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49 publications mentioning rno-mir-20a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-20a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 182
Adenovirus -mediated p300 expression significantly increased levels of all cluster members including miR-20a (1.95-fold ±0.03, p<0.0001, Figures 4C and D), while expression of an unrelated miRNA, miR-199, was unchanged (Figure 4D), confirming that p300 gain can positively regulate expression of this anti-angiogenic microRNA cluster. [score:8]
The decline in expression of these microRNAs was associated with increased expression of VEGFA, a validated miR-20a target. [score:7]
In fact, miR-20a overexpression significantly repressed most of the angiogenic genes that were differentially upregulated in p300tg hearts (Figure 5F; compare Figure 2A). [score:6]
To determine whether miR-20a could similarly repress p300 -dependent transcription in vivo, we transduced neonatal (d 1–3) p300tg mice with lentivirus encoding mature miR-20a or a scrambled sequence (ct-miR), and at 3 months of age, quantitated expression of 84 genes previously shown to be selectively upregulated by p300 in vivo [13]. [score:6]
We show that p300 is a novel target for a microRNA, miR-20a, that has been previously implicated in the negative regulation of angiogenesis through its ability to target VEGF and HIF-1 [26], [27]. [score:6]
Relative expression of most members of the 17∼92 cluster was similar in all 4 cardiac chambers and in other organs, however, significant downregulation of miR-17-3p and miR-20a occurred between 1 and 8 months of age in both wt and tg mice. [score:6]
Angiogenic genes identified as p300-regulated in the myocardial expression profile from Figure 2A were assayed by QPCR in CPCs expressing miR-20a or ct-miR. [score:5]
Grey = expression below detection threshold G. MiR-20a directly targets EP300 3′UTR. [score:5]
In addition, miR-20a was demonstrated to directly repress p300 expression through a consensus binding site in the p300 3′UTR. [score:4]
Two members of the miR-17∼92 cluster, miR-17-3P and miR-20a, were upregulated in p300tg relative to WT myocardium in both young (1 month) and adult (9 month) mice (Figure 3A). [score:4]
One member of this cluster, miR-20a, specifically targets p300 and negatively regulates the p300 -dependent angiogenic transcription program, and angiogenic differentiation of cardiac progenitor cells. [score:4]
MiR-92, another member of the cluster, has been shown to regulate myocardial angiogenesis through targets distinct from those of miR20a, including integrin subunit alpha5 [14]. [score:4]
On the other hand, unbalanced upregulation of miR-20a in this system could lead to excessive attenuation of angiogenic transcription, and could in theory account for eventual failure of compensatory blood vessel growth [12], [13], [38]. [score:4]
A. Relative upregulation of miR-17-3p and miR-20a in p300 transgenic mice. [score:4]
p300 also induces miR-20a, which provides feedback inhibition of p300, reversing both the angiogenic and hypertrophic programs and providing counter-regulatory control of the hypertrophic stress response. [score:4]
These experiments confirm that p300 is a direct target of miR-20a, likely affecting the stability of p300 mRNA, and that angiogenic transcription downstream of p300 is also repressed by miR-20a. [score:4]
Confirming this finding, both miR-17-3p and miR-20a were upregulated in neonatal rat ventricular myocytes following adenoviral transduction of p300. [score:4]
miR-20a Represses the Angiogenic Gene Expression Program in CPCs. [score:3]
Transduction of miR-20a, but not a control miR, repressed expression of a luciferase construct containing the p300 3′UTR miR17-5p/miR-20a binding site (Figure 5G, left); mutagenesis of this site eliminated miR-20a repression (Figure 5G, right). [score:3]
Note relatively higher expression of 3′ members of the cluster, miR-20a, miR-19b, and miR-92. [score:3]
D. miR-20a reverses myocardial p300 -induced gene expression profile. [score:3]
A. Low expression of miR-20a levels in cardiac progenitor cells. [score:3]
