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22 publications mentioning rno-mir-130b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-130b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 282
Other miRNAs from this paper: rno-mir-130a
Furthermore, quantitative real-time RT-PCR (Fig. 6c) and Western blot analyses (Fig. 6d) revealed that miR-130b inhibitor obviously attenuated the silencing effect of Snail siRNA on the expression of Snail, Vimentin and Collagen IV and downregulated E-cadherin expression. [score:10]
Quantitative real-time RT-PCR analysis showed that miR-130b inhibitor upregulated the mRNA level of Snail, Vimentin and Collagen IV, but downregulated E-cadherin (Fig. 3c). [score:9]
Requirement of Snail for the miR-130b antagonism effect on downstream gene expressions in vitroTo explore whether the effect of miR-130b inhibition on downstream gene expressions depended on Snail, Snail siRNA was used to treat NRK52E cells following the treatment with miR-130b inhibitor. [score:9]
As demonstrated by qRT-PCR and Western blot analyses, miR-130b inhibitor upregulated Snail, Vimentin, and Collagen IV, but downregulated E-cadherin, however, miR-130 mimic had the opposite effect. [score:9]
These data indicate high glucose as a pivotal factor for the expression of miR-130b and regulating miR-130b expression affects Snail -induced downstream gene expressions in vitro. [score:8]
Immunohistochemistry (Fig. 7e) and quantification of the staining intensity (Fig. 7g, left panel) revealed that miR-130b inhibition upregulated the expression level of SNAIL, VIMENTIN, COLLAGEN IV and α-SMA, but decreased E-CADHERIN. [score:8]
NT: non -targeting; siRNA: small interfering RNA; miR-iNC: miRNA inhibitor negative control; miR-130bi: miR-130b inhibitor; wt: wild type; mt: mutant type. [score:7]
MiR-130b mimic suppresses Snail -induced EMT in vitroTo further explore whether miR-130b overexpression could rescue the effect of Snail -induced EMT process, we therefore administered miR-130b mimic to high glucose cultured NRK-52E cells and detected the downstream gene expressions and biological features. [score:7]
To further investigate the effects of miR-130b inhibition or overexpression on downstream gene expressions in the presence of high glucose, we treated NRK52E cells with miR-130b inhibitor (miR-130bi) or miR-130b mimic (miR-130bm). [score:7]
To explore whether the effect of miR-130b inhibition on downstream gene expressions depended on Snail, Snail siRNA was used to treat NRK52E cells following the treatment with miR-130b inhibitor. [score:7]
These results suggest that miR-130b directly suppresses Snail that subsequently regulates EMT and fibrosis related gene expressions. [score:7]
MiR-130b mimic downregulated the mRNA level of Snail, Vimentin and Collagen IV, but upregulated E-cadherin as shown by quantitative real-time RT-PCR analysis (Fig. 4c). [score:6]
MiR-130b regulates the expression of EMT markers and renal tubulointerstitial fibrosis in vivoMiR-130b in plasma and tissue samples were decreased in diabetic rats and further depleted with miR-130b inhibitor treatment (Fig. 7a,b). [score:6]
High glucose inhibits miR-130b and regulates Snail -induced downstream gene expressions in vitro. [score:6]
In high glucose cultured NRK-52E cells, miR-130b depletion upregulated Snail expression and induced phenotypic transformation of the cells from sessile epithelial to invasive mesenchymal state, with increased ability to migrate and invade. [score:6]
Here, we found that miR-130b regulated the expression of Snail and downstream gene expressions associated with renal fibrosis. [score:6]
High glucose inhibits miR-130b and regulates Snail -induced downstream gene expressions in vitroTo investigate whether high glucose affects the miR-130b level, we treated NRK52E cells with increasing concentrations of glucose and detected the expression of miR-130b and downstream genes at different time points from 12 to 72 hours. [score:6]
