1 cells transfected with miR-29 inhibitor cocktail (Fig. 2D). [score:7]
We have shown in vitro that a miR-29 inhibitor cocktail could reverse Rap -mediated suppression of MCL-1 protein expression in cardiomyocytes. [score:7]
Since increased expression of different members of miR-29 family is associated with DM, we tested the effects of insulin that attenuates the progression of DM, and rapamycin (Rap) that promotes the progression of DM, on the expression of miR-29 family miRNAs in HL-1 cells. [score:5]
We undertook this study to uncover the role of microRNA miR-29 family and its target MCL-1, a pro-survival molecule that is critical for cardiomyocyte survival under stress, in the myocardium damage seen in diabetic heart disease. [score:5]
However, suppression of hyperinsulinemia by Rap in the absence of regulation of hyperglycemia as seen in Rap -treated ZDF rat promotes severe dysregulation of cardiac miR-29-MCL-1 axis that leads to disruption and loss of myofibril bundle organization. [score:5]
This would have led to the up-regulation of all miR-29 family miRNAs in their heart tissues that resulted in the severely dysregulated miR-29-MCL-1 axis in Rap -treated ZDF rats. [score:5]
Since Rap-treatment increased miR-29 levels and suppressed MCL-1 mRNA levels in mouse HL-1 cardiomyocytes, we tested whether Rap-treatment would increase cardiac miR-29 family miRNAs and suppress cardiac MCL-1 mRNA even further in young ZDF rats. [score:5]
Further studies are needed to also confirm that in in vivo rodent mo dels a miR-29 inhibitor cocktail would improve cardiac MCL-1 protein expression. [score:5]
Insulin treatment strongly suppressed miR-29a, b and c in cardiomyocytes whereas Rap treatment significantly enhanced expression levels of all three miR-29 family members in HL-1 cardiomyocytes (Fig. 1B). [score:5]
20 nM of miR-29 inhibitor cocktail (mirVana miRNA inhibitors for miR-29a, b and c) or 20 nM Allstars negative siRNA (Qiagen) was used for transfection. [score:5]
Though rapamycin has well-established cardioprotective effects, an additional increase in miR-29 family miRNAs due to mTORC1 inhibition in the heart tissues of DM patients can potentially suppress MCL-1 and exacerbate cardiomyocyte disorganization and cardiac damage. [score:5]
D) staining with anti-MCL-1 antibody and nuclear stain DAPI in HL-1 cells transfected with either (a) Allstars negative siRNA and (b) Allstars negative siRNA and treated with Rap (10 nM), or (c) miR-29 inhibitor cocktail (mirVana miRNA inhibitors for miR-29a, b and c) and treated with Rap (10 nM). [score:5]
Since insulin suppressed miR-29 in HL-1 cardiomyocytes, we posited that insulin would improve expression of MCL-1 in these cells. [score:5]
In brief, the suppression of miR-29 expression by insulin could be a previously unidentified cardioprotective mechanism in hyperglycemia. [score:5]
Regulation of miR-29 target MCL-1 by insulin and rapamycin in mouse cardiomyocytes. [score:4]
This observation implied that miR-29 family miRNAs regulate MCL-1expression in HL-1 cardiomyocytes. [score:4]
Though 11-week old ZDF rats had a mild dysregulation of miR-29-MCL-1 axis that resulted in about 45% suppression of MCL-1, no visible differences were observed in the histopathology of the RV tissues between ZL and ZDF rats. [score:4]
These data suggested that a miR-29-MCL-1 axis, similar to that seen in mouse and human pancreatic β-cells [15] exists in mouse cardiomyocytes and it is regulated by insulin and rapamycin, an mTORC1 inhibitor. [score:4]
We only observed a mild dysregulation of miR-29–MCL-1 axis at this stage and a 45% suppression of MCL-1 mRNA (Figs. 3I and 3J). [score:4]
Additionally, knock-down of miR-29c suppressed high glucose induced apoptosis of podocytes and improved kidney function [9]. [score:4]
Therefore, dysregulation of miR-29-MCL-1 axis caused by loss of insulin and mTORC1 inhibition is a major factor in promoting myocardial damage in DM in ZDF rats. [score:4]
Collectively, our data shows the steps in the dysregulation of miR-29-MCL-1 axis in heart tissues during the progression of DM as shown in Fig. 6. Briefly, at the age of 11 weeks, healthy ZL rats show basal level expression of miR-29 and MCL-1 and their myocardium is well organized. [score:4]
miR-29 family miRNA expression pattern. [score:3]
Since we observed that insulin could suppress miR-29 family miRNAs in cardiomyocyte HL-1 cells, it is conceivable that the lack of significant increase in miR-29c in the myocardium of 11-week old ZDF rats despite severe hyperglycemia could be due to their compensatory hyperinsulinemia (a 14-fold increase in plasma insulin). [score:3]
RAP for miR-29 a, b, and c. The role of the miR-29-MCL-1 axis in the progression of DM -associated heart disease is not known. [score:3]
Expression of all three miR-29 family miRNAs (a, b and c) were significantly higher (at least 2 fold for each miRNA) in ZDF myocardium. [score:3]
Though insulin treatment could induce phosphorylation of S6K1 rapidly, in this study we chose a 12 hr treatment to be consistent with the treatment time used for determining the changes in miR-29 and an MCL-1 mRNA expression in response to insulin in HL-1 cells. [score:3]
Cardiac tissues of 15-week old Rap treated ZDF-rats (Rap treatment from 9-weeks to 15-weeks) displayed a ∼2-fold increase in miR-29 family miRNAs and a 4-fold suppression of MCL-1 mRNA. [score:3]
Since insulin is an activator of the nutrient sensor kinase mammalian target of rapamycin complex 1 (mTORC1), we further posited that mTORC1-signaling mediates insulin's effects on miR-29-MCL-1 axis. [score:3]
However, qRT-PCR showed that Rap treated ZDF rats had at least a 2-fold increase in the expression of all miR-29 family members (miR-29a, b and c) (Fig. 4E). [score:3]
This observation may have important clinical relevance given the fact that patients with DM are reported to have an increase in miR-29 expression [8], [44]. [score:3]
Increased expression of diabetic marker miR-29 family miRNAs is seen in rodent mo dels of DM and in young and adult diabetic patients with T1DM or T2DM. [score:3]
Expression of miR-29a and b were significantly higher in the myocardium of ZDF rat, but miR-29c was not significantly different between ZL and ZDF myocardium. [score:3]
Therefore, we conclude that regulation of miR-29-MCL-1 axis by insulin is a cardioprotective mechanism and compensatory hyperinsulinemia in conditions of hyperglycemia would regulate miR-29-MCL-1 axis in diabetic heart and prevent significant myocardial damage in young (11- and 15-week) ZDF rats. [score:3]
Suppression of miR-29 by anti-miR-29 oligomers protects against myocardial ischemia-reperfusion injury, abdominal aortic aneurism and diabetic nephropathy [9]– [13]. [score:3]
HL-1 cells were transfected with either Allstars negative control siRNA or miR-29 inhibitor cocktail and after 8 hours of transfection subjected to treatment with Rap (10 nM) overnight. [score:3]
However, we did not see a significant increase in miR-29c expression in hyperglycemic 11-week old ZDF myocardium. [score:3]
Progressive dysregulation of cardiac miR-29-MCL-1 axis in DM and its correlation with cardiac damage. [score:2]
Based on the data presented here, we contend that the normal functioning of miR-29-MCL-1 axis is an important cardioprotective mechanism regulated by insulin that exists in female mouse atrial cardiomyocytes and male ZDF rat heart tissue. [score:2]
In contrast Rap -treated ZDF rats have very low INS, severe hyperglycemia, and severe dysregulation of miR-29-MCL-1 axis. [score:2]
These data suggest that cardiac miR-29-MCL-1 axis is mildly dysregulated in 11-week old ZDF rats that suffer from DM. [score:2]
I: qRT-PCR analysis data showing the comparative expression levels of miR-29 family miRNAs in myocardium of ZDF rats compared to that in the myocardium of ZL rats. [score:2]
To our knowledge this is the first report that shows insulin is a regulator of miR-29 family miRNAs. [score:2]
For this study, we focused on the RV of ZDF rat heart since RV dysfunction from structural and functional perspectives has been described previously in young ZDF rats [5], [6] and therefore the baseline parameters were easy to compare in the context of regulation of the miR-29-MCL-1 axis. [score:2]
Our in vitro studies on mouse cardiomyocyte HL-1 cells showed that insulin regulates miR-29 family miRNAs (mir-29a, b and c) and improves cardioprotective MCL-1 levels in cardiomyocytes. [score:2]
Mild dysregulation of cardiac miR-29-MCL-1 axis in a hyperinsulinemic DM background (ZDF rat) does not show significant cardiac myofibril disorganization or loss. [score:2]
These observations suggest that Rap treatment causes severe dysregulation of the miR-29-MCL-1 axis in cardiac tissues of ZDF rat. [score:2]
Moreover, Rap treatment of young hyperinsulinemic ZDF rats caused severe dysregulation of cardiac miR-29-MCL-1 axis and myofibril bundle disorganization indicative of myocardial damage. [score:2]
These observations suggest that the myocardium of Rap -treated ZDF rats that had a further increase in miR-29 a, b and c miRNAs and further suppression of MCL-1 (Fig. 4E and 4F) compared to age-matched control rats, exhibited significant disorganization of myofibril bundles that reflect tissue damage. [score:2]
Regulation of diabetic marker miR-29 by insulin and rapamycin in mouse cardiomyocytes. [score:2]
They have mild to moderate dysregulation of miR-29-MCL-1 axis. [score:2]
These observations revealed that a miR-29-MCL-1 axis exists in cardiomyocytes. [score:1]
QTLs associated with the rat (rno)-miR-29 a/b cluster located on chromosome 4: 58,107,760-58,107,847 are shown (Taken from Rat RGSC3.4. [score:1]
Thus, the miR-29-MCL-1 axis is a major contributor to pancreatic dysfunction and T1DM. [score:1]
In diabetic mice, an increase in miR-29c was associated with podocyte cell death that underlies diabetic nephropathy. [score:1]
In this context, the diabetic marker microRNA miR-29 family that plays a role in increasing cell death is particularly noteworthy. [score:1]
RAP for miR-29 a, b, and c. The cardiac muscle cell line HL-1 (a generous gift from Dr. [score:1]
To determine how DM progression (natural or advanced by Rap treatment) caused dysregulation of cardiac miR-29-MCL-1 axis and promoted cardiomyocyte disorganization, we used male ZDF rats, a well-established rodent mo del for advanced DM [5], [6], [26], [27] and evaluated the correlation between regulation of miR-29-MCL-1 axis and disorganization of myofibril bundles in cardiac right ventricle. [score:1]
miR-29 is also one of the several miRNAs associated with inflammatory microvesicles [14]. [score:1]
Hyperglycemia is known to significantly increase miR-29c [9]. [score:1]
In this study we used mouse atrial cardiomyocyte HL-1 cells and right ventricular tissues of ZDF rats to investigate how Rap modulates expression of miR-29-MCL-1 axis. [score:1]
The miR-29 family consists of miR-29 a, b (b1 and b2) and c that are located on two different chromosomes (chromosomes 4 and 13 in rat, 1 and 6 in mouse and 1and 7 in human) [7]. [score:1]
Further studies with primary cultures of cardiomyocytes from rat atrium and ventricle are needed to confirm that INS -mediated modulation of miR-29-MCL-1 axis is similar in atrial and ventricular cells. [score:1]
This study was undertaken to investigate whether insulin regulated the miR-29-MCL-1 axis in cardiomyocytes and if conditions that lead to progressive loss of insulin promote dysregulation of cardiac miR-29-MCL-1 axis and disorganization of cardiomyocytes. [score:1]
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[+] score: 239
Taken together, the present study shows that bladder outlet obstruction, such as that seen in elderly men with enlarged prostate glands, leads to reduced expression of miR-29b and miR-29c in the bladder and that this is associated with increased expression of miR-29 targets, including the matrix proteins elastin and Sparc. [score:7]
Expression of all six of these targets peaked at the nadir of miR-29c expression (compare Figure 3B with Figure 2A), and they declined sharply on de-obstruction when the miR-29c level recovered. [score:7]
Human detrusor cells were transfected with miR-29c inhibitor and eight validated miR-29 targets, most of which were represented among the top 50 predicted targets in Figure 3A, were examined using western blotting. [score:7]
We also demonstrate that genetic depletion of miRNAs, including miR-29, increases bladder elastin expression and stiffness independently of outlet obstruction and that miR-29 inhibitor transfection in vitro replicates several of the expression changes associated with miR-29 repression in outlet obstruction. [score:7]
Together, these circumstances may well explain the more widespread apparent impact of miR-29 repression in outlet obstruction (8/8 examined target proteins increased) compared to inhibitor transfection (4/8 examined target proteins increased). [score:6]
Four of the eight selected miR-29 targets, including Eln (elastin or tropoelastin), Fos (also known as c-Fos), Sparc (osteonectin) and sprouty homolog 1 (Spry1), were significantly increased following inhibitor transfection (Figure 3D, left row). [score:5]
For tropoelastin, whose mRNA correlated inversely and significantly with miR-29 in outlet obstruction, we found that transfection of a miR-29c inhibitor resulted in increased tropoelastin expression. [score:5]
To address the functional impact of miR-29, we transfected a miR-29 inhibitor and mimic in vitro and conditionally deleted Dicer in vivo [5] and examined the effect of these interventions on tropoelastin expression and on tissue mechanical properties. [score:5]
Currently, we can only speculate on the role of these proteins in outlet obstruction, but it is of considerable interest that the miR-29 target Spry1 [14], which is an established ERK1/2 inhibitor [49], increases after prolonged outlet obstruction. [score:5]
Of the 30 miRNAs that are highly expressed in the mouse detrusor [5, 41] none except miR-29 is predicted to target tropoelastin. [score:5]
For miR-29c inhibitor and mimic experiments, cells were transfected with miR-29c inhibitor (Thermo Scientific, Pittsburgh, PA, USA; 20nM), mimic (Mission miRNA: Sigma-Aldrich, St. [score:5]
Some predicted and confirmed miR-29 targets, including Fbn1, which is an integral part of the elastic fiber meshwork, and Lamc1, a protein present in the basement membrane, were increased in outlet obstruction but were not significantly affected at the protein level following inhibitor transfection (not shown). [score:5]
Additional regulatory inputs on miR-29 expression include c-Myc and NF-κB [11], and recent work has provided considerable insight into c-Myc -mediated repression, which appears to depend on a repressor complex consisting of c-Myc, histone deacetylae 3 (Hdac3) and enhancer of zeste homologue 2 (Ezh2) [18]. [score:4]
Detrusors from smooth muscle-specific Dicer knockout mice were used to examine if reduction of miR-29 in vivo increases tropoelastin expression. [score:4]
We found that Dicer knockout reduced miR-29b and miR-29c by about half and increased tropoelastin expression. [score:4]
Sparc, Spry and Fos were similarly reciprocally regulated by miR-29c inhibitor and mimic, and increased in outlet obstruction. [score:4]
The extracellular matrix molecule elastin is one of the best established targets of miR-29, and its message has 14 binding sites dispersed over the coding sequence and the 3’UTR [12]. [score:3]
Expression of (E) miR-29c and (F) miR-29b in vehicle -treated (control) and TGF-β1 -treated human urinary bladder smooth muscle cells. [score:3]
Time courses of (A) miR-29c and (B) miR-29b expression following rat bladder outlet obstruction. [score:3]
