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51 publications mentioning rno-mir-451

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-451. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 176
Other miRNAs from this paper: rno-mir-21, rno-mir-130b, rno-mir-132
Considering the expression of miR-451 was down-regulated in the hearts from HCM patients, we have been suggested that the expression of TSC1 could be up-regulated in HCM hearts. [score:11]
The down-regulation of miR-451 may contribute to the development of HCM and may be a potential therapeutic target for the disease. [score:9]
These data demonstrate that the miR-451 plays an important role in regulating cardiac autophagy potentially by the targeted suppression of the expression of TSC1. [score:8]
As expected, the expression of TSC1 was markedly down-regulated by overexpression of miR-451 in both neonatal cardiomyocytes and HeLa cells (Fig. 3C and D). [score:8]
In summary, our study reveals that miR-451 is one of the most down-regulated microRNAs in HCM and regulates cardiac hypertrophy and cardiac autophagy by targeting TSC1. [score:7]
Among these differently expressed microRNAs, miR-451 ranked as the most down-regulated. [score:6]
Consistently, in HCM myocardia, where the expression of miR-451 was significantly decreased, up-regulated TSC1 and activated autophagy were observed. [score:6]
In the present study, we identified the differently expressed microRNAs in HCM by using a microRNAs microarray, and found that miR-451 was one of the most down-regulated microRNAs. [score:6]
We next assessed whether miR-451 suppressed the expression of endogenous TSC1. [score:5]
These results indicated that the down-regulation of miR-451 might be involved in the development of HCM. [score:5]
However, we found that the activity of AMPK was not altered by either overexpression or knockdown of miR-451 in cultured neonatal rat cardiomyocytes (data not shown). [score:4]
In most of the myocardia from HCM patients where miR-451 was significantly down-regulated, the activity of AMPK tended to be decreased (data not shown). [score:4]
Our microRNA profiling analysis indicated that miR-451 was one of the most down-regulated microRNAs in HCM patients, which was confirmed by qRT-PCR. [score:4]
Ectopic expression of miR-451 protects cardiomyocytes from ischaemia/reperfusion injury, whereas knockdown of miR-451 exacerbates any simulated ischaemia/reperfusion -induced cell death 20. [score:4]
Previous studies reported that miR-451 inhibited the activity of AMPK by down -regulating LKB1 32, 33. [score:4]
Overexpression of miR-451 in neonatal rat cardiomyocytes decreased cell size, whereas knockdown of endogenous miR-451 induced cardiac hypertrophy. [score:4]
As TSC1 is expressed in various cardiovascular tissues and activates autophagy 4, 21, 22, we assessed whether autophagy was regulated by miR-451. [score:4]
To further investigate the mechanism by which miR-451 regulates cardiac hypertrophy, we searched for the targets of miR-451 by using the TargetScan database. [score:4]
In this study, we found that miR-451 was markedly down-regulated in heart tissues from HCM patients. [score:4]
Finally, our study unveiled that miR-451 negatively regulated cardiac hypertrophy and cardiac autophagy via targeting TSC1. [score:4]
For transfection, cells were starved for 24 hrs, and miR-451 mimics or antagomir was transfected into cells with Lipofectamine 2000 (Life Technologies) for overexpression or knockdown of miR-451, according to the manufacturer’s instructions. [score:4]
In the present study, we demonstrated that TSC1 was a direct target of miR-451. [score:4]
We observed that the LC3-II in cells with miR-451 overexpression was significantly decreased, whereas cells transfected with miR-451 antagomir showed increased LC3-II (Fig. 4C and D). [score:3]
The mutant fragment with substitution of miR-451 target site were synthesized (GenScript, Nanjing, China) and cloned into the same vector to generate a mutated pMIR-TSC1-3′UTR plasmid. [score:3]
Autophagy is inhibited by miR-451. [score:3]
Figure 1The expression of miR-451 is decreased in hearts from patients with hypertrophic cardiomyopathy. [score:3]
Secondly, we elucidated that TSC-1 was a novel functional target responsible for miR-451 in cardiomyocytes. [score:3]
Conversely, the suppression of miR-451 in HeLa cells resulted in larger amounts of EGFP-LC3 punctae (Fig. 4A and B). [score:3]
Bioinformatic analysis predicted that TSC1 was a novel target of miR-451. [score:3]
The surface area of miR-451 overexpressed cardiomyocytes was significantly decreased to 76.0% of the scramble group (P < 0.05; Fig. 2). [score:3]
MiR-451 negatively regulated the expression of endogenous TSC1 and autophagy. [score:3]
As shown in Figure 1B, the expression of miR-451 had decreased more than fourfold. [score:3]
TSC1 is a novel target of miR-451. [score:3]
MiR-451 is down-regulated in hearts from HCM patients. [score:3]
Wang et al. reported that genetic knockout of miR-451 impairs ischaemic preconditioning -mediated cardioprotection exposed to ischaemic/reperfusion injury 19. [score:2]
The 3′UTR of human tuberous sclerosis complex 1 (TSC1) containing miR-451 target sites was amplified using the following primers: forward, 5′-AGGACTAGTGGAATGATGGTCAATCAGTG-3′; reverse, 5′-AGGGAGCTCCACAGTGCCAGCTCCAG-3′. [score:2]
Thus, AMPK may not play a crucial role among the regulation of autophagy by miR-451 in cardiomyocytes. [score:2]
To test whether the predicted TSC1 was a functional target of miR-451, dual luciferase assays were performed. [score:2]
To validate the under -expression of miR-451, a qRT-PCR assay was performed with expanded tissue samples (NCM, n = 8 and HCM, n = 16). [score:2]