5-day old wt pups were transduced with the indicated lentiviruses and miR20a expression was detected by qPCR in left ventricular myocardial lysates at2 weeks. [score:3]
In addition, miR-20a has been recently reported to reduce apoptosis following hypoxia-reoxygenation of cardiomyocytes [36], and overexpression of the miR-17∼92 cluster modestly improved cardiac function in a mouse mo del of myocardial infarction [37], suggesting that members of this cluster may have more general protective effects during oxidative or biomechanical stress. [score:3]
E. Overexpression of miR-20a slows proliferation of cardiac progenitor cells (CPCs). [score:3]
These CPCs have high angiogenic differentiation potential and express endogenous miR-20a at very low levels relative to cardiomyocytes (Figure 5A). [score:3]
Luciferase vectors containing either full-length mouse p300 (NM_177821.6) 3′ UTR or a control 3′ sequence were transfected into 293T cells stably overexpressing miR-20a or a scrambled control microRNA using Lipofectamine 2000 (Invitrogen). [score:3]
Lentiviral-transduced cardiomyocytes expressing a control sequence (A, ct-miR) or miR-20a (B and C) together with EGFP (green) were visualized with anti-GATA-4 (magenta) and pan-alpha-actinin (red) antibodies and nuclear DNA was stained with DAPI (blue). [score:3]
CPC clones stably expressing GFP and miR-20a or a scrambled sequence (ct-miR) were plated and maintained at 40–60% confluency by serial passage. [score:3]
Neither vector inhibited a control sequence lacking the miR-20a binding site. [score:3]
Lentiviral overexpression of miR-20a, but not a scrambled sequence [16] increased miR-20a levels by more than 600-fold (Figure 5B) from a negligible endogenous level; this was sufficient to reduce endogenous CPC p300 mRNA levels by more than 40% (Figure 5C) and VegfA protein levels by ∼50% (Figure 5D), associated with a significant reduction in CPC proliferation (Figure 5E). [score:3]
MiR-20a recipients had significantly reduced myocardial p300 protein (Figures 7B and C), together with significant reversal of the myocardial p300 gene expression signature (Figure 7D and Table 3) relative to control miR-transduced hearts. [score:3]
0079133.g006 Figure 6Lentiviral-transduced cardiomyocytes expressing a control sequence (A, ct-miR) or miR-20a (B and C) together with EGFP (green) were visualized with anti-GATA-4 (magenta) and pan-alpha-actinin (red) antibodies and nuclear DNA was stained with DAPI (blue). [score:3]
Since sarcomeric actinins are not predicted targets of miR-20a, this could be due to loss of p300 and previously demonstrated p300 -dependent actinin transcription [28]. [score:3]
B. Successful expression of miR20a in CPCs following lentiviral transduction. [score:3]
Notably, we find that miR-20a prevents the expression of angiogenic genes not only in the intact myocardium, but also in c-kit+ cardiac progenitor cells [40]. [score:3]
0079133.g005 Figure 5 A. Low expression of miR-20a levels in cardiac progenitor cells. [score:3]
MiR-20a targets p300 and p300-regulated angiogenic genes. [score:3]
MiR-20a binding sites predicted by TargetScan. [score:2]
F. Mir-20a overexpression represses p300 -induced angiogenic genes in CPCs. [score:2]
To determine whether miR-20a could provide a counter-regulatory signal during p300 -induced angiogenic transcription, we transduced miR-20a into previously described clonal murine c-kit+ cardiac progenitor cells (CPCs) [24]. [score:2]
B. Time dependent inverse regulation of VegfA and miR-20a. [score:2]
p300 drives an angiogenic transcription program during hypertrophy that is fine-tuned in part through direct repression of p300 by miR-20a. [score:2]
The miR-20a binding site in the p300 3′UTR was mutated using a site-directed mutagenesis kit (Stratagene). [score:2]
Note that cells expressing the miR-20a-EGFP lentivirus (B and C, arrows) have greatly reduced staining for actinin, compared with adjacent non-transduced cells (B and C, asterixes), or cells taking up the scrambled sequence (compare EGFP+ cells in A). [score:2]
p300 protein was quantitated in the same lysates in (A) by Western blot 3 months after transduction with miR-20a. [score:1]