Snail has also been shown to induce the expression of α-SMA, fibronectin, collagen I, genes directly implicated in myofibroblast activation and interstitial matrix production 4. The present study highlights the notion that Snail -induced suppression of E-cadherin activity contributes to miR-130b -mediated tubulointerstitial fibrosis in diabetic nephropathy. [score:6]
These data suggest that activation of Snail signaling by miR-130b inhibitor promotes the expression of fibrosis-related genes and EMT process. [score:5]
MiR-130b targeted Snail and miR-130b abrogation enhanced the expression of markers related to EMT and fibrosis. [score:5]
To investigate the effect of miR-130b inhibition or overexpression on renal tubulointerstitial fibrosis, miR-130b inhibitor (4 ng/mm [3] ) or miR-130b mimic (2 ng/mm [3]) was injected peritoneally to diabetic rats every other day. [score:5]
The predicted 3′-untranslated regions (UTR) sequence of Snail interacting with miR-130b and mutated sequences within the predicted target sites were synthesized and inserted into the pRL-TK control vector (Promega, Madison, WI, USA). [score:5]
However, when Snail-silenced cells were further treated with miR-130b inhibitor, the expression of SNAIL restored but E-CADHERIN considerably decreased. [score:5]
NC, normal control; DM, diabete mellitus; DM_miR-iNC, diabetic rats treated with miRNA inhibitor negative control; DM_miR-130bi, diabetic rats treated with miR-130b inhibitor; MTS, Masson’ s trichrome stain. [score:5]
As illustrated using immunofluorescence microscopy, miR-130b inhibition resulted in marked increase in the expression of SNAIL and co-localized with E-CADHERIN (Fig. 3a, double arrows), the level of which decreased (Fig. 3b). [score:5]
Immunofluorescence microscopy revealed that miR-130b overexpression led to decreased expression of SNAIL but increased E-CADHERIN (Fig. 4a,b). [score:5]
To further explore whether miR-130b overexpression could rescue the effect of Snail -induced EMT process, we therefore administered miR-130b mimic to high glucose cultured NRK-52E cells and detected the downstream gene expressions and biological features. [score:5]
Four groups (9–10 per group) were studied: diabetic rats treated with miR-130b inhibitor (4 ng/mm [3]) (DM_miR-130bi), negative control miRNA inhibitor (DM_miR-iNC), miR-130b mimic (2 ng/mm [3]) (DM_miR-130bm), and negative control miRNA mimic (DM_miR-NC). [score:5]
MiR-130b inhibitor (miR-130bi), miR-130b mimic (miR-130bm), or the appropriate negative controls (NC) of miRNA inhibitor (miR-iNC) and miRNA mimic (miR-NC), respectively, were purchased from GenePharma (Shanghai, China) and transfected at a final concentration of 50–100 nM in the cells using HiPerFect Transfection Reagent (Qiagen, Hilden) according to the manufacturer’s recommendations. [score:5]
Plasma miR-130b downregulation contributes to increased tubulointerstitial fibrosis and unfavorable renal function in diabetic nephropathy (DN) patients. [score:4]
MiR-130b mimic decreases the expression of EMT markers and inhibits renal tubulointerstitial fibrosis in vivo. [score:4]
Plasma miR-130b downregulation contributes to increased tubulointerstitial fibrosis and unfavorable renal function in DN patients. [score:4]
Western blot analysis revealed that miR-130b abrogation caused considerable increase in the expression of SNAIL, corresponded with increased VIMENTIN and COLLAGEN IV but decreased E-CADHERIN (Fig. 3d). [score:3]
Western blot analysis demonstrated that miR-130b enrichment reduced the expression of SNAIL, VIMENTIN and COLLAGEN IV but increased E-CADHERIN (Fig. 4d). [score:3]
MTS (Fig. 7f) and interstitial injury score (Fig. 7g, right panel) demonstrated that miR-130b inhibitor increased renal tubulointerstitial fibrosis. [score:3]
NRK-52E cells were cultured in high glucose medium (30 mM) for 24 hours followed by treatment with miR-130b inhibitor for another 48 hours. [score:3]