The 3′UTR regions of TSC1 contained two sites complimentary to miR-451 (Fig. 3A). [score:1]
Previous studies suggest that the role of miR-451 in the heart may be protective in response to stresses. [score:1]
To analyse the effects of miR-451 on cardiac hypertrophy, we transfected primary neonatal rat cardiomyocytes with miR-451 mimics or miR-451 antagomir for 48 hrs after which the cell surface areas were analysed. [score:1]
H9c2 cells were transfected with the wild-type pMIR-TSC1-3′UTR or mutated pMIR-TSC1-3′UTR plasmids and cotransfected with either miR-451 mimics or scrambled microRNA. [score:1]
MiR-451 regulates cell surface area in vitroMiR-451 was reported to show cardioprotective roles in response to ischaemia/reperfusion stresses 19, 20, but its role remains unclear in cardiac hypertrophy. [score:1]
The binding sites of miR-451 in wild-type (WT) and mutated (Mut) 3′UTR sequences of TSC1 are shown. [score:1]
An autophagy-reporter plasmid encoding EGFP-LC3 recombinant protein was cotransfected with miR-451 mimics or antagomir into HeLa cells. [score:1]
Primary neonatal rat cardiomyocytes and HeLa cells were transfected with miR-451 mimics or scrambled microRNA. [score:1]
For the quantitative detection of mature miR-451, total RNA was reverse transcribed using High Capacity cDNA Reverse Transcription Kit (Life Technologies,Grand Island, NY, USA). [score:1]
HeLa cells were transfected with EGFP-LC3, together with miR-451, scrambled microRNA, miR-451 antagomir-451 or control antagomir, for 48 hrs and EGFP-LC3 punctae were observed and analysed with FV1000 confocal microscopy (Olympus, Tokyo, Japan). [score:1]
MiR-451 regulates cell surface area in vitro. [score:1]
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2
[+] score: 98
Other miRNAs from this paper: rno-mir-7a-1, rno-mir-7a-2, rno-mir-7b, rno-mir-375
Therefore, we speculated that the low expression of 14-3-3ζ might be regulated in part due to the over -expression of miR-451 and miR-375, and the over -expression of p53 may be caused by the down-regulation of 14-3-3ζ in spina bifida aperta. [score:11]
Thus, we speculated that the low expression of 14-3-3ζ, which may be regulated by the over -expression of miR-451 and miR-375, and the consequent up-regulation of p53 may contribute to excessive apoptosis in spina bifida. [score:9]
These data suggest that the reduced expression of 14-3-3ζ plays a role in the excessive apoptosis that occurs in spina bifida and may be partly regulated by the over -expression of miR-451 and miR-375, and the consequent up-regulation of p53 might further promote apoptosis in spina bifida. [score:9]
Up-regulated expression of miR-451 was also observed in spina bifida (E13∶1.163±0.189 vs. [score:6]
We discovered that, in contrast to the reduction of 14-3-3ζ expression, the expression of miR-451, miR-375 and p53 increased in spina bifida rat fetuses. [score:5]
We found that, as compared with control fetuses, the expression of miR-375 in spina bifida was significantly up-regulated at E13, and miR-451 was increased at E13 and E15. [score:5]
To initially explore the molecular mechanisms of apoptosis in NTDs, we investigated the expression of microRNA-7 (miR-7), microRNA-375 (miR-375) and microRNA-451 (miR-451), which are known to down-regulate 14-3-3ζ in several different cell types. [score:4]
These data suggest that the low expression levels of 14-3-3ζ in spina bifida aperta may be partially regulated by miR-375 and miR-451. [score:4]
Therefore, in this paper, we confirmed the expression of 14-3-3ζ in spinal cords from normal rat fetuses and fetuses with spina bifida from E11 to E19, and selected miR-7, miR-375 and miR-451 as upstream regulators and p53 as the downstream effector of 14-3-3ζ. [score:4]
Accompanying the reduced expression of 14-3-3ζ, miR-375, miR-451 and p53 were all increased. [score:3]
Expression of miR-7, miR-375 and miR-451 in spinal cords of rat fetuses. [score:3]
In subgroup 2, the expression of miR-7, miR-375 and miR-451 was similar to that in controls (Figure 3, A - miR-7, B - miR-375, C - miR-451). [score:3]
However, in subgroup 1, the expression of miR-375 and miR-451 was significantly different from control fetuses. [score:3]
Over -expression of miR-375 and miR-451 in Defective Spinal Cords. [score:3]
0070457.g003 Figure 3Expression of miR-7 (A), miR-375 (B) and miR-451 (C) in spinal cords of control group (blue), subgroup 1 (red) and subgroup 2 (pink) embryos at E12, E13 and E15 detected by qRT-PCR. [score:3]
To initially explore the mechanism by which 14-3-3ζ is down-regulated in spina bifida, we measured miR-7, miR-375 and miR-451 (upstream regulators of 14-3-3ζ) in normal and defective spinal cords at E12, E13 and E15. [score:3]
Furthermore, we showed that, in contrast to the reduction of 14-3-3ζ expression, the levels of miR-451, miR-375 and p53 increased in spina bifida rat fetuses. [score:3]
One-way ANOVA was used to evaluate differences in 14-3-3ζ expression (both in mRNA and protein levels), miR-7, miR-375, miR-451 and p53 protein expression among the controls, subgroup 1 and subgroup 2. If a significant P-value was reached, the SNK post-hoc test was used for pairwise comparisons to identify which means were significantly different from one another. [score:3]
However, the expression of miR-7, miR-375 and miR-451 in subgroup 2 was similar to that in control fetuses. [score:3]
Expression of miR-7 (A), miR-375 (B) and miR-451 (C) in spinal cords of control group (blue), subgroup 1 (red) and subgroup 2 (pink) embryos at E12, E13 and E15 detected by qRT-PCR. [score:3]