Transfection of miR-29c inhibitor and mimic. [score:3]
0082308.g002 Figure 2Time courses of (A) miR-29c and (B) miR-29b expression following rat bladder outlet obstruction. [score:3]
Repression of miR-29 after outlet obstruction is associated with increased levels of miR-29 target proteins. [score:3]
We first examined expression of miR-29b and miR-29c following 5 weeks of Dicer deletion and found both miRNAs to be reduced (Figure 6A, B). [score:3]
MiR-1 (not shown), miR-29b, and miR-29c returned significant associations with target mRNA levels. [score:3]
We plotted the mean expression of these mRNAs versus the mean miR-29c level in sham-operated control bladders, after 10 days and 6 weeks of obstruction, and after 10 days of de-obstruction. [score:3]
Outlet obstruction and transforming growth factor β (TGF-β1) stimulation leads to reduced expression of miR-29. [score:3]
0082308.g005 Figure 5(A) Western blots for eight miR-29 targets in sham-operated control bladders and at 6 weeks of obstruction. [score:3]
We also examined if the reduction of miR-29 correlated with altered miR-29 target mRNAs, including tropoelastin and Sparc. [score:3]
6 weeks) of the top 50 mRNA targets of miR-29 when miR-29 was repressed at 10 days and when miR-29 recovered after de-obstruction (c. f. Figure 2A and B). [score:3]
sham) of miR-29 target messenger RNAs (mRNA; black circles) and proteins (white circles). [score:3]
Considerably more time was moreover allowed for de-repression of miR-29 targets in the in vivo setting (6 wk vs. [score:3]
It may be argued that a miRNA other than miR-29 is responsible for altered tropoelastin expression in Dicer KO bladders. [score:3]
Outlet obstruction and TGF-β reduce miR-29 expression. [score:3]
MiR-29b and miR-29c were among the 63 differentially expressed miRNAs in outlet obstruction (q=0; n=6−8; GEO accession number GSE47080). [score:3]
This revealed a pronounced increase around individual cells and around muscle bundles in obstructed bladders, consistent with its increased mRNA level and with the fact that it is a miR-29 target [48]. [score:3]
We next set out to determine miR-29 expression. [score:3]
Time courses of expression for miR-29c and miR-29b from the microarray experiment are depicted in Figure 2A and 2B. [score:3]
A previous microarray study [31] with close to genome-wide coverage showed that overexpression of miR-29c reduced six mRNAs: Col4a1; Fbn1; Lamc1; collagen, type XV, α1 (Col15A1); thymine-DNA glycosylase (Tdg); and collagen, type III, α1 (Col3A1). [score:3]
Real-time quantitative PCR to confirm reduced expression of miR-29. [score:3]
The experimental support for an impact of miR-29 on protein synthesis in the bladder following outlet obstruction extends well beyond a significant correlation between miR-29b/c and target mRNAs. [score:3]
Stimulation with TGF-β1 for 48h led to reduced expression of miR-29c and miR-29b (Figure 2E and F). [score:3]
We next tested whether TGF-β1 reduces miR-29 expression using cultured smooth muscle cells from human bladder. [score:3]
Repression of miR-29 during outlet obstruction is associated with increased levels of miR-29 target messenger RNAs (mRNAs). [score:3]
The matricellular protein Sparc is a confirmed miR-29 target [13] that influences collagen fibril morphology and function [47]. [score:3]
We also predicted the free energies of miR-29c binding to proximal sites in the Eln and Sparc 3’UTRs and found them to be within the range of authentic miRNA-target pairs (Figure S1A, B). [score:3]
Bladder outlet obstruction increases miR-29 target protein levels. [score:3]
Type I and type III collagens are however established targets of miR-29 [10], and their mRNAs were largely unchanged at 10 days and at 6 weeks (Col1a1 at 10 days: up by 15%, q=2.7, p=0.05; Col3a1 at 10 days: up by 12%, q=8.7, p=0.12). [score:3]
Unlike other miRNAs, miR-29 also targets a large battery of collagens, including collagens I and III [10]. [score:3]
This would repress miR-29, and hence it would be more difficult to see an effect of miR-29 inhibition. [score:3]
Our studies support a mo del in which multiple signaling pathways converge on repression of miR-29 in outlet obstruction, facilitating matrix protein expression and leading to altered mechanical properties of the urinary bladder. [score:3]
Real-time quantitative PCR for miR-29c and miR-29b (Figure 2C and D) confirmed reduced expression of both miRNAs at 10 days. [score:3]
MiR-29 target mRNAs change in outlet obstruction. [score:2]
Thus, several independent lines of evidence support a regulatory role of miR-29 in tropoelastin synthesis in the bladder, consistent with the large number of miR-29 binding sites in its mRNA [10, 12]. [score:2]
Several of the miR-29 targets that we studied, including Col15a1, Tdg and Spry1, have not been considered previously in the context of hypertrophic growth and remo deling of the bladder. [score:2]
SMAD proteins belong to a conserved family of TGF-β signal transducers that are regulated by phosphorylation [17], and the repression of miR-29 by TGF-β was shown to involve SMAD3 [16]. [score:2]
The matricellular protein Sparc has three miR-29 binding sites clustered in its proximal 3’ UTR, and, similar to elastin, this protein is effectively regulated by miR-29 in vitro [13]. [score:2]
Real-time quantitative polymerase chain reaction (n=5-7) for miR-29b (A), miR-29c (B) and elastin (Eln, C) in control (Ctrl) and Dicer knockout (KO) mouse bladders. [score:2]
Figure S1 Free energies (ΔG [0]) of miR-29c binding to the proximal 3’UTR site in rat, mouse and human elastin (Eln, panel A) and osteonectin (Sparc, panel B), respectively. [score:1]
Our starting hypothesis was that TGF-β/SMAD3 signaling would repress miR-29 in outlet obstruction. [score:1]
Figure S2 Flow chart showing the mo del proposed for miR-29 repression in outlet obstruction and for miR-29 -mediated matrix remo deling and altered passive mechanical properties. [score:1]
The reduced level of miR-29 leads to increased levels of mRNAs encoding extracellular matrix proteins (3), including elastin and Sparc (osteonectin), but possibly also collagens and fibrillin-1. The resulting protein synthesis and matrix deposition (4) leads to increased detrusor stiffness (5) (and increased elastic modulus) which counteracts (6) further distension. [score:1]
Together, these findings support the view that repression of miR-29, independent of surgical obstruction of the urethra, leads to matrix remo deling. [score:1]
We therefore hypothesized that outlet obstruction leads to SMAD3 phosphorylation repressing miR-29, and that this in turn has an impact on protein synthesis and mechanical properties of the bladder. [score:1]
Studies using cultured cells support the idea that transforming growth factor-β (TGF-β), a central mediator in fibrogenesis, represses miR-29 [16]. [score:1]
Independent confirmation of reduced (C) miR-29c and (D) miR-29b in the obstructed bladder by real-time quantitative polymerase chain reaction (n=6). [score:1]
sham), a time point when miR-29 was reduced (c. f. Figure 2A and B). [score:1]
The miR-29 cluster has gained recognition as a modulator of extracellular matrix production [7- 10]. [score:1]
This hypothesis was based on a handful of prior studies demonstrating increased mRNA levels for different TGF-β isoforms shortly after outlet obstruction (e. g. 24), and on the documented repression of miR-29 by TGF-β/SMAD3 [11]. [score:1]
Thus we measured the eight validated miR-29 target proteins (the same ones measured after inhibitor transfection) at 6 weeks of obstruction. [score:1]
c-Myc and NF-κB are also known to repress miR-29 [11, 18], and both pathways have previously been shown to be activated in outlet obstruction and by mechanical distension [37- 39]. [score:1]
The proposed mo del fits the data presented in this article, but alternative interpretations are possible and steps upstream of miR-29 repression need in vivo corroboration. [score:1]
This supported the possibility that c-Myc and NF-κB, but not SMAD3, might be involved in the repression of miR-29b and miR-29c at 10 days. [score:1]
SMAD3 activation, which is known to be involved in TGF-β -mediated repression of miR-29, was not significantly increased at 10 days when miR-29b and miR-29c appeared to be maximally repressed. [score:1]
Our findings do not provide any further guidance as to which possibility is correct, but they do indicate that SMAD3, which is specific for the miR-29b2/c gene [11], may be involved in chronic repression of miR-29c, but not in its acute reduction. [score:1]
c-Myc -mediated repression of miR-29 involves a complex consisting of c-Myc (Myc), histone deacetylase 3 (Hdac3) and enhancer of zeste homolog 2 (Ezh2) which binds to conserved sequences in the promoters of the miR-29a/b1 and miR-29b2/c genes [18]. [score:1]
MiR-29 -mediated extracellular matrix remo deling has been demonstrated in the infarcted heart [10] and during aortic aneurysm progression [7- 9], but miR-29 also plays roles in cell proliferation, muscle differentiation and apoptosis [11]. [score:1]
It comprises three miRNAs (miR-29a, miR-29b, and miR-29c) derived from two independent genes [10]. [score:1]
Therefore, reduction of miR-29b and miR-29c could well promote collagen production at an unchanged mRNA level at these times. [score:1]
This in turn (2) activates multiple signaling pathways including c-Myc, NF-κB and TGF-β/SMAD3 that in turn repress miR-29. [score:1]
With the possible exception for tropoelastin, transfection of miR-29c mimic was associated with a reduction of these proteins (Figure 3D, right row). [score:1]
Added to the correlation between miR-29c and Col4a1 mRNA this favors a causal relationship between the repression of miR-29 and the increase of Col4a1 in outlet obstruction. [score:1]
Combined, these findings provide support for our hypothesis that miR-29 reduction contributes to increased protein synthesis in the bladder following outlet obstruction and that this in turn influences matrix properties and stiffness (Figure S2). [score:1]
We hypothesized that miR-29 repression may contribute to increased detrusor stiffness in outlet obstruction. [score:1]
We propose that bladder distension leads to repression of miR-29 via three distinct mechanisms and that this has an impact on tropoelastin and Sparc synthesis and on tissue mechanical properties. [score:1]
To address this hypothesis we examined if SMAD proteins are phosphorylated and whether miR-29 is reduced in outlet obstruction. [score:1]
Right row in D shows effect of miR-29c mimic. [score:1]
Eln correlated significantly with miR-29c (Figure 3E) and with the mean of miR-29b and miR-29c (not shown). [score:1]
De-repression of Sparc may thus also contribute to a miR-29 -mediated change of detrusor stiffness in outlet obstruction. [score:1]
Our lack of evidence for SMAD2/3 activation at 10 days, when miR-29b and miR-29c appeared maximally repressed, forced us to consider alternative mechanisms. [score:1]
In view of this outcome we tested if Eln and Sparc mRNAs were individually correlated with miR-29 in outlet obstruction. [score:1]
Sparc correlated with the mean of miR-29b and miR-29c (Figure 3F). [score:1]
For miR-29c this would give three waves of repressive influences that together ensure a rapid yet longstanding decrease in outlet obstruction. [score:1]
We therefore propose that c-Myc/Hdac3/Ezh2 and NF-κB are jointly responsible for repression of miR-29b and miR-29c at 10 days and that SMAD3 is responsible for the sustained repression of miR-29c. [score:1]
The impact of miR-29 in outlet obstruction is likely underestimated by measuring levels of mRNAs because an important mechanism of miRNAs is translational repression. [score:1]
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[+] score: 175
This was demonstrated by the data of ChIP which showed a directly targeting miR-29 promotor by p65 and result of cells incubated NF-κB inhibitor, BAY 11-7082 that leaded to abolishment of high glucose -induced upregulation of miR-29 expression. [score:11]
By luciferase reporter assays and expression analysis of Keap1 in HK [miR−29 mimic] or HK [miR−29 inhibitor] cells, we can draw a conclusion of miR-29 directly regulated Keap1 expression by targeting Keap1 mRNA 3′ UTR. [score:10]
cell treated with 45 mM + DMSO Detection of abnormal expression of miR-29 and Keap1 in HK-2 cell lead us to determine whether miR-29 directly regulates Keap1 expression. [score:7]
This finding demonstrated a novel mechanism by which high glucose causes renal tubules injury and may provide insight as to what might be acted as therapy target by providing evidence supporting a role for miR-29 overexpression in the inhibition of Keap1/Nrf2 pathway. [score:7]
By result of western blotting, we observed that high glucose induced upregulation of Keap1 and downregulation of nuclear Nrf2 was abrogated by miR-29 mimic treatment (Fig.   6b). [score:7]
a Cells were transfected with miR-29 mimic and b miR-29 inhibitor as well as respective negative control (NC) for 48 h; miR-29 level, translational activity of Keap1 and expression of Keap1 mRNA and protein were determined. [score:7]
In diabetic rat, miR-29 was downregulated and its expression is negatively correlated with both of serum creatinine and creatinine clearance. [score:6]
In this present study, we observed that NF-κB activity was enhanced mediated by high glucose induced reduction of deacetylases activity of Sirt1, which leaded to downregulation of miR-29 and inhibition of Keap/Nrf2 signal. [score:6]
Relative protein band density was quantified by image J. To achieve alteration of expression of miR-29, cells were treated with miR-29 mimic or inhibitor with the negative control (NC) of nonsense strand using Lipofectamine (Invitrogen). [score:5]
We altered miR-29 expression by cell incubated with miR-29 mimic or inhibitor. [score:5]
NF-κB was demonstrated to regulate miR-29 expression by directly binding to its promotor. [score:5]
This data suggested an expressional regulation of miR-29 by NF-κB. [score:4]
While high glucose induced down regulation of miR-29 contributed to enhancement of Keap1 expression that finally reduced Nrf2 content by ubiquitinating Nrf2. [score:4]
This was further confirmed by qRT-PCR assay which showed that inhibition of NF-κB pathway by BAY 11-7082 treatment increased miR-29 expression in high glucose-triggered cell. [score:4]
Fig.  4NF-κB regulates miR-29 expression in high glucose-triggered HK-2 cells. [score:4]
Additionally, overexpression of miR-29 effectively relieved high glucose-reduced cell viability. [score:3]
One day later, cells were co -transfected with pGL4-TK-Luc-Keap1 (0.5 μg) with control of pGL-SV40 (internal control, 0.018 μg) and miR-29 mimic or inhibitor. [score:3]
b Western blot was performed to analyze expression of Keap1 and nuclear Nrf2 in 5.5 mM and 45 mM glucose-triggered HK-2 [miR−29mimic] cells To determine the role of miR-29 on high glucose triggered cell, cell viability was examined in HK-2 [miR−29 mimic] cell. [score:3]
Calculated Keap1 mRNA expression levels were normalized to the expression levels of GAPDH and relative miR-29 level was normalized to U6 of the same cDNA sample. [score:3]
Renal tubule was obtained from rats treated with STZ for 4, 8, 12, 16 weeks and lyzed for analysis of miR-29 expression. [score:3]
Overexpression of miR-29 enhanced cell viability. [score:3]
Notably, decreased expression of miR-29 by NF-κB signal has been described in cells and tissues [12, 13]. [score:3]
Due to description of decreased expression of miR-29 by NF-κB signal in cells and tissues [12, 13], we speculated that NF-κB/miR-29 axis might be involved in high glucose incubated renal cell. [score:3]