Furthermore, plasma miR-130b level was negatively associated with albuminuria in diabetic rats treated with miR-130b inhibitor or mimic (see Supplementary Fig. S2 online). [score:3]
The mean value of miR-130b expression in glucose-free cultured cells was used as the calibrator. [score:3]
Correspondingly, miR-130b inhibition elevated the level of Snail, Vimentin, Collagen IV and α-SMA, but decreased E-cadherin as detected by qRT-PCR (Fig. 7c) and Western blot analyses (Fig. 7d). [score:3]
Moreover, miR-130b inhibitor increased renal tubulointerstitial fibrosis in diabetic rats. [score:3]
Pearson correlation analysis was used to analyze correlations between plasma miR-130b and biological parameters, and between SNAIL and E-CADHERIN expression. [score:3]
Increasing concentrations of glucose reduced miR-130b expression in a dose dependent manner (Fig. 5d). [score:3]
Under high glucose microenvironment (see Supplementary Fig. S1 online), the level of miR-130b decreased or increased with miR-130b inhibitor or miR-130b mimic treatment, respectively. [score:3]
MiR-130b regulates the expression of EMT markers and renal tubulointerstitial fibrosis in vivo. [score:3]
MiR-130b in plasma and tissue samples were decreased in diabetic rats and further depleted with miR-130b inhibitor treatment (Fig. 7a,b). [score:3]
MiR-130b inhibitor caused considerable increase in the level of BUN, serum creatinine, β2-microglobulin and albuminuria (see Supplementary Table S1 online), but miR-130b mimic had the opposite effects (see Supplementary Table S2 online). [score:3]
NRK52E cells transfected with 120 ng miR-130b inhibitor or negative controls, followed by co-transfection with 30 ng of the wild-type or mutant 3′-UTR of Snail using 0.45 μL of Fugene (Promega, Madison, WI, USA). [score:3]
We found high glucose reduced miR-130b expression level in a time dependent manner (Fig. 5a). [score:3]
Requirement of Snail for the miR-130b antagonism effect on downstream gene expressions in vitro. [score:3]
We monitored the renal interstitial changes and expression levels of miR-130b, Snail and related molecules at four, eight and 12 weeks. [score:3]
Conversely, miR-130b overexpression had the opposite effects (Fig. 8). [score:3]
Conversely, administration of miR-130b mimic to high glucose cultured NRK-52E cells and diabetic rats remarkably decreased the expression of Snail and attenuated renal fibrosis. [score:3]
MiR-130b inhibitor increases EMT markers and promotes renal tubulointerstitial fibrosis in vivo. [score:2]
MiR-130b mimic did not cause phenotypic changes of NKR-52E cells (Fig. 4e) but inhibited the cells to migrate (Fig. 4f) and invade (Fig. 4g). [score:2]
MiR-130b mimic suppresses Snail -induced EMT in vitro. [score:2]
Our findings indicate a critical role of miR-130b in regulating renal tubulointerstitial fibrosis in diabetic nephropathy. [score:2]
MiR-130b inhibitor led to a noticeable increase in the luciferase activity of wild-type 3′-UTR of Snail but not the mutant (Fig. 6f). [score:2]
To further demonstrate that Snail is directly targeted by miR-130b in NRK52E cells, we investigated whether miR-130b directly interacted with the 3′-UTR of Snail mRNA using a dual-luciferase reporter assay. [score:2]
We also found that miR-130b level was decreased in high glucose cultured NRK-52E cells, plasma or kidney tissue samples of streptozotocin -induced diabetic rats. [score:1]
Inverse correlations between plasma miR-130b with serum creatinine (Fig. 1c), β2-microglobulin (Fig. 1d), and proteinuria (Fig. 1e) were detected. [score:1]
We demonstrated that plasma miR-130b was decreased in DN patients and correlated with declined renal function. [score:1]
Given the critical role of plasma miR-130b and its possible correlation with increased tubulointerstitial fibrosis in renal biopsies of DN patients (Fig. 1), we next investigated the potential effect of miR-130b inhibition on EMT and fibrosis-related molecules using an in vitro mo del system. [score:1]