Further investigation is necessary to determine why 14-3-3ζ is expressed at low levels at E12 in spina bifida and how 14-3-3ζ is regulated by miR-375 and miR-451 at E13 and E15. [score:2]
The repression of 14-3-3ζ by the regulatory microRNA-451 (miR-451) has been confirmed under conditions of defective erythroid differentiation and erythroid oxidative stress [16], [17]. [score:2]
Similarly, the different expression levels of 14-3-3ζ, miR-7, miR-375, miR-451 and p53 among multiple developmental stages were also evaluated by one-way ANOVA and the SNK post-hoc test. [score:2]
Except for defective erythroid differentiation and erythroid oxidative stress, the repression of 14-3-3ζ by miR-451 has also been confirmed in early diabetic nephropathy and breast cancer [60], [61]. [score:1]
U6 (as the endogenous control gene), miR-7, miR-375 and miR-451 cDNA was reverse-transcribed from the total RNA (obtained from the same sample used for the mRNA expression assays) using specific primers and a TaqMan® MicroRNA Reverse Transcription Kit (Applied Biosystems, USA) in accordance with the manufacturer’s instructions. [score:1]
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3
[+] score: 76
Other miRNAs from this paper: rno-mir-16
Bar graphs showing (A) average fold expression of miR-451-5p and miR-16expression, fold expression was calculated using the 2 [- ΔCT] method, where ΔCT = CT [miRNA]—CT [U6snRNA]; and (B) semi-quantitative analysis of pathology for glomerulosclerotic index (GI) and tubulointerstitial fibrosis index (TFI) in kidney-tissue from untreated diabetic (DM), non-diabetic control (CTRL) and insulin treated diabetic rats (DM + INS) at 10 [th] week of the study 1 (n = 6-10/group). [score:5]
0154055.g006 Fig 6. Bar graphs showing (A) average fold expression of miR-451-5p and miR-16expression, fold expression was calculated using the 2 [- ΔCT] method, where ΔCT = CT [miRNA]—CT [U6snRNA]; and (B) semi-quantitative analysis of pathology for glomerulosclerotic index (GI) and tubulointerstitial fibrosis index (TFI) in kidney-tissue from untreated diabetic (DM), non-diabetic control (CTRL) and insulin treated diabetic rats (DM + INS) at 10 [th] week of the study 1 (n = 6-10/group). [score:5]
MicroRNA-451 inhibits growth of human colorectal carcinoma cells via downregulation of Pi3k/Akt pathway. [score:5]
The drop in kidney levels of miR-451-5p and miR-16 could lead to unchecked increased expression of their target IL-6 and MMP-9 levels (Fig 7) which are associated with the pathogenesis of diabetes nephropathy [52] [49– 51]. [score:5]
Furthermore, Rosenberger et al, 2015 have shown that the inhibition of miR-451 expression is related to elevated levels of IL-6 [48]. [score:5]
Relative expression of miR-451-5p and miR-16 was estimated using TaqMan microRNA expression assays (Applied BioSystems, Foster city, CA, USA) through quantitative Real Time PCR (qPCR). [score:4]
To analyze the expression of target genes of miR-451-5p and miR-16, first the kidney tissue total RNA (2μg) was reverse transcribed to cDNA using High-Capacity cDNA Reverse Transcription Kit as per manufacturer's instructions using random primers (Applied BioSystems, Foster city, CA, USA). [score:4]
Moreover, the down-regulation of miR-451 has also been associated with cardiomyopathy in diabetic mice [46]. [score:4]
In addition the levels of MMP-9, experimentally proven target of miR-451 reported in mirTarbase was also significantly increased in diabetic kidney tissue (Fig 7). [score:3]
However, renal pathology showed a strong negative association with the renal expression of miRs, i. e., for miR-451-5p, n = 14, r = 0.70, p = 0.005 for TFI, and r = 0.6 and p = 0.02 for GI, and for miR-16, n = 10, r = 0.8, p = 0.005 for TFI and r = 0.78, p = 0.008 for GI (Fig 6C). [score:3]
0154055.g005 Fig 5(A) Line diagram showing average fold expression of (A) miR-451-5p and (B) miR-16 in urinary exosomes from untreated diabetic (DM, n = 10), non-diabetic control (CTRL, n = 6) and insulin treated diabetic rats (DM + INS, n = 6) at 3 [rd], 6 [th] and 9 [th] weeks post-injection. [score:3]
Significantly higher mRNA levels of IL-6 and MMP-9 genes (predicted targets for miR-16 and miR-451-5p) were found in kidney tissue from DM rats relative to control or DM + INS rats (Fig 7). [score:3]
To determine the time course of regulation of miR-451-5p and miR-16 in urinary exosomes during diabetes, we examined UE from rats at the 3 [rd], 6 [th] and 9 [th] weeks of diabetes by Taqman -based qPCR. [score:2]
We conducted a detailed analysis of the time-course regulation of miR-451-5p and miR-16 in urinary exosomes and found them to be increased substantially on an initial screen of all urine exosomal miRNAs. [score:2]
Findings presented in our study on the regulation of miR-451-5p support the potential usefulness of urinary exosomal (UE) miRNA analysis for non-invasive serial monitoring of early renal damage in diabetes. [score:2]
The rise in miR-451-5p may be a more sensitive predictor of imminent diabetic kidney disease, as compared to albumin excretion. [score:2]
We examined the effect of diabetes on the regulation of miRNA-451-5p and miR-16 in the kidney tissue at 10 weeks (Study 1) by qPCR. [score:2]
This is in agreement with studies demonstrating a protective role of miR-451 in ameliorating diabetic complications, especially diabetic nephropathy [54, 55]. [score:1]
Thus, the rise in miR-451-5p in UE at the 6 [th] week (or even earlier if sampled) may predict an increase in urine albumin excretion and renal tissue pathology. [score:1]
Notably, mean miR-451-5p levels increased more than 1000-fold between 3 and 6 weeks, while urine albumin increased only 21% (non-significant). [score:1]