Newborn (5 day) p300tg pups (BS line [13]) received 8×10 [8] viral particles of miR-20a or control sequence (ct-miR) [16] via external jugular vein injection using a previously described method [17], with minor modifications [18]. [score:1]
In vivo Transduction of miR-20a. [score:1]
C. miR-20a reduces endogenous p300 transcript levels in CPCs. [score:1]
C. Gain of p300 induces miR-20a. [score:1]
A mo del of the miR20-p300 feedback loop during hypertrophy. [score:1]
Lentiviral transduction of miR-20a, but not a control sequence, sharply reduced the number of visible sarcomeres containing alpha-actinin in cardiac myocytes (Figure 6). [score:1]
These data further support functional repression of p300 by miR-20a. [score:1]
We have previously demonstrated long-lasting effects of microRNA transduction using this method [18]; consistent with this, miR-20a levels were significantly elevated for at least 2 weeks following injection (Figure 7A) following miR-20a but not ct-miR transduction. [score:1]
CPCs were transduced with miR-20a or scrambled control lentivirus [16]. [score:1]
In brief, 5-days old p300tg pups were placed on a transilluminator and the external jugular vein was injected with 10 µl of 8×10 [8] viral particles encoding miR-20a or ct-miR. [score:1]
We asked whether the sarcomeric organization of neonatal rat cardiomyocytes could be impacted by increased levels of miR-20a. [score:1]
Lentiviral vectors encoding miR-20a or a control sequence within a common miR-30 backbone have been previously described [16]. [score:1]
B. Reduced p300 in miR-20a-transduced hearts. [score:1]
A. Sustained in vivo transduction of miR20a. [score:1]
Shown are locations and sequences of canonical MEF2 and GATA binding sites upstream of miR-20a. [score:1]
In vivo Transduction of miR-20aNewborn (5 day) p300tg pups (BS line [13]) received 8×10 [8] viral particles of miR-20a or control sequence (ct-miR) [16] via external jugular vein injection using a previously described method [17], with minor modifications [18]. [score:1]
p300 -induced genes repressed by miR-20a transduction in vivo. [score:1]
See for miR-20a binding site sequence and mutant sequence. [score:1]
Similar negative feedback loops have been described for miR20a, E2F and Myc [30], [31], [32], [33]. [score:1]
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[+] score: 52
We also performed a predicted target analysis for miRNA-20a, which was chosen because it was highly expressed in the mo del group and downregulated in the PQR group. [score:8]
Recently, Pin et al. found that miR-20a can inhibit the expression of MKK3 and downregulate p38 pathway -mediated and VEGF -induced endothelial cell migration and angiogenesis [32]. [score:8]
qRT-PCR showed that miR-145 and miR-20a expression was downregulated in the mo del group compared with their expression in the PQR group, which was consistent with the microarray results. [score:7]
The underlying mechanism might be related to the modulation of 18 upregulated and 14 downregulated miRNAs, in particular, miR-20a, miR-145, miR-30, and miR-98. [score:7]
Furthermore, we also found differentially expressed miRNA-20a, with 38 potential target genes in rats, which demonstrated that miRNA expression might be significant in PQR treatment for rats with essential hypertension. [score:7]
We suggest that the target genes of miR-20a may be involved in the etiology of vascular remo deling through cell proliferation, apoptosis, migration, and differentiation. [score:3]
Thus, involution was obtained by miChip analysis for four selected miRNAs that showed either high (miR-145) or low (miR-30) signal intensities, or high (miR-20a) or low (miRNA-98) differential expression values among the three groups. [score:3]
Results of miR-20a Target Gene Prediction. [score:3]
The target genes of miR-20a may be involved in the etiology of vascular remo deling through cell proliferation, apoptosis, migration, and differentiation. [score:3]
These included miR-20a, miR-18b, miR-375, and miR-215 [34]. [score:1]
MiR-20a, a member of the miR-17–92 cluster, is a highly conserved miRNA within a noncoding RNA encoded by the c13 or f25 host gene localized on chromosome 13 [31]. [score:1]