Level of miR-29 was significantly downregulated in cells incubated with 30 and 45 mM high glucose compared with cell treated with 5.5 mM normal glucose (Fig.   2c). [score:3]
As shown in Fig.   5b, level of miR-29 declined by 10 fold, binding activity of miR-29 and Keap1 promotor was boosted that leads to increase of the expression of Keap1 mRNA and protein. [score:3]
We attempted to figure out the target gene for miR-29. [score:3]
The data showed that high glucose promoted ubiquitination of Nrf2 whereas this promotion was reversed by overexpression of miR-29 (Fig.   6a). [score:3]
The data of luciferase assay showed that miR-29 directly targets to Keap1 mRNA. [score:3]
The correlation analysis demonstrated that abnormal miR-29 expression is negatively related to serum creatinine (Spearman correlation is −0.96, P = 0.000; Fig.   1d) and creatinine clearance (Spearman correlation is −0.93, P = 0.000; Fig.   1e). [score:3]
c miR-29 expression was determined. [score:3]
Fig.  7Effect of overexpression of miR-29 on cell viability in glucose-triggered HK-2 cell. [score:3]
b Cells were exposed to BAY 11-7082 for 2 h before 5.5 and 45 mM glucose treatment and miR-29 expression was determined. [score:3]
MiR-29 directly regulates Keap1. [score:2]
Fig.  6Ubiquitination of Nrf2 was regulated by miR-29/Keap1 axis in high glucose triggered HK-2 cells. [score:2]
In HK-2 [miR−29 mimic] cell, level of miR-29 was significantly increased by 12.9 fold, binding activity of miR-29 and Keap1 promotor was reduced and expression of Keap1 mRNA and protein was attenuated compared with pre-NC incubated cell (Fig.   5a). [score:2]
cell treated with 45 mM + pcDNA was performed to assess whether NF-κB directly binds to miR-29 gene in high glucose cultured HK-2 cell. [score:2]
The ChIP assay was carried out to detect the possible target miR-29 gene by p65. [score:2]
All cells were incubated with glucose for 48 h. To evaluate whether NF-κB regulates miR-29 expression in high glucose incubated HK-2 cell, the cells were pretreated with BAY11-7082 (5 μmol/L) (Sigma-Aldrich Co. [score:2]
These data indicated that miR-29 is involved in pathological process of diabetes and might function as one of modulatory factors. [score:1]
Renal tubular was obtained for detection of miR-29 level. [score:1]
As shown in Fig.   7, reduction of cell viability by high glucose was effectively enhanced by miR-29 mimic treatment. [score:1]
Among these, miR-29 is observed in diabetic patients [10] and also ameliorates hyperglycemia -induced renal dysfunction [11]. [score:1]
Notably, both miR-29 and NF-κB activity play vital roles in high glucose induced decrease of cell viability. [score:1]
pre-NC or NC To determine the downstream molecule of miR-29/Keap1 axis, we examined Nrf2, a nuclear transcriptional factor that commonly activated by Keap1, in 45 mM high glucose-triggered HK-2 [miR−29 mimic] cell. [score:1]
cell treated with 45 mM + pcDNA Chip assay was performed to assess whether NF-κB directly binds to miR-29 gene in high glucose cultured HK-2 cell. [score:1]
The data showed that miR-29 level was decreased in time -dependent manner after rat mo del of diabetes established (Fig.   1c). [score:1]
Level of microR-29 (miR-29) was assessed using quantitative RT-PCR. [score:1]
We made a prediction of the possible binding site in Keap1 3′ UTR by miR-29 and this was demonstrated by online bioinformatics analysis (data is not shown). [score:1]
Thus we speculated that NF-κB/miR-29 axis might be involved in high glucose incubated renal cell. [score:1]
Acetyl-p65 HK-2 miR-29 Nrf2 Serum creatinine Diabetes mellitus is a common metabolic disorder which is associated with chronic complications such as angiopathy, retinopathy, and peripheral neuropathy. [score:1]
In summary, our data suggested that high glucose induced renal tubular injury might be a process of a signal transduction pathway of Sirt1/NF-κB/miR-29/Keap1/Nrf2. [score:1]
Combination of p65 and miR-29 promotor was assessed using chromatin immunoprecipitation. [score:1]
NF-κB binds to miR-29. [score:1]
High glucose promotes ubiquitination of Nrf2 via miR-29/Keap1 axis. [score:1]
As shown in Fig.   4a, high glucose promoted association between p65 and miR-29 promotor in a manner of time dependent. [score:1]
To assess the correlation between the serum creatinine or blood urea nitrogen (BUN) and serum miR-29 level, the Spearman correlation coefficient was used. [score:1]
a Cells were stimulated with 5.5 and 45 mM glucose for 12, 24, 48 h and combination of p65 and miR-29 gene was examined using. [score:1]
Correlated analysis was performed to assess relationship between d miR-29 level and Serum creatinine as well as e miR-29 level and creatinine clearance. [score:1]
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[+] score: 150
We confirmed this by experimentally showing that a REST expressing plasmid curtailed the miR-29c promoter plasmid expression and this inhibitory effect was removed when the REST binding sites in the miR-29c promoter were mutated. [score:7]
As REST is a suppressor of gene expression, its low levels might allow high expression of miR-29c in normal adult brain. [score:7]
Following ischemia, down-regulation of miR-29c might derepress DNMT3a translation resulting in increased amounts of DNMT3a protein as observed in the present study. [score:6]
Our studies showed that miR-29c is one of the highly expressed miRNAs in rat brain that was down-regulated in a sustained manner during the acute phase (2 h to 3 days) after focal ischemia [3]. [score:6]
We crosschecked the target-miRNA relationship using DNMT3a as an input mRNA in Microcosm which showed that rat DNMT3a is targeted by only 2 miRNAs (rno-miR-29c and rno-miR-300-3p) of which rno-miR-300-3p was unaltered after MCAO [3]. [score:5]
We also observed that knocking-down DNMT3a protein with DNMT3a siRNA decreased infarction in vivo and cell death in vitro indicating that DNMT3a induction is a potential mechanism of miR-29c down-regulation mediated ischemic damage. [score:5]
Using TargetScan and Microcosm from MiRBase, we analyzed the targets of rat miR-29c. [score:5]
Transfection with a REST plasmid inhibited miR-29c promoter vector expression which was ablated by deletion of REST binding sites (A). [score:5]
These observations show that miR-29c is a prosurvival miRNA under physiological conditions and its down-regulation after ischemia is a promoter of cell death. [score:4]
Cotransfection with REST plasmid inhibited miR-29c promoter (2 Kb rat miR-29c promoter cloned in Promega promoterless pGL-3 basic vector) expression in PC12 cells by 62±5% compared to dominant negative (DN) REST plasmid transfected group (Fig. 4A). [score:4]
Thus, miR-29c might be essential for cell survival under homeostatic conditions and its down-regulation after ischemia is derogatory. [score:4]
As the in vitro studies showed that DNMT3a is a mediator of the miR-29c down-regulation induced ischemic cell death, we tested the role of DNMT3a in post-ischemic brain damage following transient MCAO. [score:4]
These studies confirm our previous microarray studies that showed miR-29c down-regulation after focal ischemia (Dharap et al., 2009). [score:4]
This indicates that the REST binding sites in the miR-29c promoter can control miR-29c expression. [score:3]
PremiR-29c had no effect on the expression of the DNMT3a 3′UTR mutant vector containing a point mutation in the miR-29c binding site compared to control miR treated group (B). [score:3]
Disruption of the miR-29c binding site completely abrogated the inhibition of luciferase activity by premiR-29c (Fig. 2B). [score:3]
We hypothesize that a highly expressed miRNA like miR-29c might play an essential role in maintaining the cellular homeostasis in adult brain and its dysfunction contributes to ischemic brain damage. [score:3]
DNMT3a is a miR-29c target. [score:3]
Based on our results we hypothesize that controlling DNMT3a might be a conserved function of a highly expressed miRNA like miR-29c that leads to brain damage if disturbed. [score:3]
The contribution of other targets of miR-29c to ischemic brain damage can't be ruled out from the present studies, but our data firmly establishes miR-29c as a prosurvival miRNA that is under REST control and disruption of the REST, miR-29c and DNMT3a homeostasis is one of the mediators of post-stroke brain death. [score:3]
REST curtailed miR-29c promoter expression. [score:3]
In PC12 cells, OGD -induced cell death was mediated by miR-29c down-stream target DNMT3a. [score:3]
This indicates that REST induction might be responsible for miR-29c suppression (and thus derepression of DNMT3a) leading to ischemic brain damage. [score:3]
Using real-time PCR, we presently observed that miR-29c was down-regulated by 5.8±1.1 fold in the ipsilateral cortex of rats subjected to transient MCAO and 12 h reperfusion compared to sham control (Fig. 3A). [score:3]
REST mediates miR-29c expression after ischemia. [score:3]
The miR-29c is one of the highly expressed miRNAs in rat brain. [score:3]
DNMT3a is one of the predicted miR-29c targets identified by both algorithms with a very high score and energy. [score:3]
As in silico analysis showed DNA methyltransfease 3a (DNMT3a) as a robust target of miR-29c, we tested the role of DNMT3a in mediating the post-ischemic effects of miR-29c. [score:3]
A DNMT3a 3′UTR mutant plasmid was generated by creating a point mutation in the miR-29c binding site using the Site-Directed Mutagenesis Kit (Invitrogen USA) as per manufacturer's instructions. [score:3]
In silico analysis showed high score and a low mean free energy for DNMT3a and miR-29c interaction indicating that DNMT3a is a robust target of miR-29c. [score:3]
We also observed that PC12 cells die if miR-29c is knocked-down with an antagomiR-29. [score:2]
Treatment with premiR-29c or DNMT3a siRNA decreased infarction after MCAOAs the in vitro studies showed that miR-29c down-regulation is a proponent of ischemic cell death, we evaluated if providing premiR-29c decreases focal ischemia -induced brain damage in vivo. [score:2]
As the in vitro studies showed that miR-29c down-regulation is a proponent of ischemic cell death, we evaluated if providing premiR-29c decreases focal ischemia -induced brain damage in vivo. [score:2]
Furthermore, knocking-down miR-29c promotes cell death under normal conditions. [score:2]
miR-29c and DNMT3a contributes to the development of focal ischemia -induced infarction in rat brain. [score:2]
The REST mutant plasmids which are 1.9 Kb and 1.1 Kb; lacking either 2 REST binding sites or all 3 REST binding sites showed ablation of the REST -mediated suppression of miR-29c promoter by 45 and 100%, respectively compared to DN REST transfected control (Fig. 4A). [score:2]
The sequences (5′–3′) of the amplified miRNA transcripts are AUU GGC UAA AGU UUA CCA CGA U(rno-miR-29c) and UGA GGU AGU AGG UUG UAU AGU U (rno-Let-7a). [score:1]
Treatment with premiR-29c (for 12 h) increased the post-OGD miR-29c levels by 3.6 fold over control premiR treated group (Table 1). [score:1]
The miR-29c promoter (2 Kb) and 2 mutants (1.9 Kb and 1.1 Kb; lacking REST binding sites) were amplified from rat brain genomic DNA and cloned in pGL-3 basic vector (Promega USA). [score:1]
We identified 3 binding sites for the transcription factor REST within 1 Kb from transcription start site (TSS) located at −2 to −32, −94 to −124 and −838 to −868 upstream from TSS on the same strand of the DNA from which miR-29c is transcribed. [score:1]
Our studies also showed that replenishing miR-29c with premiR-29c treatment significantly decreases the infarct volume after transient MCAO confirming the role of miR-29c as an endogenous pro-survival miRNA under in vivo conditions as well. [score:1]
To understand the factors that control miR-29c after ischemia, we analyzed the transcription factor binding sites in the miR-29c gene promoter using the Genomatix search algorithm (Genomatix GmbH). [score:1]
Bioinformatics showed 3 binding sites for the transcription factor REST in the miR-29c putative promoter within 1 Kb upstream to miR-29c coding region in the same strand of DNA from which miR-29c is transcribed. [score:1]
In other experiments, cells were transfected with pGL3-miR-29c promoter plasmid or one of the mutant pGL3-miR-29c promoter plasmids (that lack REST binding sites) together with pMT-REST or pMT-dominant negative REST (DN-REST). [score:1]
We further evaluated if repressor element 1 silencing transcription factor (REST) aka neuron-restrictive silencing factor (NRSF) controls miR-29c expression. [score:1]
PremiR-29c and REST siRNA treatment restored post-ischemic levels of miR-29c. [score:1]
Whereas, rats injected with premiR-29c, but not control miR, subjected to transient MCAO showed a complete recovery of miR-29c levels by 12 h of reperfusion (Fig. 3A). [score:1]
This suggests REST as a potential transcriptional controller of miR-29c. [score:1]
The miR-29c seed sequence of DNMT3a was shown in Fig. 2A. [score:1]
We observed that treatment with REST siRNA significantly increased the levels of miR-29c, curtailed DNMT3a protein induction and decreased the cell death following ischemia. [score:1]
The miR-29c promoter has 3 upstream binding sites within 1 Kb from TSS for the transcription factor REST. [score:1]
0058039.g004 Figure 4The miR-29c promoter has 3 upstream binding sites within 1 Kb from TSS for the transcription factor REST. [score:1]
Furthermore, transient focal ischemia led to a sustained silencing of miR-29c during the acute phase of reperfusion (2 h to 3 days) during which the cell death is on-going but can be prevented with timely intervention. [score:1]
The miR-29 seed sequence in the 3′UTR of DNMT3a mRNA (A). [score:1]
0058039.g002 Figure 2The miR-29 seed sequence in the 3′UTR of DNMT3a mRNA (A). [score:1]
Thus restoring miR-29c levels protects against OGD, while providing excess miR-29c had no effect under normal conditions. [score:1]
Our data support this hypothesis by showing that restoring miR-29c levels by treatment with premiR-29c is neuroprotective after ischemia. [score:1]
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[+] score: 149
As extracellular or cytoskeletal molecules are thought to be important in maintaining normal development, and their abnormal expression may cause pathogenesis, we chose Tm1α and 2β molecules, predicted targets of the miR29 family and used Western blot analysis to examine their protein expression in cell extracts isolated from LECs transfected with miR29a or 29c inhibitors (Fig. 4). [score:10]
These novel findings were further verified by expression inhibition and overexpression experiments using miR29c inhibitor and precursor respectively. [score:9]
Expression of Tm1α/2β protein was down-regulated in LECs following miR29c transfection, further demonstrating that miR29c may regulate and control Tm1α/2β gene expression. [score:9]
As shown in Figure 6A and B, when the luciferase gene carried 3′ UTR region of TM1α's transcript, the luciferase activity was inhibited by overexpressing miR29c compared with the negative control, but was not significantly inhibited by overexpressing miR29a (Fig. 6A). [score:8]
These data imply that miR29c may directly or indirectly regulate the translation of Tm1α and Tm2β. [score:6]
These data suggest that down-regulation of let7c, miR29a and miR29c, and miR126 may be a major event during cataract formation in the SCR, as changes in miRNA expression levels were increased in cataractous lenses. [score:6]
Rat TM1α3′-UTR, rat TM2β 3′-UTR was cotransfected with miExpress™ Precursor miRNA Expression Clone for rno-miR29a mimic or rno-miR29c mimics in pEZX-MR04 vector with eGFP reporter gene, Precursor miRNA scrambled control for pEZX-MR04 or empty pEZX-MR04 vector purchased from GeneCopoeia Inc. [score:5]