Moreover, at the 9 [th] week, a significant difference was observed for miR-451-5p (p = 0.04) and miR-16 (p = 0.03) among the three groups by One Way ANOVA. [score:1]
Change in urinary exosomal miRNA-451-5p and miR-16 levels during the course of diabetes. [score:1]
Moreover, UE miR-451-5p levels at 6 [th] week significantly correlated with urine albumin excretion at 9 [th] week (Fig 5C) 10.1371/journal. [score:1]
Change in Urinary exosomal miRNA-451-5p and miR-16 levels during the course of the study in rats. [score:1]
However, urine exosomal miRNA did not correlate or predict renal miRNA levels, at least with regard to miR-451-5p and miR-16. [score:1]
Moreover, it is unclear to what extent changes in the levels of miR-16 and miR-451-5p in urinary exosomes in diabetes can predict future renal pathology. [score:1]
Moreover, UE miR-451-5p levels at 6 [th] week significantly correlated with urine albumin excretion at 9 [th] week (Fig 5C) 10.1371/journal. [score:1]
Fold change values for miR-451-5p and miR-16 obtained by real time PCR. [score:1]
In summary, we demonstrated a progressive rise in miR-451-5p levels and miR-16 in urinary exosomes in diabetic rats during the progression of diabetes. [score:1]
Surprisingly, we found significantly lower levels of both miR-451-5p and miR-16 in kidney tissue from DM rats relative to control or DM + INS rats (p = 0.007 and 0.024, respectively by One-Way ANOVA, Fig 6A). [score:1]
Kidney tissue levels of miR-451-5p and miR-16 and their association with renal pathology at the end of the study. [score:1]
The results from miR-451-5p and miR-16 corroborated with the findings from deep sequencing analysis most, and hence they were selected for further analysis. [score:1]
For miR-451-5p, the levels increased significantly in the 6 [th], and then further increased in the 9 [th] week of diabetes, relative to the 3 [rd] week (p = 0.03 and p = 0.002, respectively Fig 5A). [score:1]
Further studies are, however, warranted to establish the potential of miR-451-5p as a non-invasive tool to serially monitor diabetic renal damage in human subjects. [score:1]
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4
[+] score: 40
Therefore, we measured the expression of GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 using real-time RT-PCR to examine their expression patterns in the context of LHR downregulation (Fig. 1). [score:6]
In a similar manner, rno-miR-144 and rno-miR-376a expression peaked 12 h after the hCG treatment, and rno-miR-451 expression peaked 24 h after the hCG treatment. [score:5]
We believe that the discrepancy regarding in the expression of miR-144 and 451 between in the in vivo and in vitro experiments (Fig. 1 and 2) can be explained by the presence of blood cells in the in vivo study which express both rno-miR-144 and rno-miR-451 [22], [23]. [score:5]
uk/) revealed that rno-miR-144, rno-miR-376a, and rno-miR-451 can bind to the 3′-UTR of GRP78 mRNA (from bp 2439–2459) and negatively regulate GRP78 expression. [score:4]
Rat GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 expression in primary rat granulosa cells induced by FSH and hCG. [score:3]
Time course of rat GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 expression in rat ovaries induced by PMSG and hCG. [score:3]
The array data along with the bioinformatic analysis provided by MicroCosm Targets, which indicated that several miRNAs bind to the GRP78 mRNA 3′-UTR, led us to focus on rno-miR-144, rno-miR-376a, and rno-miR-451. [score:3]
From these, we narrowed the focus to rno-miR-376a based on the results of the in vitro experiments (Fig. 2) since rno-miR-144 and rno-miR-451 was not induced expression by hCG treatment. [score:3]
In contrast, rno-miR-144 and rno-miR-451 expression decreased significantly after the hCG treatment. [score:3]
Rat GRP78 mRNA (A), rno-miR-144 (B), rno-miR-376a (C), and rno-miR-451 (D) expression levels were measured using real-time RT-PCR as described in the. [score:1]
The amount of rat GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 in the hCG 0 h group was set at 1. Data were normalized to 18S rRNA (for GRP78 mRNA) and 4.5S RNA(H) (for rno-miR-144, rno-miR-376a, and rno-miR451) levels in each sample and represent the mean ±SE of three independent experiments. [score:1]
Total RNA was isolated, and GRP78 mRNA (A), rno-miR-144 (B), rno-miR-376a (C), and rno-miR-451 (D) expression levels were measured using real-time RT-PCR as described in the. [score:1]
Next, we investigated the effects of rno-miR-144, rno-miR-376a, and rno-miR-451 on GRP78 mRNA expression in granulosa cells isolated from DES -treated immature rats (Fig. 2). [score:1]
The amounts of GRP78 mRNA, rno-miR-144, rno-miR-376a, and rno-miR-451 in the hCG 0 h group were set at 1. Data were normalized for 18S rRNA (for GRP78 mRNA) and 4.5S RNA(H) (for rno-miR-144, rno-miR-376a, and rno-miR-451) levels in each sample and represent the mean ±SE of 3 independent experiments. [score:1]
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5
[+] score: 31
UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
0180490.g006 Fig 6 UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
miR-155 and miR-451 upregulated in HSD and UNX+HSD rats (Fig 5D). [score:4]
In glioma cells, miR-451 targets CAB39 [53], a binding partner of LKB1 [54], which in turn phosphorylates and activates AMPK [55]. [score:3]
D), E) Relative levels of miR-25, miR-155, miR-451 and miR-99b in heart normalized with sn-RNU5G; F) Relative levels of miR-25, miR-451 and miR-99b in plasma normalized with miR-30e. [score:1]
Our data also shows a surge of miR-451 and a proportionate dip in p-AMPK in the heart of HSD and UNX+HSD animals. [score:1]