miR-20a has also been shown to play an important role in vascular remo deling [33]. [score:1]
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[+] score: 28
As a result, five up-regulated miRNAs (miR-874-3P, miR-20a-5p, miR-345-3p, miR-365-5p and miR-764-3p) and one down-regulated miRNA (miR-99b-3p) were screened out for subsequent qRT-PCR confirmation. [score:7]
For instance, the expression of miR-20a was found to be up-regulated whilst the miR-99b level was significant reduced in both of these two studies. [score:6]
As shown in Figure 2, the expression of miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p was significantly increased after SE (P<0.05), whereas the levels of miR-99b-3p was markedly decreased (P<0.05). [score:3]
After analyzing the initial results of deep sequencing, six deferentially expressed miRNA (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) were screened out based on the criteria mentioned in, and qRT-PCR was performed to confirm their alterations after SE. [score:3]
0078375.g002 Figure 2The levels of six differentially expressed miRNAs (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) in the rat hippocampus at 24 hours after SE were confirmed using qRT-PCR. [score:3]
The expression of miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p and miR-764-3p were significantly increased at 24 hours after SE (P<0.05), peaked at 1 week (P<0.05) and returned to the basal levels at 3 weeks after SE (Figure 3A-3E). [score:3]
The levels of six differentially expressed miRNAs (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) in the rat hippocampus at 24 hours after SE were confirmed using qRT-PCR. [score:3]
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[+] score: 27
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-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-29c-2, rno-mir-1b, ssc-mir-26b
Heart-specific miRNAs or miRNAs abundantly expressed in the heart, B) Liver-specific miRNAs or miRNAs abundantly expressed in the liver, C) miRNAs showing strong expression in the thymus, D) Expression analysis of miR-18a and miR-20a, the miRNAs located in the miR-17-92 cluster, and E). [score:9]
Our study revealed miR-181 and miR-142-3p with relatively high expression in thymus (Figure 2C), and miR18a and miR-20a appeared to be weakly expressed in thymus (Figure 2D). [score:5]
Some miRNAs, including miR-208, miR-101, miR-18a, miR-20 and miR-142-3p, showed a weaker expression than other miRNAs tested by small RNA blot analyses (Figures 2 and 3). [score:3]
Although miR-18a and miR-20a are likely derived from the same primary-transcript, the expression levels of these mature miRNAs are not similar (Figure 2D). [score:3]
Surprisingly, the expression pattern of miR-20a's differed from that of miR18a in different tissues. [score:3]
miR-18a and miR-20a are located within the miR-17-92 cluster, which contains miRNAs known as "oncomiRs" because of their overexpression in many types of cancer cells [58, 59]. [score:3]
The miR-17-92 cluster (polycistronic miRNA gene) encodes six miRNAs (miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92-1) located in the third intron of a ~7-kb primary transcript known as C13orf25 [61]. [score:1]
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[+] score: 21
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, 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, rno-mir-451, 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
In contrast, ICI 182,780 increased the expression of miR-20a and miR-21 in MSMC and LSMC, and miR-26a in MSMC, while inhibiting the expression of miR-26a in LSMC [210]. [score:7]
After 6 and 12 wks of E [2] exposure, 15 miRNAs were down-regulated, e. g., miR-22, miR-99a, miR-106a, miR-127, miR-499, and 19 miRNAs were-up-regulated, e. g., miR-17-5p, miR-20a, miR-21, miR-129-3p, miR-106a, miR-22, and miR-127. [score:7]
Genes targeted by three of the altered miRNAs were examined: miR-20a regulates E2F1, miR-106a regulates RBI, and miR-127 regulates BCL6. [score:6]
Western blot of mammary gland lysates after 12 wks of E [2] showed that levels of RBI and E2F1 were decreased and BCL6 protein was increased, data that are in agreement with the increase miR-20a and miR-106a and the decrease in miR-127 detected [198]. [score:1]