NC, normal control; DM, diabete mellitus; DM_miR-NC, diabetic rats treated with miRNA mimic negative control; DM_miR-130bm, diabetic rats treated with miR-130b mimic; MTS, Masson’ s trichrome stain. [score:1]
For miRNA expression analysis of the cells, human plasma samples and rat kidney tissues or plasma samples, RNA was reverse transcribed using miRScript PCR System and analyzed by qRT-PCR with the miScript SYBR Green PCR Kit using the specific miR-130b miScript Primer Assays (Qiagen, Hilden, Germany) according to the manufacturers’ instructions. [score:1]
These results suggest that plasma miR-130b negatively correlates with serum creatinine, β2-microglobulin, and proteinuria in DN patients. [score:1]
Plasma miR-130b can be extrapolated to quantifying the severity of renal tubulointerstitial fibrosis in diabetic nephropathy. [score:1]
The mutant Snail binding site was generated in the complementary site for the seed region of miR-130b. [score:1]
In conclusion, this study provides a novel mechanism that miR-130b attenuates tubulointerstitial fibrosis in diabetic nephropathy through repression of Snail -induced EMT. [score:1]
To investigate whether high glucose affects the miR-130b level, we treated NRK52E cells with increasing concentrations of glucose and detected the expression of miR-130b and downstream genes at different time points from 12 to 72 hours. [score:1]
MiR-130b ablation enhances Snail -induced EMT in vitroGiven the critical role of plasma miR-130b and its possible correlation with increased tubulointerstitial fibrosis in renal biopsies of DN patients (Fig. 1), we next investigated the potential effect of miR-130b inhibition on EMT and fibrosis-related molecules using an in vitro mo del system. [score:1]
These data clearly suggest a role of miR-130b in repressing the EMT process in high glucose cultured NRK-52E cells in vitro. [score:1]
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2
[+] score: 57
Other miRNAs from this paper: rno-mir-130a, rno-mir-132, rno-mir-152, rno-mir-184, rno-mir-212
Concerning the miRNAs studied here, we previously showed that miR-130a expression is downregulated with increased glucose concentration in Wistar rat islets 10, which was supported by our findings in INS-1 832/13 cells for miR-130a, miR-130b and miR-152 (Supplementary Fig. S2). [score:6]
The transient modulation of miR-130a, miR-130b, or miR-152 in INS-1 832/13 cells by either over -expression or knock-down resulted in reciprocal effects on GSIS, but not KCl -induced insulin secretion agrees with targets primarily involved in modulating the cytosolic ATP concentration. [score:6]
Over -expression and co -expression of miR-152, miR-130a, and miR-130b in pancreatic islets. [score:5]
Here, we validated our array findings by qPCR, and showed that miR-130b, which harbours an identical seed sequence as miR-130a and belongs to the miR-130 gene family, was also upregulated in the pancreatic islets of hyperglycaemic GK rats (Fig. 1A). [score:4]
Upregulation of miR-152, miR-130a and miR-130b in GK rat islets, and in human islets from donors with impaired glucose tolerance and type-2 diabetes. [score:4]
The similar ATP dynamics profile of miR-130a and miR-130b confirmed the similar regulatory targets of these miRNAs by virtue of their identical seed sequence. [score:4]
Moreover, despite different chromosomal locations of the three miRNAs in the human genome (chr11/miR-130a; chr22/miR-130b; chr17/miR-152), there was a notable co -expression among them, indicating highly-coordinated transcriptional regulation of these miRNAs in the human pancreatic islets (Fig. 1C). [score:4]
To conclude, we could show that miR-130a, miR-130b and miR-152 influence the metabolic control of GSIS via modulation of ATP levels, partially through targeting of PDHA1 and GCK in the pancreatic beta cell (Fig. 7). [score:3]