Relative expression of miRNAs let7b, let7c, miR-29a, miR29c and miR126, which are significantly up- or down-regulated during the progression of lens development, were measured following RNA extraction using RT-PCR. [score:5]
let7b, let7c, miR29b, miR29c and miR204 showed significant, gradual up-regulation (>2 times) after birth and during progression of lens development (ED16<4W<14W). [score:5]
We found very interesting molecules, Tm1α, which is a target of miR29c (Figs 6), as demonstrated by protein expression analysis. [score:5]
Although further work is necessary for a more precise definition of the processes involved, this initial delineation of the level of miRNA expression in lens provides a beginning, along with our identification of the specific miR29c and its target gene, Tms. [score:5]
We believe that optimizing the expression levels of Tms by manipulating the expression of miR29c may postpone or delay posterior cataract opacification (PCO), anterior subcapsular fibrosis (ASF) and severe nuclear cataracts resulting from overinduction of abnormal cellular changes such as fibrosis in LECs. [score:5]
These results suggest that Tm1α expression may be directly regulated by miR29c, not miR29a. [score:5]
Tm2β expression may be indirectly regulated by miR29c. [score:5]
To further determine whether miR29a or miR29c regulates Tm1α/2β expression, we transfected LECs isolated from cataractous SCRs with precursors (pre) of these miRNAs. [score:4]
These findings suggest that aberrant expression of miR29c during progression of lens development or cataract formation may be one cause of cellular abnormalities that in turn result in abnormal cellular organization or defective organogenesis, leading to age -associated degenerative disorders including cataractogenesis. [score:4]
On the other hand, when the luciferase gene carried 3′ UTR region of TM2β's transcript, the luciferase activity was not significantly inhibited by overexpressing miR29a and miR29c compared with the negative control (Fig. 6B). [score:4]
This regulation of miR29c may have effects in other disorders associated with aberrant Tms expression [37]. [score:4]
In protein blot, delivery of miR29c inhibitor to LECs significantly enhanced the abundance of Tm2β protein (Fig. 4). [score:3]
Direct regulation of miR29c to TM1α's transcripts. [score:3]
These experiments revealed that, indeed, Tm1α and Tm2β are targets of miR29c in lenses or LECs of SCRs without cataract and/or SCRs with cataract. [score:3]
This was the first demonstration that Tm1α is a target gene for miR29c, at least in lens. [score:3]
As shown in Figure 3, Let 7c, miR-29a and miR29c were up-regulated in non-cataractous LECs/lenses compared with cataractous. [score:3]
Cells were overexpressed with let7b, miR29a and miR29c by transfecting them with miRNA precursors. [score:3]
miR29c affects Tm2β by modulating the Tm2β translation (Fig. 4). [score:3]
2XUp  let-7b poly (ADP-ribose) polymerase family, member 3, Glutaredoxin-2, Fibroblast growth factor 20 (FGF-20), FGF -binding protein 1, Multiple EGF-like domains 6 precursor, Hsp70 -binding protein 1, IGF2 mRNA -binding protein 3, Myc proto-oncogene protein (c-Myc), Hsp70 -binding protein 1 (HspBP1), FGF receptor activating protein 1, Tumor protein p53-inducible nuclear protein 1, Vimentin, Thioredoxin mitochondrial precursor (Mt-Trx)  let-7c poly (ADP-ribose) polymerase family, member 3, Vascular endothelial growth factor C precursor (VEGF-C), FGF-20, IGF2 mRNA -binding protein 3, Glutaredoxin-2, NF-kappa-B essential modulator (NEMO) (NF-kappa-B essential modifier), Hsp70 -binding protein 1, c-Myc, Heat shock factor 2-bindlng protein, AQP-2, Tumor protein p53-inducible nuclear protein 1, Vimentin, Mt-Trx  miR-29a Tropomyosin alpha-1 chain (Tropomyosin-1) (Alpha-tropomyosin), glutathione peroxidase 7, PDGF B-chain, Dicer1  miR-29c Tropomyosin-1, Dicer1, TGF-beta-2, glutathione peroxidase 7, PDGF A-chain, Multiple EGF-like domains 6 precursor, FGF receptor–activating protein 1, SMAD 6, AQP-11  miR-204* Tropomyosin-1, Hsp70 -binding protein 1, Mitogen-activated protein kinase 4, Gamma crystallin D, IGFBP-1, Glutathione S-transferase P (GST class-pi), Sulfiredoxin 1 To predict genes targeted by miRNAs, Sanger miBase Software was utilized. [score:3]
However, let7c, miR-29a, miR29c and miR126 were significantly down-regulated in SCR with cataract lenses compared with SCR without cataract lenses at both ages 7 and 21 weeks. [score:3]
Relative expression levels of miRNAs, let-7b, let-7c, miR-29a, miR-29c, miR-204, miR-126, miR-451 in ED16, 4W and 14W lenses are represented as histograms with normalized averages ± SD. [score:3]
The increased expression of these molecules was inversely related to miR29 in LECs of SCRs with cataract. [score:3]
Figure 5 shows the expression levels of Tm1α/2β proteins in LECs transfected with miR29a and miR29c precursors isolated from SCR with cataract. [score:3]
Data revealed that let7c, miR29a and miR29c were significantly up-regulated in 21W lenses compared with 7W SCR without cataract (Cat−) or SCR with cataract (Cat+). [score:3]
Levels of let-7b, let-7c, miR-29a, miR-29c and miR-204 were dramatically altered during the progression of development. [score:2]
In parallel experiments, we used miR29a inhibitor, and found it ineffective compared with miR29c. [score:2]
Mouse lens epithelial cells were cotransfected with rat TM1α (A) or rat TM2β (B) with rno-miR29a mimic, rno-miR29c mimics in pEZX-MR04 vector with eGFP reporter gene, precursor miRNA scrambled control for pEZX-MR04 or empty pEZX-MR04 vector. [score:1]
The seven miRNAs (let7b, 7c, miR29a, miR-29c, miR204, miR126, miR51) listed in Table 3 were used for validation experiments. [score:1]
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[+] score: 146
Conversely, upregulation of miR-29 levels was observed after stimulation of HSC with the antifibrotic mediator HGF (Figure 8), previously shown to inhibit expression of various collagens [21], [48], [49]. [score:8]
Upregulation of miRNA-29 by HGF and downregulation by TGF-β take part in the anti- or profibrogenic response of HSC, respectively. [score:7]
Indeed, our in vitro data reveal a definite inhibition of collagen type IV, that is the most upregulated collagen form in the fibrotic liver [6], by miR-29. [score:6]
Whereas TGF-β stimulation leads to decreased miR-29 levels, but to pronounced upregulation of collagen synthesis, HGF stimulation leads to elevated miR-29 expression, but to repression of collagen synthesis. [score:6]
However, overexpression of miR-29 in myofibroblastic HSC did not affect the expression of SMA (Figure S1 D). [score:5]
Together, these data demonstrated that miR-29 specifically inhibits transcription and protein expression of collagen I and IV. [score:5]
After demonstrating that repression of the collagen-inhibiting miR-29 is an important downstream TGF–β effect, we studied if miR-29 overexpression can overcome the profibrogenic features mediated by TGF-β such as col1A1 induction. [score:5]
TGF-β treatment resulted in highly increased col1A1 expression in HSC cells treated with scrambled miRNA or with antago-miR-29, but only a moderate col1A1 induction in miR-29 overexpressing HSC after transfection with ago-miR-29. [score:5]
Therefore, miR-29 expression appears to be reciprocally regulated by profibrogenic (TGF-β) and antifibrogenic growth factors (HGF) in HSC, suggesting that miR-29 occupies a central role in responding to the antagonistic actions of HGF and TGF-β in regulating collagen synthesis in activated and transdifferentiated HSC. [score:5]
In agreement with the data on rat HSC, miR-29 is repressed by TGF-β, but upregulated by HGF (Figure S2). [score:4]
While miR-29 and HGF expression was significantly reduced (C,D), hydroxyproline and collagen mRNA were signifcantly increased in BDO livers (B) (*: p<0.05 **:p<0.01; ***: p<0.001). [score:3]
Since miR-29 is thought to be involved in modulating expression of extracellular matrix components (Table S3) [30], [31], [32], [34], this makes them promising candidates for collagen I and IV repression after HGF stimulation of HSC. [score:3]
Keeping with the antifibrotic function of miR-29, miR-29 is reduced in liver biopsies after liver intoxication in mice and after chronic liver disease in humans [35]. [score:3]
Figure S2 miR-29 expression in human skin fibroblasts after stimulation with HGF. [score:3]
Thus, whereas TGF-β stimulation leads to a reduction in miR-29 expression and de-repression of collagen synthesis, stimulation with HGF was definitely associated with highly elevated miR-29 levels and markedly repressed collagen-I and -IV synthesis. [score:3]
In order to analyze if other features of myofibroblastic transition were affected by miR-29, we determined SMA expression in miR-29 treated HSC, because increased SMA assembly is one of the most important features of myofibroblastic transition (Figure S1 A). [score:3]
Diminished effect of TGF-β on col1A1 expression in miR-29 treated HSC. [score:3]
Overexpression of miR-29 can overcome TGF-β mediated induction of col1A1. [score:3]
Table S3 Ranking list of putative collagen targets from miR-29*. [score:3]
Therefore, in addition to collagen-1, the collagen-4 mRNA could be an important target of miR-29 in HSC after HGF stimulation. [score:3]
Next, we induced experimental fibrosis by bile duct occlusion (BDO) in rats and studied the miRNA-29 expression during liver fibrogenesis. [score:3]
Thus, our findings convincingly demonstrate that HGF mediates antifibrotic signals by influencing miR-29 expression and thereby counteracting the profibrotic activity of TGF-β. [score:3]
Reciprocal expression of the collagen subunits, col1A1 and col4A2, and primary and mature miR-29. [score:3]
Consistent with the antifibrogenic and inhibitory function of miR-29 in collagen I and IV synthesis and the increase of col1A2 and col4A2 (Figure 7 B), we observed a significant reduction in hepatic miR-29a and miR-29b levels in this experimental BDO mo del (Figure 7 C). [score:3]
Contrary effects of HGF and TGF-β on miR-29 expression in HSC. [score:3]
Insertion of the miR-29 binding sites (wt), but not with mutated binding site (mu), resulted in reduced reporter gene expression by miR-29a treated HSC (A–D). [score:3]
Among the putative miR-29 binding sites of the collagen mRNA (shown in the Table S4), the following sites were chosen for our further analyses, due to the suggestions of Bartel et al. [50] to function most likely as an inhibitory miR-29 interaction sequence: the region of positon 29–35 in the col4A1 3′-UTR, of postion 404–410 in the col4A5, positon 903–909 in the col1A1, and of position 506–512 in the col1A2 3′-UTR (Table S4). [score:3]
miR-29 synthesis in HSC is suppressed by TGF-β, but promoted by HGF. [score:3]
In the present study, we now collect evidence that in response to the counteracting HGF / TGF-β signals the miR-29 levels in HSC are contrarily regulated. [score:2]
To demonstrate the specificity of miR-29 for the binding sites, in the 3′-UTRs two point mutations were incorporated to abolish the putative miR-29 recognition sequences of the collagen-4 mRNA (col4A1, col4A5) and collagen-1 transcripts (col1A1 and col1A2). [score:2]
These findings are in agreement with the data of Du et al. [33] and recent reports showing the miR-29 regulation of elastin, fibullin and collagen I synthesis [30], [31], [32], [34], [35]. [score:2]
The interaction of miR-29 with 3′-untranslated mRNA regions (UTR) was analyzed by reporter assays. [score:2]
Putative miR-29 binding sites in the collagen col1A1 (A), col1A2 (B), col4A1 (C) and col4A5 (D) 3′-UTR (wt) and the corresponding mutated sequences (mu) carrying two point mutations (bold and underlined) were cloned into psiCHECK [TM]-2 vector. [score:2]
0024568.g005 Figure 5Putative miR-29 binding sites in the collagen col1A1 (A), col1A2 (B), col4A1 (C) and col4A5 (D) 3′-UTR (wt) and the corresponding mutated sequences (mu) carrying two point mutations (bold and underlined) were cloned into psiCHECK [TM]-2 vector. [score:2]
Strikingly, all of the collagen-1 and -4 transcripts contained binding sites for members of the miRNA-29 family in their 3′UTR (Table 1). [score:1]
Furthermore, our in vitro and in vivo studies on HSC or on BDO -treated fibrotic livers, respectively, suggest that the loss of miR-29 in HSC after TGF-β exposure and during liver fibrogenesis leads to the abolishment of collagen type I and IV repression. [score:1]
For this purpose, HSC-T6 cells were transfected with miR-29a mimics (ago-miR29a) in comparison to scrambled or miR-29-silencing miRNA (antago-miR-29). [score:1]
We therefore studied the influence of HGF and TGF-β on the miR-29 collagen axis in HSC. [score:1]
Recently, miR-29 has been reported to be involved in ECM synthesis. [score:1]
0024568.g009 Figure 9 The myofibroblastic HSC-T6 cells were transfected with scrambled miRNA, miR-29 mimic (ago-miR-29), or with a miR-29 silencer (antago-miR-29). [score:1]
miR-29 interaction with the 3′-UTR of col4A1 and col4A5 transcripts. [score:1]
The synthesis of extracellular matrix proteins is modulated by microRNA-29 (miR-29) in extrahepatic tissue [30], [31], [32], [33]. [score:1]
The genes for miR-29a and miR-29b [1] are both located on chromosome 7, whereas the genes for miR-29c and miR-29b [2] are located on chromosome 1. Each gene pair is transcribed in tandem resulting in a common pri-miRNA from which the mature miR-29 members are released after further processing [36], [37]. [score:1]
The miR-29 family consists of miR-29a, miR-29b (b [1], b [2]), and miR-29c, which differ in only two or three nucleotides, respectively. [score:1]
Thus, our data provide detailed evidence for the antifibrotic action of miR-29 in response to HGF signalling that is counteracted by the profibrotic growth factor TGF-β. [score:1]
Recent reports suggest that miR-29 is also involved in the synthesis of collagen type I in liver fibrosis [34], [35]. [score:1]
In order to study miR-29 function in collagen synthesis, we inserted the 3′-UTR sequences downstream of a luciferase reporter (Figure 4 A). [score:1]
Conversely, a decrease in miR-29 levels is observed during collagen accumulation upon experimental fibrosis, in vivo, and after TGF-β stimulation of HSC, in vitro. [score:1]
The myofibroblastic HSC-T6 cells were transfected with scrambled miRNA, miR-29 mimic (ago-miR-29), or with a miR-29 silencer (antago-miR-29). [score:1]
The repressive effect of miR-29 on collagen synthesis was studied in HSC treated with miR-29 -mimicks by Real-Time PCR and immunoblotting. [score:1]
We demonstrate that miR-29 is not only involved in collagen type I but also in type IV synthesis of myofibroblastic HSC. [score:1]
The 3′-UTR of the collagen-1 and −4 subtypes were identified to bind miR-29. [score:1]
The importance of miR-29 in hepatic collagen homeostasis is underlined by our in vivo data that shows the lack of miR-29 in severe experimental fibrosis after bile duct obstruction. [score:1]
This loss of miR-29 is suggested to be due to the response of HSC to exposure to profibrogenic mediators as shown by our in vitro findings on TGF-β stimulated HSC. [score:1]
The level of miR-29 transfected into HSC-T6 cells was analyzed by Real-Time PCR, demonstrating stable levels between 8 h and 48 h post-transfection. [score:1]
In this respect, the members of the miR-29 family are the most promising candidates because they are repressed during myofibroblastic transition and they hold highly conserved binding sites in the 3′-UTR of the various subunits of collagen 1 and 4 (Table 1). [score:1]