Roles of miR-25 [14], miR-155 [15] & miR-451 [16] in various murine CVDs have been reported but their role in high salt diet -induced CV complications in uninephrectomized rats is not yet reported. [score:1]
Micro RNAs quantified were hsa-miR-25-3p (Cat# 204361), mmu-miR-155-5p (Cat# 205930), hsa-miR-99b-3p (Cat# 204064) and mmu-miR-451(Cat# 204734) and normalized with RNU5G (a small nuclear RNA) in heart and hsa-miR-30e-5p (Cat# 204714) in plasma. [score:1]
[1 to 20 of 8 sentences]
6
[+] score: 31
Interestingly, miR-29b was drastically down-regulated by GH (21-fold, p = 0.008) (Figure 2b), GH-treatment did not affect the levels of 5S rRNA level (Figure 2a), suggesting a specific inhibitory effect of GH on miR-451 and miR-29b and putative roles for these miRNAs in the regulation of GH -dependent gene products. [score:7]
miR-451 was significantly down-regulated (3.1-fold, p = 0.01) by GH (Figure 2c), whereas miR-122a expression was unaffected by this treatment (Figure 2d). [score:6]
miR-451 had only one predicted target in common between the databases, whereas miR-148a, miR-21 and miR-205 had 200 to 300 putative target genes. [score:5]
As illustrated in figure 3, the level of miR-451 was significantly up-regulated in males (7.4-fold, p < 0.001) and females (9.7-fold, p = 0.03) after mild starvation, without any sex-differences (Figure 3c). [score:4]
We conclude that mild starvation up-regulated the levels of miR-451, miR-122a and miR-29b significantly in both sexes, when compared to the postabsorptive state. [score:3]
Based on qRT-PCR analysis, the expression of miR-451, miR-148a, miR-21, miR-205 and miR-193a were not different between the sexes and therefore contrasted the microarray results. [score:3]
However, miR-451, miR-148a and miR-193 have recently been detected in liver by a high-throughput sequencing approach (Sarah Leigh-Brown, personal communication). [score:1]
Selected miRNAs (miR-122a, miR-29b and miR-451), and 5S rRNA as reference gene, were further examined using the miRCURY™LNA Real-time PCR kit (Exiqon, Danmark), according to the manufacturer's protocol. [score:1]
Furthermore, 1 week of continuous GH-treatment in male rats reduced the levels of miR-451 and miR-29b, whereas mild starvation (12 hours) raised the levels of miR-451, miR-122a and miR-29b in both sexes. [score:1]
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7
[+] score: 24
miR-451 has recently been suggested as a prognostic biomarker of hepatocellular carcinoma (HCC), with decreased expression in HCC tissues correlating with advanced stage, metastasis, and worse disease-free or overall survival [78]. [score:5]
The expression of miR-451 was significantly increased relative to the 5–21-week-old baseline group when basophilic foci were present, i. e., increased expression was seen in the livers of 78 (1.8-fold increase) and 104-week-old (1.5 fold increase) females and not in any of the males or 52-week-old female livers. [score:5]
Increased expression of miR-451 and decreased expression of miR-18a were associated with the presence of hepatic basophilic loci, which are considered pre-neoplastic lesions [53]. [score:4]
The expression of specific miRNAs (miR-451, miR-18a, miR-99a, and miR-203) was found to associate with sexually dimorphic histopathology findings of basophilic foci and bile duct hyperplasia. [score:3]
A total of 43 miRNAs met these criteria and are shown in Additional file 5. The expression of two miRNAs was associated with the presence and absence of basophilic foci, miR-18a, and miR-451 (Table  3). [score:3]
The expression of miRNAs (miR-18a, miR-99a, and miR-203, miR-451) was also found to associate with specific sexually dimorphic hepatic histopathology. [score:3]
In addition, increased serum levels of miR-451 were recently found in patients with NAFLD [80]. [score:1]
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8
[+] score: 17
Most importantly, the predicted target genes for miRNAs also included the cytoskeleton remo delling protein tropomodulin (target for miR451) and Tm 1α and 2β, the latter of which is a molecule essential for maintaining structural biology of several organs including eye lens [53]. [score:5]
Of the latter, miR126, miR136, miR206, miR451 and miR551b showed significant, gradual down-regulation (>2 times) after birth or during development (ED16>4W>4W). [score:5]
In contrast, miR126 and miR-451 were significantly down-regulated (Fig. 2). [score:4]
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]
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9
[+] score: 11
miR-21-5p, miR-34a-5p, miR-146b-5p, miR-149-3p, miR-224-5p, miR-451-5p, miR-1949, miR-3084a-3p, and miR-3084c-3p demonstrated more abundant expression and a two-fold or greater significant increase in expression with Cd treatment. [score:5]
miR-21-5p, miR-34a-5p, miR-146b-5p, miR-149-3p, miR-224-5p, miR-451-5p, miR-1949, miR-3084a-3p, and miR-3084c-3p were more abundantly expressed and demonstrated a two-fold or greater increased expression in the Cd-treatment group. [score:5]
Using a streptozotocin -induced diabetic rat mo del, Mohan et al. demonstrated the utility of urinary exosomal miR-451-5p as an early biomarker of diabetes -associated nephropathy, and the elevated levels of miR-451-5p appeared to be protective against kidney fibrosis [48]. [score:1]
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10
[+] score: 11
Analysis at P21 revealed 74 mature miRNAs with differential expression between LPD -induced IUGR rat lungs and control lungs (Fig 1): 10 showed more than twofold differential expression: miR-184, miR-127-3p, miR-378a-5p and miR541-5p were downregulated, and miR-30e-5p, miR-23b-5p, miR-451-5p, miR-1839-5p, miR-449a-5p, and miR-19b-3p were upregulated in LPD -induced IUGR versus control lungs. [score:11]