Specific primers and probes from TaqMan [®] MiRNA Assays (Applied Biosystems, CA, USA) were used to measure the expression levels of miR-130a-3p (#TM_000454), miR-130b-3p (#TM_000456), miR-152-3p (#TM_ 000475) and mRNA expression of their targets: Rat Pdha1 (Rn01424346_m1), Rat Gck (Rn00561265_m1), Human PDHA1 (Hs01049345_g1), and Human GCK (Hs01564555_m1). [score:3]
html) 29 to identify putative targets of miR-130a-3p, miR-130b-3p, and miR-152-3p. [score:3]
We found that miR-130a, miR-130b and miR-152 or combination of miR-130a/miR-152 resulted in significant decrease in the expression of Pdha1 both in the mRNA and protein levels (Fig. 4A,B). [score:3]
How to cite this article: Ofori, J. K. et al. Elevated miR-130a/miR130b/miR-152 expression reduces intracellular ATP levels in the pancreatic beta cell. [score:3]
Subsequently, we could show negative regulatory effects of miR-130a and miR-130b on glucokinase and PDHA1, and the direct biochemical interaction of miR-152, with Pdha1 mRNA using the AGO2 RIP assay. [score:2]
Hypothetically, LNAs that knock down miR-130a/miR-130b/miR-152 would affect the glucose conversion pathway in the mitochondria and assist in stabilizing the intracellular ATP to an optimal level. [score:2]
We did not see enrichment in ATP -binding category for genes containing only miR-130a/miR-130b putative binding sites (Supplementary Table 3). [score:1]
The characteristics of human pancreatic islet donors are in Supplementary Table 1. We found that the levels of miR-152, miR-130a and miR-130b were upregulated in the islets of hyperglycaemic donors (IGT/T2D) compared to those of normoglycemic (NGT) donors (Fig. 1B). [score:1]
Effect of modulating miR-130a, miR-130b, and miR-152 levels on insulin secretion in INS-1 832/13 cells. [score:1]
In this study, we showed that islets from hyperglycaemic human donors contain elevated levels of miR-130a, miR-130b and miR-152. [score:1]
For instance, we could observe that miR-152 impacted less on the ATP:ADP ratios during GSIS than either miR-130a or miR-130b. [score:1]
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3
[+] score: 54
Expression of miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588 were uniquely suppressed in mid dose but then elevated in high dose, with opposite expression to their target genes. [score:9]
In agreement with sequencing data, miR-129, miR-130b and miR-141 were down-regulated in CM and up-regulated in CH, although no signicance was found in miR-141. [score:7]
Interestingly, our results showed that OTA induced up -expression of miR-130b in the 4 and 13 weeks groups, then a down -expression in the 26 weeks groups, indicating the different effect of OTA on miR-130b between the short- and long-term treatment. [score:5]
The expression of target genes of miR-129, miR-218b, miR-141,miR-130a, miR-130b, miR-3588 at 13 weeks. [score:5]
Both of miR-130b and miR-141 were up-regulated after administrated with OTA for 4 weeks (Figure  10a). [score:4]
In the 26-week group, the expression of miR-129 and miR-130b were decreased, while miR-141 was increased (Figure  10c). [score:3]
The expression of miR-129, miR-130a, miR-130b and miR-141 was also examined in kidneys of rats in groups of 4 weeks and 26 weeks. [score:3]
Among these 77 miRNAs, those with ≥ 2-fold down-regulation in CM compared to CK (miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588) were selected for bioinformatic analysis. [score:3]
The mRNA expression of Smoc2/Dcn (miR-129), Emp1/Rapgef5 (miR-218b), lgfbp3/sepp1 (miR-141), lgfbp3/Sepp1/Col1a2/Edem1 (miR-130a/miR-130b) and Edem1/Dpt (miR-3588) at 13 weeks are strongly correlated with its corresponding miRNAs shown in the parentheses. [score:3]
Figure 10 analysis of miR-129, miR-130a, miR-130b and miR-141 expression in the kidneys of the rats in 4 weeks (BK, BM and BHgroups, Figure 10 a), 13 weeks (CK, CM and CH groups, Figure 10 b) and 26 weeks (DK, DM and DH groups, Figure 10 c). [score:3]