The reduced levels of miR-29 during fibrosis are associated with an increase of extracellular miR-29 in serum depending on the fibrotic stage (manuscript in preparation). [score:1]
Table S4 Putative binding sites of the members of the miR-29 family to the 3′-UTR of different collagens. [score:1]
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[+] score: 84
Although there are presumably additional targets regulated by miR-29 and miR-203, our experiments suggest that VEGFA suppression is mediated, at least in part, by overexpression of these miRNAs. [score:8]
Relative expression levels of miR-29 family members (A) and miR-203 (B) in isolated (ISO) rats are in comparison to control levels expressed as 1 on the graph. [score:5]
These data suggest that overexpression of miR-29 and miR-203 contributes to isolation -induced delays of wound healing, partially by suppressing VEGFA. [score:5]
0072359.g004 Figure 4(A) The predicted miR-203 and miR-29 targeting sequences located in the 3’-untranslated region (3’-UTR) of VEGFA mRNA. [score:5]
Cells were co -transfected with constructs containing the predicted targeting sequence (WT) or mutated targeting sequence (Mutant) cloned into the 3’-UTR of the reporter gene, along with miRNA mimics of miR-29 or miR-203. [score:5]
Based on bioinformatics analysis, a highly conserved miR-29 isoform -targeting sequence and a miR-203 -targeting sequence were identified in the VEGFA mRNA 3’ UTR (Figure 4A). [score:5]
miR-29a, miR-29c (Figure 4B) and miR-203 (Figure 4C) significantly reduced activity of firefly luciferase by directly targeting the rat VEGFA 3′ UTR. [score:4]
MiR-203 and miR-29 directly target VEGFA mRNA. [score:4]
As shown in Figure 4D, ectopic transfection of miR-29a, miR-29c and miR-203 in HEK293 cells led to a significant decrease in VEGFA protein expression. [score:3]
Expression of miR-29 family members, miR-203 and SOCS3 mRNA in wounded tissues by qRT-PCR. [score:3]
In this study, VEGFA was the only healing -associated mRNA targeted by miR-29 and miR-203 (out of the nine that were tested). [score:3]
0072359.g003 Figure 3 Expression of miR-29 family members, miR-203 and SOCS3 mRNA in wounded tissues by. [score:3]
In accordance with these findings, our results demonstrate that miR-29 family members and miR-203 were persistently overexpressed across healing in isolated rats. [score:3]
Furthermore, co-transfection of miR-29c and miR-203 mimics produced an additive effect on reducing VEGFA expression in vitro. [score:3]
For functional analysis, miR-29 (a, b, c) mimics, miR-203 mimics and non -targeting miRNA mimics (Dharmacon, Lafayette, CO, USA) were transfected into cells using DharmaFECT Transfection Reagent 1 (Dharmacon) per the manufacturer’s instructions. [score:3]
Reduced expression of miR-29 family members was recently reported in different fibrotic organs [31- 33]. [score:3]
MiR-29 is a typical multifunctional miRNA which is involved in regulating the epithelial-mesenchymal transition, cellular differentiation, extracellular matrix remo deling, and angiogenesis [29, 30]. [score:2]
Mutation of the putative miR-203 binding site abolished the effect of miR-203 while leaving the action of all three miR-29 isoforms unaffected (B). [score:2]
Similarly, mutation of the putative miR-29 site led to abolishing the action of the miR-29 isoforms (Figure 4C). [score:2]
Intriguingly, both miR-29 and miR-203 are important regulators of wound-specific cell functions and the cytokine network [38, 39]. [score:2]
Similarly, mutation of the putative miR-29 binding site abolished the action of the miR-29 isoforms (C). [score:2]
As expected, mutation of the putative miR-203 binding site abolished the effect of miR-203 while leaving the action of all three miR-29 isoforms unaffected (Figure 4B). [score:2]
In this study, we hypothesized that social isolation delays oral mucosal wound healing, and healing -associated genes and miRNAs (i. e., miR-29 and miR-203) play a role in this process. [score:1]
Isolation Stress and Levels of miR-29 and miR-203. [score:1]
Considering the important role of miR-29 and miR-203 in both dermal and mucosal repair, these results suggest a putative mechanism for isolation -induced healing impairments through the modulation of VEGFA. [score:1]
This suggests there are novel roles of miR-29 and miR-203 in isolation-impaired healing. [score:1]
Intriguingly, the isolated rats persistently exhibited higher levels of miR-29 family members and miR-203. [score:1]
To test this, we selected and determined the levels of two miRNAs in wounds: miR-29 and miR-203. [score:1]
In both the putative miR-29 and miR-203 binding sites, the 6 to 8 nucleotides of the “seed region” were replaced with a restriction enzyme site with minimal complementarity to the miRNA sequence (see Materials and). [score:1]
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[+] score: 57
Our results show that obesity -induced pathological cardiac remo deling leads to an increase in cardiac pathological hypertrophy markers and downregulation of microRNA-29c expression, which can be associated with the increase in the LV collagen volumetric fraction. [score:6]
In contrast, AET restored the pathological expression of microRNA-1 and microRNA-29c and their target genes, which likely counteracted the pathological cardiac remo deling and cardiac dysfunction in obesity. [score:5]
Studies have shown that AET increases microRNA-29 expression in the heart and consequently decreases collagen expression and protein levels [24, 25]. [score:5]
To confirm the involvement of obesity-regulated microRNAs in pathological CH, we analyzed the cardiac microRNA-29 family (microRNA-29a, microRNA-29b and microRNA-29c), whose expression affects collagen content. [score:4]
In conclusion, obesity downregulated microRNA-29c in OZR possibly leading to increased cardiac collagen content. [score:4]
Our study demonstrates for the first time that AET was efficient in restoring the microRNA-1 and microRNA-29c to nonpathological levels in obesity, as well as its targets NCX1 and collagen, respectively. [score:3]
The LV interstitial collagen volumetric fraction (CVF) was inversely proportional to the microRNA-29c expression level. [score:3]
Previous data reported by our group showed that physiological CH induced by different amounts of AET is related to reduced cardiac collagen expression via elevated cardiac microRNA-29c levels in healthy rats [24]. [score:3]
Animals trained on a higher intensity protocol presented an increase of 123% in microRNA-29c expression and decreases of 33% and 48% for COLIAI and COLIIIAI, respectively [24]. [score:3]
AET resulted in microRNA-29c expression in the OZR + TR group approaching control levels (LZR: 100 ± 16.2%; LZR + TR: 92 ± 6.1%; OZR: 43 ± 4.7%; and OZR + TR: 118 ± 24.2%) (Figure 4(c)). [score:3]
Soci et al. [24] demonstrated that different intensities of swimming training lead to different magnitudes in the expression of microRNA-29c levels. [score:3]
Animals trained on the same protocol as the current study showed that the microRNA-29c levels decreased by 52% and that COLIAI and COLIIIAI expressions decreased by 27% and 38%, respectively. [score:3]
The relative expression of COLIAI, COLIIIAI, ANF, α-MHC, α-actin skeletal, β-MHC, microRNA-1, microRNA-29a, microRNA-29b, and microRNA-29c was analyzed using real-time polymerase chain reactions (real-time PCR) as described previously [24]. [score:3]
Thus, AET was able to normalize cardiac microRNA-29c expression and CVF in OZR + TR, and these results suggest that AET has a cardioprotective effect against pathological CH as shown in Figure 8. In our previous study, although there was no statistical difference (p = 0.07), a 25% reduced time E/A wave ratio was found when OZR was compared with untrained LZR [4], suggesting damage in the contractile myocardium. [score:2]
In the present study, obesity decreased the cardiac microRNA-29c expression in OZR by 47% compared with LZR, which induced an increase in the cardiac CVF. [score:2]
The microRNA-29 family has been described to negatively regulate collagen content and to be highly responsive to AET [22, 24, 25]. [score:2]
Thus, further studies are needed to assess whether modulation of the microRNA-1 and microRNA-29c in vivo in the obesity phenotype would play a key role in preventing pathologic cardiac remo deling. [score:1]
In addition, Melo et al. [25] showed that AET restored the levels of microRNA-29c in infarcted rats, contributing to a reduction in cardiac collagen content. [score:1]
MicroRNA-29c expression was decreased in the OZR group compared with LZR, LZR + TR, and OZR + TR. [score:1]
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[+] score: 50
For instance, during postnatal aortic development, miR-29 was found to be differentially expressed to downregulate elastin [14]. [score:7]
Last but not least, in a very recent study [30], a comparison of miRNA expression profile between the dermis tissues of the young and elderly revealed that, several miRNAs, including miR-29, were upregulated in aged dermis. [score:6]
In cells haploinsufficient for elastin and in bioengineered vessels, inhibition of miR-29 could increase elastin expression levels [15]. [score:5]
Rats were assigned into six experimental groups (n = 12 each): (1) control, sham-operated rats to serve as healthy control; (2) PFD, vaginal distention was performed on the rats to induce PFD symptoms, and saline was injected 2 weeks after the operation; (3) BMSC (control) + bFGF, PFD rats were injected with control BMSCs and free bFGF 2 weeks after the operation; (4) BMSC (control) + PLGA-bFGF, PFD rats were injected with control BMSCs and bFGF -loaded PLGA 14 days after the operation; (5) BMSC (anti-miR-29) + bFGF, PFD rats were injected with miR-29a-3p -inhibited BMSCs and free bFGF 2 weeks after the operation; (6) BMSC (anti-miR-29) + PLGA-bFGF, PFD rats were injected with miR-29a-3p -inhibited BMSCs and bFGF -loaded PLGA 2 weeks after the operation. [score:5]
Four different in vitro cultures were established: (1) BMSC (control) + bFGF, control BMSCs with 20 ng/ml free bFGF; (2) BMSC (control) + bFGF-PLGA, control BMSCs with 20 ng/ml equivalent bFGF -loaded PLGA NPs; (3) BMSC (anti-miR-29) + bFGF, miR-29a-3p inhibited BMSCs with 20 ng/ml free bFGF; (4) BMSC (anti-miR-29) + bFGF-PLGA, miR-29a-3p -inhibited BMSCs with 20 ng/ml equivalent bFGF -loaded PLGA NPs. [score:5]
Downregulation of elastin by miR-29 family miRNAs has been wi dely reported. [score:4]
from the above studies consistently point to an important role of miR-29, miR-29a-3p in particular, in our current work, in regulating the expression of elastin in the mammalian system, including BMSCs. [score:4]
Recently in a study performed in vascular smooth muscle cells, miR-29 -mediated elastin downregulation was found to contribute to osteoblastic differentiation induced by inorganic phosphorus [16]. [score:4]
[##] P < 0.01 vs BMSC (control) + bFGF-PLGA and BMSC (anti-miR-29) + bFGF We next established a rat PFD mo del to test the effect of miR-29a-3p -inhibited BMSC transplantation on PFD symptoms in vivo. [score:3]
Importantly in rats receiving injections of miR-29a-3p -inhibited BMSCs, the decreased void volume and bladder void pressure were both rescued (Fig.   6b and c, fifth and sixth columns), with defects in BMSC (anti-miR-29) + bFGF-PLGA group rats almost completely restored to similar levels of the sham-operated control rats (Fig.   6b and c, sixth column). [score:3]
[$] P < 0.05 vs PFD, BMSC (control) + bFGF, BMSC (control) + bFGF-PLGA and BMSC (anti-miR-29) + bFGF from the LPP test displayed a very similar pattern. [score:1]
[$] P < 0.05 vs PFD, BMSC (control) + bFGF, BMSC (control) + bFGF-PLGA and BMSC (anti-miR-29) + bFGF Results from the LPP test displayed a very similar pattern. [score:1]
[$$] P < 0.01 vs PFD, BMSC (control) + bFGF, BMSC (control) + bFGF-PLGA and BMSC (anti-miR-29) + bFGF Taken together, regardless of bFGF source, transplant of control BMSCs did not exhibit any alleviating effect on the PFD rats. [score:1]
[$$] P < 0.01 vs PFD, BMSC (control) + bFGF, BMSC (control) + bFGF-PLGA and BMSC (anti-miR-29) + bFGF Taken together, regardless of bFGF source, transplant of control BMSCs did not exhibit any alleviating effect on the PFD rats. [score:1]
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[+] score: 46
Interestingly, ZL-F had higher cardiac Med13 expression than ZL-M. (d– f) Graphs show qRT-PCR data on the expression of cardiac microRNA miR-29a, b and c. Expression of all miR-29 family miRNAs were increased in ZDF-F and ZDF-M. miR-29c was the most differentially expressed miRNA between male rats (f) whereas miR-29b was the most differentially expressed miRNA between female rats (e). [score:11]
Since increased expression of miR-208a is associated with cardiac hypertrophy, the female-specific increase in cardiac miR-208a expression could have contributed to the increased susceptibility to cardiac hypertrophy in ZDF-F. Increases in the circulating levels of miR-29 family miRNAs in children with T1DM and adults with T2DM 42, 43 emphasize the clinical relevance of this biomarker in DM. [score:5]
DM -associated dysregulation of miR-208a-MED13 signaling and increase in miR-29 family miRNAs occur in both male and female ZDF rats, however, only ZDF-F rats exhibited myocardial damage indicating that cardiac repair is impaired in ZDF-F. It is conceivable that the higher expression of cardio-reparative Agtr2 in ZL-F compared to ZL-M (Fig.   9a) could have provided increased protection despite the higher expression of pro-hypertrophic miR-208a in ZL-F heart compared to ZL-M heart. [score:4]
Here we show for the first time that while all miR-29 family miRNAs increased in response to diabetes in both sexes, there was a sex difference in their expression patterns. [score:3]
Thus, increases in the expression levels of the individual DM -associated miR-29 isoforms are also largely dependent on sex. [score:3]
Cardiac miR-29 family miRNA expression patterns are different in male and female diabetic rats. [score:3]
Thus, there were sex differences in miR-29 family miRNA expression. [score:3]
Cardiac expression of AT2R (Agtr2), Med13, miR-208a, and miR-29 family miRNAs were determined using mRNA and miRNA isolated from frozen heart tissues as described previously [44]. [score:3]
Figure 9Expression patterns of cardioprotective Agtr2 and Med13, and cardio- deleterious miR-208a and diabetic marker miR-29 family miRNAs in heart tissues of 5-month old healthy and diabetic, male and female rats. [score:3]
Cardiac expression of all members of the miR-29 family increased in both ZDF-F and ZDF-M compared to ZL-F and ZL-M (Fig.   9d–f, p < 0.05). [score:2]
Given the critical role of miR-29 in both DM and cardiac structure, we compared the cardiac expression of miR-29a, b and c between our groups. [score:2]
We previously showed that increased miR-29 family miRNAs correlate with DM -induced cardiomyocyte disorganization [44]. [score:1]
We showed that elevated miR-29 family miRNAs correlate with increased cardiomyocyte disarray in 15-week old ZDF-M [44]. [score:1]
miR-29b is implicated in the development of early aortic aneurysm [68], whereas miR-29c is considered as a signature molecule of hyperglycemia [69]. [score:1]
Members of the microRNA miR-29 family (miR-29a, b, and c) serve as mechanistic biomarkers for diabetes (T1DM and T2DM) and cardiovascular damage. [score:1]
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[+] score: 34
The findings illustrated that fish oil may restore the expression of circadian clock-related Per3 via inhibiting the WD -induced overexpression of rno-miR-29c and that FOH upregulated the expression of rno-miR-328, possibly resulting in the inhibition of Pcsk9. [score:14]