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11
[+] score: 10
Down-regulation of miR-451 and miR-885-5p in neuron-like cells has been shown to increase Bcl-2 expression and lead to reduction of apoptosis activity [48]. [score:6]
Alural B. Duran G. A. Tufekci K. U. Allmer J. Onkal Z. Tunali D. Genc K. Genc S. EPO mediates neurotrophic, neuroprotective, anti-oxidant, and anti-apoptotic effects via down-regulation of miR-451 and miR-885-5p in SH-SY5Y neuron-like cells Front. [score:4]
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12
[+] score: 10
The qRT-PCR confirmed changes of the selected miRNAs (Figure  4B), decreased expression of miR-96, miR-141, miR-182, miR-183, miR-200a, miR-200b, miR-429 and miR-451 in F2-SSS compared to F0-S animals, whereas miR-23b and miR-200c showed increased expression levels. [score:4]
Moreover, miR-451 is expressed in the uterus [58, 59] and regulated by estrogen and progesterone [58]. [score:4]
In order to validate miRNAs, we performed quantitative real time PCR (qRT-PCR) analysis of these differentially regulated miRNAs (n = 3 per group for F0, F1 and F2 generations, three replicates per sample): miR-23b, miR-96, miR-141, miR-181a, miR-182, miR-183, miR-200a, miR-200b, miR-200c, miR429 and miR-451. [score:2]
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13
[+] score: 10
Similarly, the specific miRNA profile of AFL consisted of five downregulated (miR-93, miR-451, miR-221, miR-17-5p and miR-146a) and three upregulated (miR-200c, miR-490 and miR-195) miRNAs, in comparison to the control group. [score:7]
Wiskott-Aldrich syndrome protein family member 1 (Wasf1), which was found to be regulated by miR-17-5p, miR-93, miR-191, miR-451, miR-146a and miR-140, has been shown to be a protective alcohol-responsive gene in the prefrontal cortex of human alcoholics (38). [score:2]
Among the dysregulated miRNAs, miR-490 exhibited an increment in the ASH and AFL groups, while miR-140, miR-7a, miR-451, miR-93, miR-146a and miR-191 levels exhibited a decline in the ASH and AFL groups compared with the respective controls (Table II). [score:1]
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14
[+] score: 9
According to this observation, Caruso et al. (2010) showed that, during the onset of pulmonary arterial hypertension (PAH) after hypoxia, there is a reduced Dicer expression leading to miR-22, miR-30, and let-7f down-regulation and, at the same time, to miR-322 and miR-451 up-regulation in two different PAH rat mo dels. [score:9]
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15
[+] score: 9
Other miRNAs from this paper: mmu-mir-155, mmu-mir-451a, mmu-mir-451b, rno-mir-155
[18] The absence of the passenger strand from the miR-451 scaffold provides a better safety profile for therapeutic shRNAs or miRNAs since it reduces the chance for off-target suppression of other genes by the passenger strand. [score:5]
In this study, we showed that the miHTT construct processed from the miR-451 scaffold is able to strongly suppress mutant HTT aggregation and ultimately dramatically reduce the generation of striatal lesions at two months post-injection. [score:3]
We did not observe any reads belonging to the passenger strand, confirming the absence of a passenger strand associated with the miR-451 precursor. [score:1]
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16
[+] 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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17
[+] score: 8
IPA identified 4 focus miRNAs related to metastasis and upper gastrointestinal tract cancer (≥4 fold change) that were downregulated in metastasis positive samples versus metastasis negative samples: 1) miR-92a-3p (p = 0.0001, fold change >14), miR-141-3p (p = 0.0022, fold change >9), miR-451-1a (p = 0.0181, fold change >12) and miR133a-3p (p = 0.0304, fold change >9) (S2 Fig. ). [score:4]
miRNome analysis identified four down-regulated miRNAs in metastasis positive primary tumors compared to metastasis negative tumors: miR-92a-3p (p=0.0001), miR-141-3p (p=0.0022), miR-451-1a (p=0.0181) and miR133a-3p (p=0.0304). [score:3]
The 4 focus miRNAs symbols miR-92a-3p, miR-141-3p, miR-451-1a, and miR133a-3p were mapped from the dataset ID rno-miR-32-5p, rno-miR-141-3p, rno-miR-451-5p, and rno-miR-133b-3p respectively. [score:1]
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18
[+] score: 8
MiR-451, which was over-expressed in SP-HCCs, is involved in activating the expression of P-glycoprotein (P-gp), the MDR1 gene product that confers the SP phenotype [54]. [score:4]
Among the moderately up-regulated miRNAs, miR-451 and miR-181a have been well studied. [score:4]
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19
[+] score: 7
These data support the hypothesis that there are no distinct differences in miRNA profiles between these major organs and peripheral blood cells with some exceptions, such as miR-451 and miR-144, and that expression profiles for the majority of miRNAs were not markedly affected by remaining peripheral blood. [score:3]
Moreover, our data showed that miR-451 and miR-144 were specifically expressed in hematopoietic tissues e. g., spleen and bone marrow (refer to the original dataset for details). [score:3]
As shown in Figure 1, blood-cell–specific miRNAs (e. g., miR-451 and miR-144) [21] were clearly evident in nonperfused samples, but not in perfused samples. [score:1]
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20
[+] score: 7
Levels of miR-144, miR-451, and miR-770 were significantly down-regulated in CCA rats (p < 0.05 vs. [score:4]