KEGG and GO enrichment analyses were further performed in the six differentially expressed miRNAs (miR-129, miR-130a, miR-130b, miR-141, miR-218b and miR-3588), demonstrating that “phosphatidylinositol signaling system”, “pancreatic cancer” and “MAPK signaling pathway” were mostly significantly enriched. [score:3]
Among the six miRNAs that selected by STEM analysis, 4 miRNAs (most of the pathways were enriched by the targets of miR-129, miR-130a and miR-130b. [score:3]
Notably, regulation of the pathways and GOBPs were strongly associated with miR-129, miR-130a and miR-130b. [score:2]
No change was found in miR-130b according to (Figure  10b). [score:1]
[1 to 20 of 14 sentences]
4
[+] score: 38
Therefore, we speculate here that downregulation of miR-93 and miR-130b can result in elevated expression of tumor suppressor TP53INP1, which in turn can cause growth arrest of AR42J-B13 cells leading to transdifferentiation. [score:8]
Using these hepatocyte and non-hepatocyte cell lines and primary tissues, we performed unsupervised clustering analysis by selecting 7 down-regulated miRNAs (miR-17-5p, miR-18a, miR-93, miR-106a, miR-106b, miR-130b and miR-375) and 4 up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182). [score:7]
Total RNA extracted from Dex/OSM treated AR42J-B13 cells (7 Days) and mock controls were used for Northern blot analysis using antisense probes against down-regulated miRNAs (miR-93, miR-106b and miR-130b) and up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182). [score:7]
Both up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182) and down-regulated miRNAs (miR-17-5p, miR-18a, miR-93, miR-106a, miR-106b, miR-130b and miR-375) were chosen as a parameter for comparison. [score:7]
Interestingly, Yeung et al. reported that miR-93 and miR-130b have a potential to target tumor suppressor protein p53 -induced nuclear protein 1 (TP53INP1) in HTLV-1 infected/transformed cells [39]. [score:5]
Mature miRNA of miR-93, miR-106b, miR-130b, miR-21, miR-22 and miR-182 were differentially expressed after transdifferentiation. [score:3]
As shown in Table 1, both miR-93 and miR-130b were reduced in transdifferentiated hepatocytes. [score:1]
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5
[+] score: 30
We indeed confirmed the upregulation of miR-124a and miR-383 and the downregulation of miR-181a and miR-130b observed by microarray (Fig.   2a–d). [score:7]
The islets of these animals displayed modifications at the level of several miRNAs, including upregulation of miR-34a, miR-124a and miR-383, and downregulation of miR-130b and miR-181a. [score:7]
In contrast, beta cell proliferation was unaffected by overexpression of miR-383 and miR-124a or downregulation of miR-130b (Fig.   6e–g). [score:6]
Downregulation of miR-130b and overexpression of miR-383 did not affect apoptosis of rat (Fig.   5c, e) or human (Fig.   5d, f) islet cells, whereas they exerted a protective effect when the cells were treated with cytokines. [score:6]
Indeed, downregulation of miR-130b or induction of miR-383 improved the survival of beta cells under proapoptotic conditions. [score:4]
[1 to 20 of 5 sentences]
6
[+] score: 19
Male-biased miRNA expression was associated with pathways related to cancer (miR-130b, miR-214, miR-181b, miR-199a, miR-150, miR-135a, miR-142-3p, miR-142-5p, miR-185), hematological disease (miR-22*, miR-142-3p, miR-142-5p, miR-150, miR-181b), and renal inflammation/nephritis (miR-130b, miR-223, miR-150, miR-142-5p, miR-296*, miR-185-3p) (Additional file 2). [score:5]
Several miRNAs also exhibited substantial male-biased expression, including miR-142-5p (7.8-fold), miR-130b (5.9-fold), and miR-206 (4.6-fold). [score:3]
MiRNAs associated with young age expression showed the highest enrichment for pathways involved in renal inflammation/nephritis (miR-130b, miR-363, miR-296*) and cancer (miR-214, miR-130b, miR-18a, miR-181a, miR-363, miR-196a). [score:3]