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[+] score: 20
In contrast, expression of miR-19a and miR-20a was downregulated in mouse NS cell differentiation. [score:6]
In contrast, antiapoptotic miR-20a was mainly downregulated throughout neural differentiation. [score:4]
In fact, transfection of hematopoietic progenitors with miR-20a increased the proliferation of monocytes and blocked differentiation, whereas inhibition of miR-20a caused a decrease in proliferation and more rapid differentiation and maturation. [score:3]
Expression of specific proapoptotic (miR-16, let-7a and miR-34a) and antiapoptotic miRNAs (miR-20a and miR-19a) were analyzed by quantitative Real Time-PCR from 10 ng of total RNA using specific Taqman primers and GAPDH for normalization. [score:2]
However, additional studies are required to determine the specific role of both miR-20a and miR-19a during cell differentiation, and also evaluate if their expression is restricted to a specific cell type. [score:1]
Recently, additional functions have been assigned to this cluster, particularly to miR-20a and miR-19a. [score:1]
miR-19a and miR-20a are members of the miR-17-92 cluster [61], which consists of seven mature miRNAs, previously linked to tumorigenesis. [score:1]
Specifically, miR-20a was shown to control monocyte differentiation [62]. [score:1]
Our results, showing that miR-20a decreases during mouse NS cell differentiation, are in agreement with this previous report. [score:1]
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[+] score: 20
These selected miRNAs included the seven most strongly upregulated miRNAs (miR-330, miR-338, miR-223, miR-20a, miR-181a, miR-592, miR-212) in the Ago2 IP at 30 min, the only downregulated miRNA (miR-29b) in the Ago2 IP at 30 min, and the three most strongly upregulated miRNAs (miR-219, miR-384, let-7f) in the Ago2 IP at 120 min post-HFS (significant by t-test with Dunn–Bonferroni correction and 1-Way ANOVA with LSD test). [score:10]
Five miRNAs (miR-384, miR-29b, miR-219, miR-592, and miR-20a) exhibited 2 to 5-fold greater increases in expression in the Ago2 immunoprecipitate than in the input samples, relative to contralateral control values (Figures 3C,D). [score:3]
When comparing miRNA Ago2/input expression ratios, eight miRNAs (miR-384, miR-29b, miR-219, miR-592, miR-20a, miR-330 miR-223, and miR-34a) exhibited increases relative to the contralateral dentate gyrus, whereas five miRNAs (miR-let7f, miR-338, miR-212, miR-19a, and miR-326) showed decreases in this ratio. [score:3]
Target gene list sizes for miRNAs with activity -dependent association with Ago2 for the 8 enhanced miRNAs were 97 (miR-20a), 156 (miR-219), 58 (miR-223), 114 (miR-29b), 30 (miR-330), 91 (miR-34a), 156 (miR-384), and 53 (miR-592) and for the 5 depleted miRNAs were 52 (let-7f), 55 (miR-338), 47 (miR-212), 255 (miR-19a), 32 (miR-326). [score:3]
Seven miRNAs (miR-384, miR-29b, miR-219, miR-592, miR-20a, miR-330, and miR-223) showed enhanced, NMDAR -dependent association with Ago2. [score:1]
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[+] score: 19
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
In addition, the miR-17-19 cluster, which comprises seven miRNAs (miR-17-5p, miR-17-3p, miR-18, miR-19a, miR-20, miR-19b, and miR-92-1) and promotes cell proliferation in various cancers, has been demonstrated to be significantly upregulated at the clonal expansion stage of adipocyte differentiation. [score:4]
Some of the circulating miRNAs identified in this study have also been reported in the adipose tissue of DIO mice or implicated in adipogenic processes [11– 13], including Let-7, miR-103, miR-15, the miR-17-92 cluster (miR-17, miR-20a, and miR-92a), miR-21, miR-221, and miR-30b. [score:1]
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[+] score: 15
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-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-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Furthermore, we and Gorter et al. 24 observed the up-regulation of miR-17-5p, miR-20a-5p, miR-23a-3p and the down-regulation of miR-139-5p, whereas we and Bot et al. 23 observed the down-regulation of miR-551b-3p. [score:10]