Our findings indicated that fish oil feeding reduced the expression of rno-miR-29c and increased the expression of rno-miR-328 and rno-miR-30d in FOH group, and target regulated the expression of Per3, Pcsk9, and Socs1, respectively. [score:10]
The results showed that fish oil feeding inhibited the expression of rno-miR-29c and stimulated the expression of miR-30d and miR-328, where all were consistent with our miRNA transcriptomic results. [score:7]
The expression of rno-miR-29c, rno-miR-328, and rno-miR-30d in WD, FOH, and CON groups was further examined using qRT-PCR to validate the findings of comparative miRNA sequencing. [score:3]
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[+] score: 33
In addition, accumulating evidence suggests that miR-29 downregulation inhibits dilation of aneurysms and is helpful in an early fibrotic response at the aortic wall by increasing target gene expression in murine mo dels of experimental aneurysms and human aneurysm tissues [29]. [score:10]
In recent years, some studies have reported that miR-29 is a novel diagnostic biomarker and therapeutic target for cancer, because it plays an important role in angiogenesis, invasion, and metastasis of tumors by regulating MMP2 expression [30]. [score:6]
Furthermore, all members of the miR-29 family were downregulated in myocardial tissue adjacent to the infarct and during cardiac fibrosis after acute myocardial infarction in mice and humans [28]. [score:4]
The miR-29 family (miR-29a, miR-29b-3p, and miR-29c) has been previously implicated in multiple pathological changes in cardiovascular diseases. [score:3]
), as shown in Figure 2. These data suggested that miR-29 may be involved in vascular calcification through mediation of MMP2 expression. [score:3]
To further characterize the mechanisms involving miR-29b-3p -mediated MMP2 expression, a luciferase assay was performed to determine whether miR-29 can directly target MMP2. [score:3]
The rat miR-29 family includes three members: miR-29a, miR-29b-3p, and miR-29c, whose dysregulation has been reported in many studies. [score:2]
In addition, the miR-29 family is involved in aneurysm development by mediating extracellular matrix protein synthesis, including Col1a1, Col3a1, Col5a1, and Eln. [score:2]
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[+] score: 33
Based on the finding that the miR-29 family is expressed in the rat retina [14] and that one miRNA has several targets, we hypothesize that miR-29b could regulate the genes in the pro-apoptotic pathways that are involved in the apoptosis of the retinal neurons of STZ -induced diabetic rats. [score:6]
The computational prediction programs suggested that RAX is a target of the miR-29 family (miR-29a, miR-29b, and miR-29c), and miR-29b showed the highest score of prediction. [score:3]
A: The firefly luciferase reporter construct (pISORAX plasmid) contains a partial-length 3′-UTR of RAX mRNA in the 5′ to 3′ orientation with respect to the firefly-luc open reading frame with the firefly luciferase start and stop codons and the potential miR-29 target site. [score:3]
The results of the computational analysis indicated that one of the miR-29 targets is RAX mRNA. [score:3]
The expression profiles of miR-29a and miR-29c were similar to that found for miR-29b (data not shown). [score:3]
The firefly luciferase start and stop codons and the potential miR-29 target site are also shown. [score:3]
The localization of the binding sites of these paralogs of miR-29 to on the RAX 3′-UTR overlap, and there is only a single target site on RAX for each miRNA studied. [score:3]
We found that the three paralogs of miR-29 (miR-29a, miR-29b, and miR-29c) have a complementary sequence to the seed sequence on RAX with minor divergences (Figure 3B), suggesting that the three paralogs potentially target RAX mRNA. [score:3]
The retinas were dissected and used either for the analysis of RAX mRNA and miR-29 expression and protein analysis or processed for in situ hybridization and immunofluorescence. [score:3]
The bioinformatic algorithms TargetScan, miRanda, and FindTar were used to predict miR-29 binding sites in the 3′-UTR of RAX mRNA. [score:3]
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[+] score: 32
HL-1 atrial cardiomyocytes transfected with miR-29 and miR-200 (Fig 8) significantly down-regulate Cacna1c, Hnc4 and Ryr2 expression, while Camk2a was significantly decreased with miR-200 but not miR-29 (Fig 8). [score:6]
miR-29 over -expression in HL1 atrial cardiomyocyte deregulate Cacna1c, Hnc4 and Ryr2, influencing therefore both the calcium handling and pacemaker activity, whereas miR-200 regulated Cacna1c, Ryr2 and Camk2a, in addition to Scn5a as previously reported [64], impacting therefore also in calcium handling. [score:5]
Observe that miR-29 and miR-200 over -expression leads to significant decreased of Cacna1c, Hcn4, Ryr2 and Camk2a (except for miR-29a) expression. [score:5]
We provide herein evidences that miR-29 and miR-200 over -expression also contributes to ion channel expression remo deling. [score:5]
Thus these data demonstrate that miR-29 and miR-200 impaired expression also contributes to develop pro-arrhythmogenic substrates. [score:3]
We have previously demonstrated that Pitx2 modulates expression of miR-29 and miR-200, among other microRNAs [16] and furthermore we have demonstrated in this study that modulation of distinct ion channel is greatly influenced by H [2]0 [2] administration while microRNA signature is mostly dependent on Pitx2c but not H [2]0 [2] administration. [score:3]
Whereas it is wi dely documented that redox signaling can compromise ion channel functioning and calcium homeostasis in cardiomyocytes [67], in our system we observed no influence of H [2]O [2] administration on the regulatory impact of Pitx2 in distinct ion channels such as Scn5a, Kcnj2 and Cacna1c as well as multiple Pitx2-regulated microRNAs such as miR-1, miR-26, miR-29 and miR-200, in which redox impairment impact is less documented [68]. [score:3]
Importantly, miR-29 and miR-200 are not significantly impaired in SHR atrial chambers, suggesting that Wnt-microRNA might be a pivotal candidate establishing fundamental differences between HTD and HTN in atrial arrhythmogenesis susceptibility. [score:1]
Modulation of miR-29 and miR-200 alters cardiac action potential determinants. [score:1]
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[+] score: 27
We demonstrate that either miR-200c or miR-29c can down-regulate the expression of Klf4. [score:6]
0125153.g009 Fig 9(A) Log2 plots of microarray and qPCR expression profiles for miRNAs and their predicted target genes: miR-214, and Xbp1; miR-29c, miR-200c and Klf4; and miR-30a, miR-200a, and Sox11. [score:5]
As development proceeds, the observed increases of miR-29c, miR-375, miR-148, and miR-200c may drive the observed decreased expression of Klf4 mRNA. [score:4]
Klf4 does not decrease in expression until late in postnatal development when miR-29c increases. [score:4]
This includes miR-29c, which has been shown to regulate Klf4 expression in breast cancer cells. [score:4]
Fig 9A shows the Log2 relative expression of miR-29c during acinar differentiation compared to that of Klf4 mRNA. [score:2]
Transfection experiments confirmed repression of rat Klf4 by miR-29c (Fig 9B). [score:1]
Loss of miR-29c in those cells results in dedifferentiation due to Klf4, leading to a population of stem-like cells [57]. [score:1]
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[+] score: 25
The miR-29 family members are induced by estrogen and reduce fibrosis by inhibiting expression of collagens [43]. [score:5]
The role of the miR-29 family, including miR-29b, in fibrosis disease has been recently reviewed and additional targets appear to be collagens [59]. [score:5]
In addition, the miR-29 family members appear to play a significant role in the development of liver fibrosis, possibly through the regulation of collagen expression [59]. [score:5]
The expression of six (miR-29a, miR-29b, miR-29c, miR-34a, miR-375, and miR-466b-2*) was altered in both males and females (Table  1). [score:3]
As rats mature from adults to old-age, miRNAs involved in cell death, cell proliferation, and cell cycle (miR-29 family and miR-34a) were found to change expression. [score:3]
The miR-29 family and miR-34a, whose expression was altered in both older males and older females, are relatively well-studied miRNAs, and their roles in cell proliferation and apoptosis are established [75, 76]. [score:3]
In addition, miR-29 family members may be involved in susceptibility to fibrosis. [score:1]
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[+] score: 22
For the microRNAs that were downregulated at 3 dpo, miR-29c and miR-107 were significantly repressed in the injured animals compared only to the control group, whereas miR-219-5p was significantly downregulated in comparison to both the control and the sham groups. [score:6]
Moreover, the downregulation of miR-29, which is a modulator of ECM homeostasis [106], may induce the overexpression of key pro-regenerative matrix molecules, such as laminin, collagen, and fibronectin. [score:6]
Similarly, we analyzed proapoptotic miR-29c, which regulates p53 -mediated apoptosis [29], as well as miR-145 and miR-107, which belong to the group of 25 microRNAs whose targets were significantly enriched in the mRNA expression patterns following spinal cord injury reported by De Biase et al. (2005). [score:6]
Conversely, the expression of miR-219-5p, miR-107 and miR-29c were repressed at 7 dpo. [score:3]
We validated the changes in the levels of the microRNAs miR-21, miR-223, miR-146a, miR-219-5p, miR-29c, miR-468, miR-145 and miR-107 using Q-PCR. [score:1]
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[+] score: 19
MicroRNA-29 overexpression and knockdown studies in cardiac cells and other cell types have reported its inhibitory action on the TGF- β1 pathway (Cushing et al. 2011; Luna et al. 2011; Roderburg et al. 2011; Zhang et al. 2014). [score:5]
Angiotensin II also has been reported to regulate expression of microRNA-29 via Smads. [score:4]
In summary, as outlined in Fig. 10 our study provides evidence that elevated IS levels caused by renal damage secondary to MI has a direct effect of on the expression of and microRNA-29. [score:4]
MicroRNA-21 and microRNA-29 are among the most abundantly expressed microRNAs in heart and are known to regulate fibrosis by their action on mRNA of extracellular matrix proteins and TGF- β1 (van Rooij et al. 2008; Liang et al. 2012). [score:4]
Chronic angiotensin II infusion in wild-type mice resulted in significant reduction in microRNA-29 while in Smad3 knockout mice this reduction was prevented (Zhang et al. 2014). [score:2]
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[+] score: 17
Figure 5The effects of MIAT suppression on the expression of miR-29 and Sp1 in high glucose -induced rMC-1 cells(A) MIAT suppression significantly reversed the decreased expression of miR-29 induced by high glucose. [score:9]
The effects of MIAT suppression on the expression of miR-29 and Sp1 in high glucose -induced rMC-1 cells. [score:5]
miR-29b belongs to the miR-29 family, which acts as a tumour suppressor in many tumour researches. [score:3]
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[+] score: 17
Therefore, increased expression of miR-29 and miR-24 and reduced expression of miR-34, miR-130 and miR-378 may be responsible for the beneficial effects exerted by MSC-Exo. [score:5]
Previous studies have shown that enhanced expression of miR-29 prevented kidney fibrosis by reducing the expression of collagen [32]. [score:5]
The expression of miR-29 and miR-24, which positively regulate cardiac functions, was relatively high (Figure 3(a)). [score:4]
Our results showed high expression of miR-29 and miR-24 in both MSC-Exo and MSCs. [score:3]
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[+] score: 17
Remarkably, the main direction of changes of these genes (decrease in mRNA expression during maturation) is in agreement with the developmental increase of miR-29 expression under the assumption that miRNAs negatively regulate gene expression. [score:10]
Notably, previously published studies provide some information about possible interactions between developmentally regulated miRNAs and genes, for example, regarding the miR-29 family. [score:3]
One of the most strongly altered miRNA during postnatal development is the miRNA-29 family (miRNA-29a, -29b and -29c), that is associated with different signaling cascades. [score:2]
Therefore, the finding of an established interaction between miR-29 and structural genes reported in the previous literature and our observation of differently expressed miR-29 and mRNA for collagen and elastin strongly suggest a possible interaction between these miRNAs and the regulated structural genes in the vessel investigated in our study. [score:2]
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[+] score: 17
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-1b, ssc-mir-26b
For instance, miR-29c was expressed abundantly in stomach but only in trace amounts in thymus and ovary and miR-30c was relatively strongly expressed in heart, lungs, stomach and endometrium (Figure 3B). [score:5]
miR-22, miR-26b, miR-29c, miR-30c and miR-126 exhibited almost similar expression patterns in all tissues examined (Figure 3B). [score:3]
The observation that miR-22, miR-26b, miR-126, miR-29c and miR-30c are ubiquitously expressed in 14 different tissues of pig is interesting. [score:3]
miR-22, miR-26b, miR-29c and miR-30c showed ubiquitous expression in diverse tissues. [score:3]
Additionally, many other miRNAs, such as let-7, miR-98, miR-16, miR22, miR-26b, miR-29c, miR-30c and miR126, were also expressed abundantly in thymus (Figure 3). [score:3]
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[+] score: 16
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
Among their shared miRNAs, previous research showed that miR-29 is significantly down-regulated and expressed in mesenchymal cells in the lungs of bleomycin -treated mouse [43]. [score:6]
We used TargetScan and miRanda database queries to obtain miRNAs, which had higher targeting combined with N4bp2, namely, miR-200, miR-429, miR-29 and miR-30. [score:5]
Our qRT-PCR results show that the expression of miR-29 and MRAK088388 was highly correlated in lung tissue. [score:3]
Based on these results and preliminary analysis, MRAK088388 possibly regulated lung myofibroblast growth and subsequent collagen deposition by sponging miR-29, which could bind to N4bp2. [score:2]
[1 to 20 of 4 sentences]
[+] score: 15
From P4 to P28, miRNAs displayed very similar expression between both progeny: 0–22 (<5%) miRNAs displayed differential expression and 0–7 of them (<2%) had expression differences higher than 3. Ratios of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p or miR-1843-5p expressions relatively to miR-124-3p expression calculated from RT-qPCR at P28 data matched those calculated from HTS data (Fig. 3B). [score:7]
As the U6 snRNA was excluded from small RNA fractions and could not been used as an internal reference to quantify miRNA expressions, we quantified the expression of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p and miR-1843-5p relatively to that of miR-124-3p, at P4, P8, P14.4 and P21.4 relatively to P28, from RT-qPCR amplification or sequencing data (Fig. 3A). [score:5]
Expression of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p and miR-1843-5p were quantified relatively to those of miR-124-3p, and relatively to those of stage P28, by using the ΔΔCt method 25 and experimentally ascertained amplification efficiencies. [score:3]