Significant age differences in the expression of miR-34a, miR-223, and miR-130b (Figure  7A,E,F) were confirmed by qPCR. [score:3]
More than 15 cancer-related pathways ranked among the top findings for the young age group and included common miRNAs: miR-363, miR-181a, miR-130b, and miR-18a (Figures  5 and 6). [score:1]
These miRNAs showed high representation in renal inflammation and nephritis pathways, and included miR-214, miR-130b, miR-150, miR-223, miR-142-5p, miR-185, and miR-296*. [score:1]
MiR-181a and miR-130b have also been shown to be involved in endothelial cell proliferation [43]. [score:1]
These six miRNAs are miR-130b, miR-296*, miR-223, miR-142-5p, miR-185, and miR-150. [score:1]
For example, miR-130b was found in pathways related to cancer, renal inflammation, and organismal injury and abnormalities, while miR-150 was found in both cancer and renal inflammation pathways. [score:1]
[1 to 20 of 9 sentences]
7
[+] score: 17
We applied this approach to all significantly up- or down-regulated miRNAs at each time point as follows: For the only dysregulated miRNA at 1 hours (rno-miR-130b), we searched through the IPA database to identify potential mRNA targets among stretch-regulated genes in response to 1, 4, and 12 hours of stretching. [score:8]
In response to 4 hours of mechanical stretch, rno-miR-322, let-7f, miR-103, miR-126, miR-494, miR-126*, miR-130b and miR-195 were significantly dysregulated (Fig.   7A and Supplementary Dataset  5), so we sought potential mRNA targets for these dysregulated miRNAs among the stretch-regulated genes in 4 and 12 hours timepoints. [score:6]
In response to 1 hour of mechanical stretching, only one miRNA, rno-miR-130b showed differential expression compared to controls (P < 0.05), whereas 8 miRNAs (rno-miR-322, rno-let-7f, rno-miR-103, rno-miR-126, rno-miR-494, rno-miR-126*, rno-miR-130b, rno-miR-195; P < 0.05) were dysregulated in response to 4 hours of stretch (Supplemental Dataset  5). [score:3]
[1 to 20 of 3 sentences]
8
[+] score: 14
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]
Moreover, the low expression of miR-130 and miR-378 in both MSC-Exo and MSCs found in our study is in line with other reports that high expression of the miR-130 and miR-378 caused K ion channel dysfunction in cardiac stem cell and cardiac hypertrophy [37, 38]. [score:5]
We found that the expression of miR-130, miR-378, and miR-34, which negatively regulate cardiac functions, was relatively low. [score:4]
[1 to 20 of 3 sentences]
9
[+] score: 9
Inhibition of FGF signaling through SU5402 -treated primitive streak regions of chick embryos identified up-regulation of let-7b, miR-9, miR-19b, miR-107, miR-130b, miR-148a, miR-203, and miR-218 and down-regulation of miR-29a and miR-489 (Bobbs et al. 2012). [score:9]
[1 to 20 of 1 sentences]
10
[+] score: 7
Other miRNAs from this paper: rno-mir-21, rno-mir-132, rno-mir-451
In total, three microRNAs (miR-21, miR-130b and miR-132) were significantly up-regulated (≥2-fold, P < 0.01), whereas 10 down-regulated (≤0.5-fold, P < 0.01) in hearts from HCM patients (Fig. 1A). [score:7]
[1 to 20 of 1 sentences]
11
[+] score: 7
Seven overexpressed miRNAs (miR-20a, miR-199a-5p, miR-199, miR-323, miR-301a, miR-301b and miR-130b) showed the most target mRNAs. [score:5]
The miRNAs including miR-301a, miR-301b and miR-130b regulated some important genes, including TGF-βR1, TGF-βR2, Smad2, Smad4 and Smad5 and, therefore, might be of great importance to the activation of the organ of Corti. [score:2]
[1 to 20 of 2 sentences]
12
[+] score: 7
Other miRNAs from this paper: rno-mir-130a
miR-130 suppresses adipogenesis by inhibiting peroxisome proliferator-activated receptor gamma expression. [score:7]
[1 to 20 of 1 sentences]
13
[+] score: 5