First, a subgroup of miRNAs (miR-15b-5p, miR-17-5p, miR-18a-5p, miR-19a-3p, miR19b-3p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23b-5p, miR-24-3p, miR-27a-3p, miR-92a-3p, miR-93-5p, miR-142-3p, miR-344b-2-3p, miR-431, miR-466b-5p and miR-674-3p) displayed increased expression levels during latency (4 and 8 days after SE), decreased their expression levels at the time of the first spontaneous seizure and returned to control levels in the chronic phase (Fig. 2, Supplementary Fig. S1). [score:5]
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[+] score: 13
miR-17 and miR-20a inhibitors and mimics were used as positive controls, since these two miRNAs were previously shown to target HIF-1α. [score:5]
Independent transfection of HeLa cells with anti miR-17/-20a/-335/-93 exhibited an increase in the relative luciferase activity, whereas introduction of miR-17/-20a/-335/-93 mimics resulted in a reduction in luciferase activity suggesting that, apart from miR-17 and miR-20a, miR-335 and miR-93 are also direct regulators of Hif-1α (Fig 2B). [score:3]
Among these miRNAs, miR-17 and miR-20a have been reported to directly regulate HIF-1α in lung cancer cells [16]. [score:3]
Furthermore, interaction between miR-20a and Hif-1α was not found to be significant in our study. [score:1]
miR-93 was observed to share the same binding site as miR-17 and miR-20a while miR-335 had two binding sites. [score:1]
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[+] score: 12
The study of these miRNAs could be a good basis for the identification and analysis of potential immuno-modulatory effectors in immuno -mediated diseases like multiple sclerosis, where a down-regulation of miR-17 and miR-20a associated with T-cell activation was demonstrated [80], or like inflammatory myopathies. [score:6]
The mir-17 family is the one most enriched (p = 3.24 E-4; Table S6) and comprises mir-17, mir-18a, mir-19a, mir-20a, mir-19b-1 and mir-92-1. This family is expressed as polycistronic units, revealing a common regulatory mechanism [62], that is confirmed by the similarity of their expression profiles (Figure 4 D). [score:6]
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[+] score: 11
However, miR-15b, miR-16, miR-20a, miR-20b [17], [18], miR-205 [23] and miR-195 [22] down-regulate angiogenesis by directly targeting VEGF. [score:7]
Recent studies also indicate that a panel of miRNAs (i. e., miR-10, miR-15b, miR-16, miR-20a, miR-20b, miR-27a, miR-126, miR-145, miR-195, miR-205, and miR-210) is involved in the regulation of VEGF expression in ECs and tumor cells [16]– [26]. [score:4]
[1 to 20 of 2 sentences]
[+] score: 11
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
From the top twenty miRNAs showing highest expression in A2B5+ GalC− cells, miR-130a, miR-16, miR-17, and miR-20a were also in the top twenty expressed miRNAs from our GPs. [score:5]
Similarly, miR-17, miR-20a, miR-21, miR-16, miR-103, and miR-107 identified in A2B5-GalC+ cells showed overlapping expression with our OPs. [score:3]
Additionally, miR-17 and miR-20a were predicted to target membrane associated guanylate kinase, WW and PDZ domain containing 3 (MagI-3), a junctional protein found in astrocytes [40]. [score:3]
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[+] score: 9
In addition, miR-20a/b was reported to target the 3’ UTR of vascular endothelial growth factor (VEGF) and repress VEGF expression in nasopharyngeal carcinoma cell line [8]. [score:5]
The miR-17 microRNA (miRNA) precursor family is a group of small non-coding RNA genes that regulate gene expression, and it includes miR-20a/b, miR-93 and miR-106a/b. [score:4]
[1 to 20 of 2 sentences]
[+] score: 8
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
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[+] score: 7
stress downregulated abundance of miR-329, miR-380, miR-20a, and miR-500 (all p≤0.05; Figure 2B-C). [score:4]
C, Table of target genes for miRNAs modulated by gestational stress (miR-329, miR-380, miR-20a, and miR-500; p≤0.05), and their physiological implications. [score:3]