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[+] score: 15
MiRNAs exhibiting old-age expression included miR-21, miR-146a (Figure  6A,C), and members of the miR-29 family (miRa/b/c), which exhibit low expression at young age with increasing expression at older ages (78 and 104 weeks) (Figure  5J-L). [score:7]
The miRNAs showing the highest expression within this group were three members of the miR-29 family (miR-29b, miR-29a, and miR-29c). [score:3]
Furthermore, in diabetic conditions, expression levels of miR-195 and miR-29 have been shown to be elevated and reduced, respectively, in podocytes where they play a role in apoptosis and fibrosis [4]. [score:3]
Old age -associated miRNAs showed enrichment in pathways related to endocrine system disorders (miR-129-1, miR-375, miR-223, miR-664, miR-29b, miR-34a), cancer (miR-223, miR-29b, miR-375, miR-96), and cellular movement/invasion of cells (miR-29b, miR-29c, miR-7a, miR-96, miR-34a, miR-375). [score:1]
MiR-29 family repression of DNA methylation activities in older animals would suggest multiple levels of epigenetic regulation. [score:1]
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[+] score: 15
Finding out biological function of miRNAs, proved its expression and regulation mechanism eventually, will have profound significance for better understanding of IBS-D. In a word, our findings may lead to new therapeutic targets [34] for the treatment of IBS-D with increased intestinal permeability via miR-29 regulation. [score:7]
Study displayed the up-regulated miRNA-29 resulted in the increased intestinal permeability [24]. [score:4]
Zhou [24] found that miR-29 targets on nuclear factor-κB-repressing factor and Claudin 1 to increase intestinal permeability. [score:3]
MiRNA-29a is a member of miRNA-29 family. [score:1]
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[+] score: 13
miRNAs that had approximately 2-fold upregulation included members of miR-29 family and miR-34 family and that were downregulated by about 2-fold were members of the miR-181 family and miR-183 family. [score:7]
The expression levels of two miRNAs (rno-miR-29c and rno-miR-29a) were reduced in the mature rat cochleae. [score:3]
The inconsistency between Zhang’s report and our study suggested that miRNA patterns in the organ of Corti change with aging and that miRNAs such as miR-183 and miR29 play different roles in the development of organ of Corti in newborn, younger and older animals. [score:2]
miRNAs that increased mostly in the adult basilar membrane includes miR-296, mi-130b and miR-183 and that those that decreased mostly include miR-29c and miR-29a. [score:1]
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[+] score: 12
Among the miRNAs, miR-214, miR-199a-5p, miR-150, miR-199a-3p, miR-351, miR-145, miR-764, miR-497 and miR-92b were upregulated, whilst miR-7a, miR-325-5p, miR-485, miR-708, miR-344-3p, let-7f, miR-26b, miR-129, miR-29c and let-7a were downregulated. [score:7]
He et al (23) reported an elevated expression of the miR-29 gene family in skeletal muscle, liver and adipose tissues of diabetic GK rats. [score:3]
These miRNAs include miR-214, miR-199a-5p, miR-150, miR-351, miR-145, miR-92b, miR-7a, miR-485, miR-708, let-7f, miR-26b, miR-129, miR-29c and let-7a. [score:1]
Among the 19 miRNAs, four miRNAs have already been reported to be correlated to diabetes in previous studies, including miR-29c, let-7a, let-7f and miR-7 (23– 25). [score:1]
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[+] score: 12
Almost all the up-regulated miRNAs (22 our of 25 miRNAs) such as miR-122, miR-192, miR-685, miR-193, and miR-29c were also up-regulated in our rat mo del, suggesting that common plasma miRNAs seem to be up-regulated in APAP -induced liver injury independent of species. [score:10]
5 miR-503* −5.7 miR-376c* −4.0 miR-215 −1.4 miR-30b* −1.3 miR-29c* −1.2All groups except the BDL and HFD groups showed necrosis and inflammation. [score:1]
5 miR-503* −5.7 miR-376c* −4.0 miR-215 −1.4 miR-30b* −1.3 miR-29c* −1.2 All groups except the BDL and HFD groups showed necrosis and inflammation. [score:1]
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[+] score: 12
In the present study the mRNA microarray experiment showed that many of the targets of miR-29 were indeed significantly down-regulated, both in WKY and SHR. [score:6]
MiR-29 has previously been related to aging and dilation of the aorta, associated with down-regulation of extracellular matrix molecules [18]. [score:3]
Thus, maturation in both WKY and SHR vessels was associated with a prominent increase in expression of the miR-29 family. [score:3]
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[+] score: 12
Park and colleagues [69] have shown that family members of miR-29 upregulate the expression of p53 through regulation of transcription of cdc42 and p85α in tumor cells and as such induce apoptosis. [score:7]
Another recent study found that miR-29 family could regulate DNA methylation via DNA methyltransferase 3A and 3B transcriptional regulation [71]. [score:3]
Our findings that miR-29b is upregulated in astrocytes and neurons after ischemia in vitro opens the path for further investigations to the role of miR-29 in apoptosis in other forms of dementia that have been related to lacunar brain ischemia. [score:2]
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[+] score: 12
More direct evidence comes from a study using a mouse mo del of peritoneal dialysis, in which microRNA-29 (miR-29) was identified to be an inhibitor of peritoneal fibrosis through suppression of TGF-β signaling pathway [29]. [score:6]
The role of miR-29 family members in various fibrotic diseases such as renal and liver fibrosis has been reported, and the results indicate that they function through modulation of collagen related gene expression and formation of extracellular matrix [51, 52]. [score:5]
miR-29b is a member of the miR-29 family which shares the same seed sequence. [score:1]
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[+] score: 12
Treatment Group MiRNA changed Log2 (G/CT) Validated targets 80 kVp/0.1 Gy 2 Low fold change – 80 kVp/0.1 Gy Low signals – – 80 kVp/1 Gy miR-34a 1.55 E2F3, Tagln, INHBB miR-29c −1.02 Tpm1 miR-20b-5p −1.65 – miR-204 −1.39 – 30 kVp/2.5 Gy miR-34a 1.08 E2F3, Tagln, INHBB miR-20b-5p −1.55 – miR-98 −1.16 – miR-127 2.08 – The elevated expression of miR-34a was interesting to us, and we decided to proceed with identifying protein levels of its targets E2F3 and transgelin as well as p53, the key protein in DNA damage response. [score:7]
Treatment Group MiRNA changed Log2 (G/CT) Validated targets 80 kVp/0.1 Gy 2 Low fold change – 80 kVp/0.1 Gy Low signals – – 80 kVp/1 Gy miR-34a 1.55 E2F3, Tagln, INHBB miR-29c −1.02 Tpm1 miR-20b-5p −1.65 – miR-204 −1.39 – 30 kVp/2.5 Gy miR-34a 1.08 E2F3, Tagln, INHBB miR-20b-5p −1.55 – miR-98 −1.16 – miR-127 2.08 – Relative miR expression values are represented in folds in the irradiated cells in comparison to non-irradiated control cells as analyzed by miRNA microarray. [score:5]
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[+] score: 12
In an elegant study, Van Rooij [14] showed that downregulation of miRNA-29 increased collagen expression and fibrosis in the heart after MI. [score:6]
Recently, our group showed that swimming training increases cardiac miRNA-29c expression and decreases collagen expression in the heart of healthy rats [18] and in the board and remote regions of the myocardium after MI [17], which is in accordance with the improved LV compliance observed after ET. [score:5]
Wang G, Kwan BC-H, Lai FM-M, Chow K-M, Li PK-T, Szeto C-C. Urinary miR-21, miR-29, and miR-93: novel biomarkers of fibrosis. [score:1]
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[+] score: 11
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
Among these differentially expressed miRNAs, miR-1, miR-133, miR-29, miR-126, miR-499, miR-30, miR-21, miR-195, miR-155, miR-199, miR-214, and miR-140 have been reported to be related to MI [25– 36], while the other miRNAs have not been reported directly in MI. [score:4]
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[+] score: 11
We also identified differential expression of a number of miRNAs which target histone modification enzymes; miR-145 suppresses histone deacetylase 2 (HDAC2) [51], miR-129 is predicted to target HDAC2 mRNA and miR-29 targets HDAC4 mRNA [52]. [score:11]
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[+] score: 11
The analysis based on their fold changes showed a significant (P < 0.05) upregulation of miR-200c-3p (predicted to regulate IL-13 and VEGF-alpha), miR203a-3p (predicted to regulate IL-24 and PRKC α), miR29-3p (predicted to regulate TNFRS1A), and miR-21-5p (predicted to regulate NFk-B activity), in ocular tissues of LPS+RvD1 -treated rats compared to the vehicle+LPS group (Figure 4). [score:7]
Interestingly, upregulation of miR29-3p and miR-21-5p induced by RvD1, significant already at the lowest dose of 10 ng/kg, was concomitant with the decrease of TNF- α and NF- κB levels in the ocular tissue (Figures 5 and 6). [score:4]
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[+] score: 11
S1 Fig The expression of MiR-29 was determined by qRT-PCR in the EDL muscle from 35 weeks old normal littermates (NL) and chronic kidney disease (CKD) rats. [score:4]
The expression of MiR-29 was determined by qRT-PCR in the EDL muscle from 35 weeks old normal littermates (NL) and chronic kidney disease (CKD) rats. [score:4]
We demonstrated in CKD skeletal muscle tissue there is higher stem cell activation (decreased Pax-7, increase MyoD) and differentiation (myogenin) with the lower expression of a pro-myogenic factor, miR-29. [score:3]
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[+] score: 10
The miR-29 family directly target at least 16 extracellular matrix genes and are relevant to renal and cardiovascular injury [29]– [31]. [score:4]
Recent research suggests that miR-29 inhibits cell proliferation and induces cell cycle arrest [32], modulates oxidative injury [33] and promote apoptosis through a mitochondrial pathway that involves Mcl-1 and Bcl-2 [28]. [score:3]
Several miRNAs (e. g., miR-29) that showed a dynamic change with hypoxic durations in this work regulate the process of oxidative stress and inflammation and are involved in regulation of apoptotic and survival signal pathways,. [score:3]
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[+] score: 10
Among myocardial infarction-regulated miRNA members, the miR-29 family (miR-29a, miR-29b copy 1 and copy 2, and miR-29c) is down-regulated in the peri-infarct region of the heart [8], which is associated with collagen production by fibroblasts, subsequent collagen deposition, and eventually leads to heart failure [11]. [score:5]
miR-29 overexpression in combination with the Tri-P may facilitate iPSC [NCX1+] migration and survival, as well as permit neovascularization of the infarct, leading to improvements in LV functional performance after the occurrence of ischemic heart disease. [score:5]
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[+] score: 9
Of the 46 increased miRNA, sICAM-1 was the predicted target of 6 (miR-23b, miR-27a, miR-99a, miR-100, miR-324-5p, miR-363); PAI-1 was the predicted target of 4 (miR-30a, miR-30d, miR-182, miR-384-5p), E selectin the predicted target of 2 (miR-16; miR-195) and the alpha chain of fibrinogen the predicted target of miR-29c [26]. [score:9]
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[+] score: 9
The over -expression of miR-29 in 3T3-L1 adipocytes inhibited insulin-stimulated glucose uptake [37]. [score:5]
The miR-29 group of microRNAs was found to be up-regulated in muscle and fat tissues of Goto–Kakizaki rats, a non-obese rat mo del of diabetes mellitus (T2DM). [score:4]
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[+] score: 9
One differentially expressed miRNA in the liver has important functions in regulation of the expression of extracellular matrix proteins (miR-29c). [score:6]
Various other miRNAs, such as miR-29c and miR-98, were differentially expressed in the spleen and lungs of the infected animals respectively. [score:3]
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[+] score: 9
MiR-29 family members are often down-regulated in cancer and forced expression of miR-29a is reported to reduce proliferation and invasiveness presumably via CDC42 and p85alpha dependent up-regulation of p53 [36], [37]. [score:9]
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[+] score: 9
Other miRNAs from this paper: rno-mir-29c-1
The majority of upregulated transcripts have a function in the cell nucleus (Upregulated: Abt1, Adar, Arid5b, Atf4, Casc3, Cdkl1, Chd2, Cstf2t, Deadc1, Erg, Eya4, Gnl3, Hdac1, Hdac11, LOC100125368, Mbnl2, Mir29c, Morc2, Morg1, Nap1l5, Nr2c1, Prmt8, Prpf38b, Rfc2, Sfrs3, Taf1a, Tarsl2, Tspyl2, Tspyl5, Xbp1, yars, Zbtb25, Zbtb26, Zcchc12, Zfp110, Zfp143, Zfp235, Zfp385b, Zfp385d, Zfp397os, Zfp9, Zfr, Zmym1, Znf23, Znf507, Zswim3, Zwilch) or are involved in cell signaling (Upregulated: Acvr1b, Adap2, Adra1a, Aktip, Alkp1, Arfrp1, Arhgap10, Arl1, Arrdc4, Eltd1, Galnt11, Galnt14, Gfra1, Gprasp2, Grem1, Gtbpb8, Hcrtr1, Inpp1, Inpp5j, Olr1148, Olr121, Pde3a, Pde8b, Psd2, Rab24, Rab5a, Rasgef1c, Rasl11b, Rem2, Rerg, Rhoq, V1rf5, V1rg13, Vom2r66). [score:9]
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[+] score: 9
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Finally, other subsets of miRNAs were either up-regulated (miR-23a-3p, miR132-3p, miR-146a-5p, miR-154-3p, miR-181d-5p, miR-212-3p, miR-212-5p, miR-344b-5p, miR-380-3p, miR-410-3p, miR-433-3p and miR-3584; Fig. 2, Supplementary Fig. S4), or down-regulated (miR-29c-5p, miR-30a-5p, miR-30c-2-3p, miR-30e-3p, miR-138-5p, miR-140-3p, miR-551b-3p and miR-652-3p; Fig. 2, Supplementary Fig. S5) during all phases of the disease. [score:9]
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[+] score: 8
Other miRNAs from this paper: rno-mir-27a, rno-mir-29c-1, rno-mir-192, rno-mir-377
In addition, downregulation of miR-29c reduces podocyte apoptosis and decreases ECM protein accumulation, both in vitro and in vivo 37. miR-377 is upregulated in human and mouse MCs exposed to HG and indirectly stimulates increased fibronectin protein production 38. [score:8]
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[+] score: 8
Of these miRNAs, rno-miR-129-1-3p, rno-miR-153-3p, rno-miR-29b-3p, rno-miR-29c-3p and rno-miR-451-5p were down-regulated, whereas rno-let-7a-1-3p, rno-miR-322-5p, rno-miR-3574 and rno-miR-628 were observed to be highly upregulated with p < 0.01 (Fig.   3). [score:7]
9 miRNAs (rno-miR-129-1-3p, rno-miR-153-3p, rno-miR-29b-3p, rno-miR-29c-3p, rno-miR-451-5p, rno-let-7a-1-3p, rno-miR-322-5p, rno-miR-3574 and rno-miR-628) showed statistically significant change. [score:1]
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[+] score: 8
MicroRNA-29a and 29b-1 are processed from chromosome 7, and miR-29b-2 and 29c are transcribed from chromosome 1. Since forced overexpression of miR-29 markedly suppresses collagen 1 A1 mRNA and protein expression [16, 17], miR-29 plays an anti-fibrotic role in the liver and other organs [18]. [score:7]
The miR-29 group is composed of miR-29a, 29b-1, 29b-2, and 29c. [score:1]
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[+] score: 7
The let-7d 27 and miR-29 28 down-regulation, and the miR-21 up-regulation 29 contribute to PF. [score:7]
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[+] score: 7
It has been shown that miR-29, miR-15 and miR-107 are upregulated; while miR-124, miR-34 and miR-153 are downregulated in patients with AD (Delay et al., 2012; Lau et al., 2013). [score:7]