Expression changes respect to control/sham 1 dpo 7 dpo Name Liu Present Liu Present rno-miR-130b 1.42 NE rno-miR-146a 1.72 INC S rno-miR-15b 1.15 DEC NS rno-miR-17 1.74 INC NS rno-miR-18a 2.71 NE 3.41 NE rno-miR-200c 4.12 NE rno-miR-206 3.26 NE rno-miR-20a 1.69 NC rno-miR-20b-5p 1.83 NE rno-miR-21 1.37 INC S rno-miR-214 2.01 INC NS rno-miR-219-5p −1.82 DEC S rno-miR-221 1.1 NE rno-miR-223 3.58 INC S 3.4 INC S rno-miR-24-2* 2.41 DEC NS rno-miR-290 3.66 INC NS 2.96 DEC S rno-miR-378 1.31 INC NS rno-miR-410 −1.21 NE rno-miR-466b 3.05 DEC S rno-miR-541 1.11 INC S rno-miR-874 2,8 NEData restricted to microRNAs with significant changes in expression (2-fold or greater) according to Liu et al. [6]. [score:5]
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14
[+] score: 5
Other miRNAs from this paper: rno-mir-301a, rno-mir-130a, rno-mir-146a, rno-mir-301b
For example, TAp63, a p53 family member, has been reported to coordinately regulate Dicer and miR-130b to suppress metastasis [52]. [score:4]
MiRNA-301a (miR-301a) is the member of miR-130/301a family. [score:1]
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15
[+] score: 4
Among these differentially expressed miRNAs, rno-miR-130b-3p, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, rno-miR-351-5p, and rno-miR-21-3p had the largest positive fold changes, while rno-miR-335, rno-miR-192-3p, rno-miR-194-5p, rno-miR-192-5p, rno-miR-499-5p, and rno-miR-210-3p had the largest negative fold changes (Table 1). [score:3]
Although the magnitude of changes differed between the two methods, these results demonstrated a high consistency between the microarray and RT-qPCR based results except for rno-miR-130b-3p and Cyp2c11. [score:1]
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In fact, these autophagy linked genes’ mRNA includes, the target sequence for miRNAs related to diverse families 5, 6. The gene networks regulating autophagy pathway were determined using a system biology and unrevealed miR-130, miR-98, miR-124, miR-204, and miR-142 as presumed posttranscriptional modulators of this pathway at different levels [6]. [score:4]
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MiRNA-21 (A), miRNA-199a (B), miRNA-130b (C), miRNA-138-1 (D), miRNA-9 (E), miRNA-27a (F), miRNA-125a (G), and miRNA-320 (H) expression was not validated at 3 days after treatment with BM-MSC. [score:3]
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Additional miRNAs involved in the regulation of the AhR include has-mir-26a-5p, hsa-mir-130b-3p, has-mir-124-3p, has-miR-625-5p and has-miR-98-5p with proven experimental evidence for their participation in the regulation of genes coding for lipid transport most notable CD36, fatty acid binding proteins FABP1, FAB6, FAB7, low density lipoprotein receptor, RXRß and others based on miRTarBase data analysis and PubMed searches. [score:3]
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MiR-98, miR-124, miR-130, miR-142, and miR-204, might regulate autophagy [25, 26]. [score:2]
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The other highly significant miRNAs displaying a steep decrease from younger to older animals (miR-301b, miR-130b, miR-20a, and miR-15b) are known to be involved in cancers (Attar et al. 2012; Funamizu et al. 2014; O’Donnell et al. 2005; Zhu et al. 2015), suggesting a role for these miRNAs in regulating MEC cell proliferation immediately after birth. [score:2]
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Other miRNAs from this paper: rno-mir-27a, rno-mir-146a, rno-mir-200a, rno-mir-182
23, 32, 33 Several miRNAs, such as microRNA-130b, [34] microRNA-182, [35] microRNA-146a [36] and microRNA-200a, [37] have been found dysregulated in diabetes. [score:2]
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MicroRNA-130b promotes cell proliferation and invasion by inhibiting peroxisome proliferator-activated receptor-gamma in human glioma cells. [score:2]
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