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[+] score: 6
Significant mechanical allodynia was observed in rats overexpressing miR-18a, miR-19a, miR-19b or miR-92a, but not in those overexpressing miR-17 or miR-20a (Fig. 2e). [score:5]
Clone IDs of TuD were as follows: NC000001 (negative control), RH000611 (miR-17), RH000323 (miR-18a), RH000643 (miR-19a), RH000352 (miR-19b), RH000277 (miR-20a) and RH000184 (miR-92a). [score:1]
[1 to 20 of 2 sentences]
[+] score: 6
miR-17 is a member of the miR-17/92 cluster, one of so far, the best-studied microRNA clusters that codes six mature miRNAs: miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1. Members of this cluster are expressed in a variety of tissues and carry out essential functions both in normal development and in diseases. [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
While the reduction in expression of miR-17-5p, miR-18a, miR-20a, and miR-92 were well coordinated in transdifferentiation, the expression of miR-19a was not concordant with its neighboring microRNA genes. [score:5]
The genes encoding for miR-17-1/miR-17-5p, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1 are clustered on chromosome 15 [35]. [score:1]
[1 to 20 of 2 sentences]
[+] score: 5
miR-20a also inhibits expression of the apoptotic factor Egl nine homolog 3 to protect cardiomyocytes from H/R injury [11]. [score:5]
[1 to 20 of 1 sentences]
[+] score: 5
hsa-miR-93 and hsa-miR-20a have been found to be overexpressed in a multiple cancer types, induce cell proliferation and deletion of these miRNA clusters, in mice, are lethal, and cause lung and lymphoid cell developmental defects [39]. [score:4]
hsa-miR-mit-3 has two matches with hsa-miR-93 and hsa-miR-20a. [score:1]
[1 to 20 of 2 sentences]
[+] score: 5
Fang W Microrna-20a-5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and pten expressionJ. [score:5]
[1 to 20 of 1 sentences]
[+] score: 5
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]
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[+] 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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[+] score: 5
For instance, we observed a decrease in the levels of 5 miRNA with predicted target sites in the Foxa1 3′UTR (miR-106b, miR-194, miR-30c, miR-30b-5p and miR-20a) along with increased Foxa1 mRNA expression on methamphetamine exposure. [score:5]
[1 to 20 of 1 sentences]
[+] score: 5
Other miRNAs from this paper: rno-mir-126a, rno-mir-132, rno-mir-155
Moreover, STDP was reported to attenuate atherosclerotic lesions in ApoE(-/-) mouse mo del via reducing the aortic expression of miR-21a, miR-132, miR-126a, miR-155 and increasing expression of miR-20a [16]. [score:5]
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[+] score: 4
We found clear upregulation of miR-146a and miR-155, but not of miR-29a, miR-29b, miR-19b, or miR-20a in skin (Figure 4A and data not shown). [score:4]
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[+] score: 4
Low-dose (0.5 Gy) irradiated cells showed a decrease in onco-miRNAs - miR-20 and 21, while high-dose irradiation (10 Gy) caused upregulation of miR-197 that can stimulate carcinogenesis [10]. [score:4]
[1 to 20 of 1 sentences]
[+] 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
In hippocampus, a total of 475 targets of rno-miR-101b-3p, rno-miR-217-5p, rno-miR-375-3p, rno-miR-20a-5p, rno-miR-19b-3p, and rno-miR-182 were predicted. [score:3]
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[+] score: 3
Jee et al. [33] reported that miR-20a was highly expressed in SCI mice and could lead to persistent degeneration of motor neurones. [score:3]
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[+] score: 3
Wei, L. & Ran, F. MicroRNA-20a promotes proliferation and invasion by directly targeting early growth response 2 in non-small cell lung carcinoma. [score:3]
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[+] score: 3
In our previous study [12], we found that miR-17, miR-19a, miR-20a, miR-19b and miR-92a, but not miR-18a, were highly expressed in the heart of C57BL/6 mice. [score:3]