Some alteration in miRNA expression following cocaine exposure may persist for a long time, even still being evident after a long-term abstinence from cocaine administration, such as miR-144, miR-451 and miR-770 in this study. [score:3]
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21
[+] score: 7
On day 2, miR-31, miR-223, miR-18a, and miR-18b were up-regulated, whereas miR-451 and miR-499-5p were down-regulated. [score:7]
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22
[+] score: 6
Cluster IV included miR-451, -341 and -376b-3p and their expression decreased from E20 to P2. [score:3]
MiR-376a, -376b-3p and -451 were localized to exocrine cells (miR-451 only at E20). [score:1]
We detected two mature species for miR-451, which may be due to its unusual structure where the mature miRNA extends into the loop sequence [27]. [score:1]
Interestingly, INS-1E cells contained precursor miRNA species for miR-451 and miR-376b-3p, but absence of mature miRNAs (Fig. S2). [score:1]
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23
[+] score: 6
Expression of miR-486-5p by RT-qPCR was in the same range as miR-451-5p suggesting reads for miR-486-5p were detected at a much higher ratio by miRNA-seq in rat blood. [score:3]
Though miR-16-5p was not among the top 10 miRNA in bovine blood 16 but is abundant in human erythrocytes 17, we checked expression by RT-qPCR and found it was also in the same range as miR-451-5p and 486-5p. [score:3]
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24
[+] score: 6
Only five miRNAs (mmu-miR-451, mmu-miR-223, mmu-miR-92a, mmu-miR-200c, and mmu-miR-873) were differentially expressed, implying that the majority of miRNA downregulation associated with obesity could be reversed by LFD treatment. [score:6]
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25
[+] score: 6
Besides, miR-140, miR-181a-5p and miR-451 expression were all highly increased during fracture healing process [18] and miR-21 overexpression [19] or miR-92a knockdown [20] would enhance fracture healing property. [score:6]
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26
[+] score: 5
To validate the microarray profiling data, qRT-PCR was used to confirm the upregulated miRNAs including miRNA-339, miR-223, miR-145, and miR-451. [score:4]
There was no significant increase in miR-451 between acupuncture group and mo del group or normal group (data not shown). [score:1]
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27
[+] score: 5
Importantly, the expression of hematopoiesis -associated miRNA (miR-451), brain-enriched miRNA (miR-143), hepatoblastoma -associated miRNA (miR-125) and of the short non-coding RNA RNU6 remained unchanged during the observed period (Fig. 6, lower row), indicating that the amount of these vesicle -associated miRNAs is not modulated at 2, 4 and 6 days after PHx. [score:3]
Other small non-coding RNAs included in the panel [i. e., RNU6, miR-143, miR-451 and miR-125 (close to significance, P = 0.057)] shows a constant expression throughout 2, 4 and 6 days after PHx and a trend of downr-egulation compared to the expression measured at day 0 (See Fig. 7, lower row). [score:2]
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[+] score: 5
After normalizing the signal intensities for all miRNA expression levels, miR-124-3p, miR-9a-3p, miR-34a-5p, miR-9a-5p, miR-125b-5p, miR-let-7c-5p, miR-29a-3p, miR-23b-3p, miR-451-5p, and miR-30c-5p were the miRNAs expressed at the highest levels (Figure  1). [score:5]
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[+] score: 4
MiR-451 was differentially expressed in the livers of infected animals, which suggests that erythroid differentiation may be altered following S. japonicum infection [36, 37]. [score:2]
It was found that miR-494, miR-365 and miR-451 were present in liver, miR-206, miR-468 and miR-691 in spleen, and miR-223, miR-98 and miR-206 in lung. [score:1]
33rno-miR-19b−1.590.33rno-miR-451−4.370.05rno-miR-196c*−1.660.32Tissue/LungLog2(infected/control)Fold changemmu-miR-32*−2.170.22rno-miR-2062.234.69mmu-miR-328*−2.630.16rno-miR-2231.823.53rno-miR-32*−2.850.14rno-miR-981.22.3mmu-miR-468−3.490.09mmu-miR-4681.192.28mmu-miR-691−4.040.06mmu-miR-669d1.112.16mmu-miR-297a−4.620.04rno-miR-328a*1.12.14mmu-miR-467h−4.960. [score:1]
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[+] score: 4
Although the most upregulated miRNAs in three rats were miR-383, miR-451 and miR-219-5p (with logs [FC]: -2.15, -2.21, -2.60) respectively, we wanted to focus on miRNAs that were altered in different rats simultaneously. [score:4]
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[+] score: 3
Intriguingly, a large number of cocaine-responsive miRNAs identified so far (miR-8 family, miR-145, miR-451) can putatively target genes implicated in addiction, including TrkB receptor, which transduces the actions of BDNF in brain and play a crucial role in activity -dependent synaptic plasticity. [score:3]
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[+] score: 3
Recent studies indicated that Epac modulated the expression of miRNAs in other cell types, as it is the case of miR-20 in macrophages [27], and miR-451 in astrocytoma cells [28]. [score:3]
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[+] score: 3
Among these 21 differentially expressed miRNAs, 17 (miR-10b-5p, miR-223-3p, miR-208a-5p, miR-434-3p, miR-190a-5p, miR-30d-5p, miR-347, miR-493-5p, miR-29a-5p, miR-451-5p, miR-190b-5p, miR-466c-5p, miR-883-5p, miR-466b-1-3p, miR-21-3p, miR-3596c, miR3584-3p) were proven significant (P < 0.05) by qRT-PCR, one (miR-487b-3p) had a tendency to be significant (P = 0.06), and three (miR-138-2-3p, miR-1188-3p, miR-665) were not confirmed to be significant (Table  2). [score:3]