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Downregulation of mir-29 (mir-29a and mir-29c) by antisense inhibitor also protected H9c2 cardiomyocytes from simulated IR injury. [score:6]
Antagomirs against mir-29a or mir-29c significantly reduced myocardial infarct size and apoptosis in hearts subjected to IR injury [28]. [score:1]
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[+] score: 7
Importantly, the miR-29 family was exclusively downregulated in the frontal cortex, resulting in upregulation of methyltransferase DNMT3a [21, 23]. [score:7]
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[+] score: 7
Since the expression of LOXL2 is also influenced by hypoxia,, and microRNAs (miR-26 and mIR-29), there are also other potential strategies for targeting LOXL2 expression or activity (Wong et al., 2014). [score:7]
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[+] score: 6
Northern blot analysis confirmed the up-regulation of all three miR-29 paralogs in muscle, adipose tissue and liver. [score:4]
He et al. (2007) [19] profiled miRNA expression in skeletal muscle in the Goto-Kakizaki (GK) rat, a well-characterized mo del of T2D, and compared it to normal Wistar rats; miR-29 paralogs were found to be over-expressed in the GK rat. [score:2]
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[+] score: 6
In diabetic nephropathy, the miRNA-29 family protects the kidney from fibrotic damage, and the DPP-4 inhibitor linagliptin has been shown to inhibit TGF-β -induced endothelial to mesenchymal transition (EndMT) by restoring the miRNA-29s’ levels [64]. [score:5]
Nevertheless, the miR-29 family might serve as a candidate for monitoring of treatment effects. [score:1]
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[+] score: 6
For example, miR-29 expression is downregulated in human and murine liver fibrosis, which is mediated by TGF-β and other inflammatory signals [16]. [score:6]
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[+] score: 6
Moreover, miR-29 has target specific sites on BACE1 mRNA and its down-regulation increases AD progression [65]. [score:6]
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[+] score: 6
Another gene family that we evidenced prevalently expressed in the WBCs is mir-29 (mir-29a, mir-29b, mir-29c; p = 2.19 E-4). [score:3]
We found that miRNAs with higher expression in WBCs includes different miRNA families: mir-15, mir-17, mir-181, mir-23, mir-27 and mir-29 families. [score:3]
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[+] score: 5
Other miRNAs from this paper: rno-mir-29a, rno-mir-29c-1
However, our group showed the expression of microRNA-29c, which targets the collagen gene and is associated with less collagen deposition in heart tissue in swimming exercise. [score:5]
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[+] score: 5
Some of the deregulated miRNAs (miR-181, miR-26, miR-1, mir-29, miR-214, miR-126, and miR-499) are reported to be related to hypoxia, cell development, and cell growth [1, 5, 7, 25]. [score:3]
Recently, some miRNAs for example miR-21, miR-1, miR-216[10], and miR-29 family[11], were reported to be deregulated in myocardial infarction. [score:2]
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[+] score: 5
Comparatively, the miR-29 family showed consistent regional expression [25] while the miR-200 family were differentially expressed. [score:5]
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[+] score: 4
Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. [score:2]
Expression of MicroRNA-29 and collagen in cardiac muscle after swimming training in myocardial-infarcted rats. [score:2]
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[+] score: 4
Du Y Upregulation of a disintegrin and metalloproteinase with thrombospondin motifs-7 by miR-29 repression mediates vascular smooth muscle calcificationArterioscler. [score:4]
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[+] score: 4
A recent study reiterated the role of miR-29 in neuronal survival by knocking down miR-29 in the mouse brain [73]. [score:2]
miR-29 knockdown resulted in massive neuronal death in the hippocampus and cerebellum. [score:2]
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[+] score: 4
Dramatical down-regulation of miR-29 was observed in the region of the fibrotic scar after MI [31]. [score:4]
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[+] score: 4
Recent studies have identified that many miRs [11], such as miR-1, miR-21, miR-29, miR-31, miR-143/145, and miR-221/222, play important roles in neointimal hyperplasia by regulating the functions of VSMCs. [score:2]
A number of miRs, such as, miR-1, miR-21, miR-29, miR-31, miR-143/145 and miR-221/222, were verified to be involved in neointimal hyperplasia by regulating the functions of VSMCs [11]. [score:2]
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[+] score: 4
Further microRNA-gene networks indicated that the key microRNAs were Homo sapiens (hsa)-miR-570, hsa-miR-122, hsa-miR-34b, hsa-miR-29c, hsa-miR-922 and hsa-miR-185, which negatively regulated ~79 downstream target genes to modulate hepatocyte immune response, inflammatory response and glutathione metabolism (10). [score:4]
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[+] score: 4
Gomes PR Long-term disruption of maternal glucose homeostasis induced by prenatal glucocorticoid treatment correlates with miR-29 upregulationAm. [score:4]
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[+] score: 4
The members of the miR-29 family showed the highest increase in expression level from younger to older animals (Fig.   1d; log fold-change (LFC) of up to 5.5 from P2/P9 to P23/P45). [score:3]
Three of the top five most significant miRNAs that increased from early to late age were members of the miR-29 family. [score:1]
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[+] score: 4
For instance, some miRNAs, such as miR-29, miR-21 and miR-221, has been reported to regulate tumor cell growth, apoptosis, migration and invasion by targeting proteins involved in those cellular pathways [7- 9]. [score:4]
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[+] score: 3
Treatment with resveratrol in cancer cell line SW480 results in decreased level of miR-21 and miR29c whereas it was increased in healthy heart when treated with resveratrol. [score:1]
1 up 3.7 down 12 down 1.1 miR-10a up 6.4 up 5.2 up 3.5 down 116 down 1.6 snoRNA202 up 3.8 up 4.7 up 3.2 down 6 down 3 miR-27b down 1.4 up 1.9 up 3.2 up 1 up 1 miR-29c up 5.4 up 4.5 up 3.1 up 1.5 down 1.5 miR-345-5p up 14.3 up 31.7 up 2.4 down 4.7 up 1.1 rno-miR-24-1 down 25.3 up 1.2 up 2.1 down 1.2 down 1.9 miR-687 up 3.8 up 1.8 up 2 down 1.7 down 11.5 miR-27a up 34 up 12. [score:1]
However, in few miRNAs such as miR-29c, longevinex have opposing effect to resveratrol and the difference may be due to many possibilities including presence of other ingredients in commercial formulation, bioavailability of resveratrol etc. [score:1]
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[+] score: 3
We identified a group of mRNA and microRNA previously associated with amyloid-ß induced toxicity (e. g. Frp2 and Ppif), or implicated in Alzheimer’s disease processes, (miR-29 and miR-9) [35- 47], (Table  4). [score:3]
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[+] score: 3
For example, it has been reported that miR-221 [15], miR-199a/b [16][17], miR-27b [18], miR-195 [11] and miR-34a/b/c [19] positively regulate cardiac hypertrophy, while miR-378 [9], miR-29 [20], miR-150 [11], miR-223 [21] and miR-1 [22] negatively regulate cardiac hypertrophy. [score:3]
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[+] score: 3
Other miRNAs from this paper: rno-mir-29c-1, rno-mir-34a, rno-mir-200b, rno-mir-155
Pogribny I. P. Starlard-Davenport A. Tryndyak V. P. Han T. Ross S. A. Rusyn I. Beland F. A. Difference in expression of hepatic microRNAs miR-29c, miR-34a, miR-155, and miR-200b is associated with strain-specific susceptibility to dietary nonalcoholic steatohepatitis in miceLab. [score:3]
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Melo S. T. F. Fernandes T. Baraúna V. G. Matos K. C. Santos A. A. Tucci P. J. F. Oliveira E. M. Expression of microRNA-29 and collagen in cardiac muscle after swimming training in myocardial-infarcted rats Cell. [score:3]
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[+] score: 3
Other miRNAs from this paper: cel-let-7, cel-lin-4, hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-29b-1, mmu-mir-101a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-132, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-199a-1, hsa-mir-199a-1, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-132, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-138-1, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-92a-2, rno-let-7d, rno-mir-7a-1, rno-mir-101b, mmu-mir-101b, hsa-mir-181b-2, mmu-mir-17, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-101-2, cel-lsy-6, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7a-2, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-92a-1, rno-mir-92a-2, rno-mir-101a, rno-mir-128-1, rno-mir-128-2, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-199a, rno-mir-181a-1, rno-mir-421, hsa-mir-181d, hsa-mir-92b, hsa-mir-421, mmu-mir-181d, mmu-mir-421, mmu-mir-92b, rno-mir-17-2, rno-mir-181d, rno-mir-92b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, mmu-mir-101c, mmu-let-7j, mmu-let-7k, rno-let-7g, rno-mir-29b-3, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Examination of the temporal clusters revealed that probes with similar sequences showed correlated expression, as exemplified by miR-181a, miR-181b, miR-181c, smallRNA-12 (Figure 4a) and miR-29a, miR-29b and miR-29c (Figure 4b), respectively. [score:3]
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Overexpression of miR-34a, miR-146a, miR199a-5p or miR-29 in MIN6 cells negatively impacts on beta cell function [6]. [score:3]
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[+] score: 3
By individual TaqMan qRT-PCR analysis of dysregulated serum miRNAs uncovered by serum TLDA and dysregulated liver tissue miRNAs uncovered by microarray hybridization in primary screening, 6 serum miRNAs, including miR-122, miR-192, miR-193, miR-200a, miR-21 and miR-29c, exhibited a high correlation with primary screening results. [score:3]
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A previous study suggested that miR-29 regulates liver fibrosis and together with TGF- β and nuclear factor- κB forms part of a signaling nexus in HSCs [40]. [score:2]
It has also been shown that hepatic levels of miR-29 are significantly increased in mice with CCl4 induced liver damage and also in the livers of patients with advanced fibrosis. [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
As an example, this situation has been demonstrated for miR-29 released from cancer tissue and targeting skeletal muscle cells, which triggers cytopathic effect and cachexia [120]. [score:3]
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[+] score: 3
Hepatocyte growth factor (HGF) inhibits collagen I and IV synthesis in hepatic stellate cells by miRNA-29 induction. [score:3]
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[+] score: 3
Combining in silico and in vivo studies, He et al identified a potential miR-29 target, insulin -induced gene 1 (INSIG1, or growth response protein CL-6) [17]. [score:3]
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[+] score: 3
This result was consistent with previous reports that Smad3 signaling promotes renal fibrosis by inhibiting miR-29 [15, 38]. [score:3]
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[+] score: 3
As shown in Table 2, we found increased expression of liver specific miRNAs in transdifferentiated hepatocytes, including miR-122a, miR-21, miR-22, miR-182, miR-29 and miR-30. [score:3]
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MiR-29, miR-133 and miR-30c are the most strongly fibrosis -associated miRNAs targeting a number of extracellular-matrix-related mRNAs [31], [32]. [score:3]
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[+] score: 3
Qi H Activation of AMPK attenuated cardiac fibrosis by inhibiting CDK2 via p21/p27 and miR-29 family pathways in ratsMol. [score:3]
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[+] score: 3
Members of the miR-29 family suppress the protein phosphatase PPM1D, increasing apoptosis [30], and may function as markers of senescence because they can reduce the levels of type IV collagen, potentially weakening the basal membrane in senescent tissues [28]. [score:3]
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[+] score: 3
Notably, it was the miR-29 isoform more expressed in this Ras -driven rat thyroid cell transformation system. [score:3]
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miR-21, miR-155 and miR-221/222 have recently been shown to regulate AngII signaling in cardiac fibroblasts [14– 16] and in endothelial cells [17], while miR-29 regulates fibrotic pathways [18]. [score:3]
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[+] score: 2
Relative expression levels of the selected miRNAs and mRNAs were depicted in Figure 3. Consistent with the microarray data, real-time PCR confirmed that, compared with controls, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, and rno-miR-351-5p were significantly increased, while rno-miR-192-3p, rno-miR-194-5p, rno-miR-29c-3p, rno-miR-185-5p, and rno-miR-30c-5p were significantly decreased in stone-forming rat kidneys. [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
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[+] score: 2
miR-29 regulates the activation of hepatic stellate cells (HSCs) mediated by transforming growth factor-β (TGF-β) [8]. [score:2]
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[+] score: 2
MicroRNA-29c correlates with neuroprotection induced by FNS by targeting both birc2 and bak1 in rat brain after stroke. [score:2]
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[+] score: 2
And Mir375 is one of a number of involved in insulin synthesis and secretion (for instance Mir9 and Mir29a/b/c), insulin sensitivity in target tissue (Mir143 and Mir29) or glucose and lipid metabolism (Mir103/107 and Mir122) and thus, having potential roles in diabetes [see for instance, [52], [53]. [score:2]
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[+] score: 2
The miRNAs miR-29 family and miR-133 regulate mRNAs that encode proteins involved in fibrosis during the pathologic cardiac remo deling [32, 33]; however, the participation of these miRNAs in physiologic cardiac remo deling induced by pregnancy is still unknown. [score:2]
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[+] score: 1
The human miR-29 family of microRNAs has three mature members, miR-29a, miR-29b, and miR-29c. [score:1]
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MiRNAs such as hsa-let-7f, hsa-miR-499, hsa-miR-373, hsa-miR-372, hsa-miR-371, hsa-miR-369-5p, hsa-miR-34c, hsa-miR-34b, hsa-miR-34a, hsa-miR-29c, hsa-miR-217, and hsa-miR-20a might influence senescence or aging [42]. [score:1]
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A number of miRNAs have been shown to be relevant to fibrotic processes in diabetic nephropathy, including miR-29 and miR-200 families, miR-192 and miR-21 [14– 17]. [score:1]
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The BLV microRNAs associate with Argonaute and mimic cellular analogs (e. g., BLV-miR-B4 for miR-29). [score:1]
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