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[+] score: 3
Further we found that expression of four miRNAs (miR-20a, miR-98, miR-107 and miR-126) showed a trend similar to that observed in microarray but was not statistically significant (Figure 3). [score:3]
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[+] score: 3
We unexpectedly identified miR-17-5p, along with other miRNAs (miR-20a and b, miR-106a and b, and miR-93) sharing the same seed motif as miR-17-5p, as a potential common regulator of Hsp70, Hsc70, CANX, and Golga2 (Figures S2-S5 in File S1). [score:2]
MiR-17-5p belongs to the miR-17~92 cluster, located on the human chromosome 13q31, and is a prototypical example of a polycistronic miRNA gene encoding six miRNAs (miR-17-5p, miR-18, miR-19a, miR-19b, miR-20 and miR-92). [score:1]
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[+] score: 2
Since the first report on the role of miRNA in VSMCs was published in 2007, miRNAs such as miR-143/145, miR-21, and miR-20a have been shown to regulate various aspects of VSMC biology 18– 21. [score:2]
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[+] score: 2
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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[+] score: 2
The following miRNAs, also present in the VTMs list of Fig 5, were found by RT-PCR to be dysregulated in mouse lung tissue: miR-21, miR-146, miR-20, miR-302, miR-19, miR-98, let-7a, miR-15a. [score:2]
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[+] score: 1
Among the spleen-specific miRNAs identified, five of them belong to the mir17 miRNA cluster, which comprise miR-17, miR-18, miR-19a, miR-19b, miR-20, miR-25, miR-92, miR-93, miR-106a, and miR-106b [59]. [score:1]
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[+] score: 1
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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[+] score: 1
In human mesenchymal stem cells, naringin promotes osteogenic differentiation through miR-20a and PPAR γ [16]. [score:1]
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[+] score: 1
We began by measuring the levels of several miRNAs reportedly associated with cardiovascular diseases, including mir-129, mir-106, mir-26a, mir-20, mir-197, mir-17, mir-27 and mir-30d, 24, 25, 26, 27, 28, 29 in cardiomyocytes under both normal and high-glucose conditions. [score:1]
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[+] score: 1
A number of other miRNA species that might affect collagen type-I and -IV synthesis, such as miR-106a/b, miR-20a/b, miR-26a/b, miR-374a/b, miR-186 were also identified by in silico analyses (summarized in Table 1). [score:1]
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[+] score: 1
As a result, miR-16, miR-17-5p, miR-20a, miR-20b-5p, miR-21 and miR-199-5p were extracted as candidates. [score:1]
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[+] score: 1
hsa-miR-20b, hsa-miR-20* and hsa-miR-20-5p). [score:1]
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[+] score: 1
For instance the mature miRNA sequence of MP-56 has only two mismatches with mmu-mir-17, mmu-mir-20 and mmu-mir-106a. [score:1]
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For example, nine miRNAs (miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805, and miR-194) have been identified in C57BL/6 mice as promising biomarkers of kidney injury after renal ischemia reperfusion injury (IRI) [15]. [score:1]
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In addition, some of the plasma miRNAs (miR-146a and miR-20a) positively correlated with peak exercise capacity and cardiorespiratory fitness (Colombo et al., 2014). [score:1]
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hsa-mir-17 belonged to a polycistronic cluster (also containing hsa-mir-18a, hsa-mir-19a, and hsa-mir-20a) residing in a large genomic region highly enriched with TF binding sites, let-7a and let-7f, also likely to be transcriptionally coupled, were also enriched with TFBSs, and mir-7-1 was also found in a large genomic region with high density of TFBSs. [score:1]
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