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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-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, 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, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Cortex let-7c-1, miR-10a, miR-21, miR-124a-1, miR-128a, miR-135b, miR-150, miR-199a, miR-217, miR-329, miR-451. [score:1]
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]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, 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-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
E [2] decreased miR-146a, miR 125a, miR-125b, let-7e, miR-126, miR-145, and miR-143 and increased miR-223, miR-451, miR-486, miR-148a, miR-18a, and miR-708 expression in mouse splenic lymphocytes [199]. [score:3]
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[+] score: 3
Recent studies have demonstrated that miRNAs also play a role in obesity -induced cardiac pathophysiology 20, 21. miR-451 is involved in diabetic cardiomyopathy, such as cardiac hypertrophy through suppression of the LKB1/AMPK pathway in mice fed HFD [20]. [score:3]
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37
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Several miRNAs were found to be highly expressed in particular tissues: miR-204, -218, and -129-2-3p in brain tissues, miR-30a, -30e, -30d, -200a and -200b in kidney, miR-192 in liver, miR-451 in spleen, miR-21 in spleen and thymus, miR-193b, -378 in LDM muscle. [score:3]
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[+] score: 3
Dueck et al. (2012) demonstrated that ectopically expressed miR-451 in HEK293 cells is not only processed by Ago2 but also loaded exclusively onto Ago2 -associated RISC. [score:3]
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39
[+] score: 3
U6 was chosen for normalization of tissue miRNA expression whereas miR-451 was used for normalization of plasma miRNA [19]. [score:3]
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40
[+] score: 2
Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
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[+] score: 2
miR-125b, miR-146, miR-150, miR-199a, miR-21, miR-129, miR-341 and miR-451 have been confirmed to play an important role in the different developmental stages of the cardiovascular system (4– 18). [score:2]
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42
[+] score: 2
MiR-451 inhibits synovial fibroblasts proliferation and inflammatory cytokines secretion in rheumatoid arthritis through mediating p38MAPK signaling pathway. [score:2]
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43
[+] score: 2
In contrast, microRNAs that were detected in the present study but not in previous studies (Table 4) include the Exiqon miR-plus probes as well as several newly released microRNAs, for which no previous data have been published, and more interestingly, the miR-451 cluster and miR-144, which are both important gene regulators of erythrocyte homeostasis and cardiomyocyte ischemia [23], [24]. [score:2]
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[+] score: 2
Some of these miRNAs, i. e. rno-miR-34c, rno-miR-449a, rno-miR-301b, rno-miR-532-5p, rno-miR-219-5p, rno-miR-451, and rno-miR-152, were even 10-fold more abundant at E10 than at any other stages, providing a hint that these 7 miRNAs may play important roles in the regulation of progenitor cell proliferation. [score:2]
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[+] score: 2
Several miRNAs, such as miR-122, miR-451, miR-200b and miR-27, have been found to be deregulated in different diet -induced NAFLD rat mo dels [15]. [score:2]
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[+] score: 2
Comparison of whey and serum qPCR analyses using the same volumes of samples showed that only miR-192, miR-150, and miR-223 (apart from the tissue-specific miRNAs miR-451 and miR-122) were detected at higher levels in serum than in whey. [score:1]
Tissue-specific miRNAs (miR-451 and miR-122) were only detected in whey at very low levels by qPCR (Fig. 6D). [score:1]
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[+] score: 1
Other miRNAs from this paper: rno-mir-221
It has been reported that the MVs obtained from cardiac progenitor cells enriched in miR-451 might be a promising cellular cardioprotection strategy [37]. [score:1]
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[+] score: 1
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, 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-29c-2, rno-mir-1b, ssc-mir-26b
Sharbati-Tehrani et al., [67] have reported 4 new miRNAs (miR-326, miR-423-3p, miR-484 and miR-451,) that could not be identified in our study, which could be attributed to the use of very specialized tissues (Jejunium, spleen, ileum and kidney) for their study. [score:1]
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[+] score: 1
For example, miR-451 and miR-142-3p were much more abundant in exosomes than in MIN6B1 cell extracts, whereas the levels of miR-32 and miR-194 were clearly higher inside the cells. [score:1]
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[+] score: 1
Related reports by Shen and Bai et al. revealed that alteration of miRNAs such as miR-126, miR-451, miR-199a, et al., contributed to the retinal neovascularization, which is consistent with our results [17, 18]. [score:1]
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[+] score: 1
Erythrocytes have high levels of miR-16 and miR-451, which correlate to the degree of hemolysis in plasma samples [52]. [score:1]
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