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9 publications mentioning rno-mir-495

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-495. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 113
Other miRNAs from this paper: rno-mir-10a, rno-mir-26a, rno-mir-103-2, rno-mir-103-1
Therefore, the goals of this study were to provide a potential mechanistic explanation for EtOH -induced effects on gene expression by quantifying the expression of EtOH sensitive miRs (miR-10a-5p, miR-26a, miR-103 and miR-495) during normal pubertal development in the male rat hippocampus, and then elucidate how peri-pubertal binge EtOH exposure alters the expression of those miRs. [score:8]
Therefore, we identified putative target genes of miR-10a-5p, miR-26a, miR-103 and miR-495 that were relevant to known dorsal and ventral hippocampus functions using target prediction software programs, Targetscan and MirDB. [score:7]
Therefore, mid/peri-pubertal disruption of miR-26a and miR-495 expression by binge EtOH exposure could result in altered BDNF expression throughout pubertal development. [score:6]
The most striking effects of mid/peri-pubertal binge EtOH exposure in the ventral hippocampus were observed in miR-103 and miR-495 expression, as their normal developmental expression levels at both mid/peri-puberty and late-puberty were opposite following mid/peri-pubertal binge EtOH exposure. [score:6]
Therefore, we quantified the expression of miR-10a-5p, miR-26a, miR-103, and miR-495 in the ventral hippocampus across pubertal development in untreated rats to determine if there were region specific miR expression patterns in the hippocampus. [score:6]
Notably, miR-495 expression in the ventral hippocampus demonstrated the most dynamic expression profile throughout pubertal development, as it had distinct expression levels at each time point measured. [score:6]
Therefore, we first quantified the normal developmental expression profile of miR-10a-5p, miR-26a, miR-103 and miR-495 in the rat hippocampus at three time points in pubertal development (early, mid/peri, and late). [score:5]
Taken together our data revealed that the expression of each miR tested (miR-10a-5p, miR-26a, miR-103 and miR-495) is dynamic across pubertal development and that the developmental profiles for each miR are distinct between the dorsal and ventral hippocampus. [score:5]
org) [40], [41], [42], we identified brain-derived neurotrophic factor (BDNF) as a target gene of miR-10a-5p, miR-26a, miR-103 and miR-495, and sirtuin 1 (SIRT1) as a target gene of miR-26a, miR-103 and miR-495. [score:5]
Consistent with our hypothesis, decreased expression of miR-26a and miR-495 correlated with increased BDNF gene expression in the dorsal hippocampus immediately following mid/peri-pubertal binge EtOH exposure and this increase remained significantly elevated up to one-month post EtOH exposure. [score:5]
Moreover, mid/peri-pubertal binge EtOH exposure altered normal pubertal development expression patterns of miR-10a-5p, miR-26a, miR-103, miR-495, Dicer, Drosha, BDNF and SIRT1 in an age- and brain region -dependent manner. [score:4]
Overall, our data reveal novel findings about the age and brain-region specific expression of miR-10a-5p, miR-26a, miR-103, and miR-495 during pubertal development in male rats. [score:4]
Therefore, we first determined the normal developmental profile of mature miR-10a-5p, miR-26a, miR-103 and miR-495 expression in the dorsal hippocampus using untreated male Wistar rats. [score:4]
Repeated adolescent binge EtOH exposure differentially alters expression of miR-10a-5p, miR-26a, miR-103 and miR-495 in the ventral hippocampus. [score:3]
Our results demonstrated a significant main effect of EtOH treatment on the expression of miR-26a and miR-495 and there was also a significant interaction between age and treatment, demonstrating that the effects of EtOH were age dependent (Table 1). [score:3]
Notably however, expression levels remained significantly below normal even one-month post EtOH exposure (Fig. 2D), suggesting a potential long-term effect of pubertal binge EtOH exposure on miR-495 in the dorsal hippocampus. [score:3]
0083166.g003 Figure 3 miR-10a-5p (A), miR-26a (B), miR-103 (C), and miR-495 (D) expression levels in untreated (solid line) and EtOH -treated (dashed line) pubertal male rats. [score:3]
The histone deacetylase sirtuin 1 (SIRT1) was also predicted by computer algorithms to be a putative gene target of miR-26a, mir-103 and miR-495. [score:3]
For instance, miR-495 is predicted to target as many as 754 genes in the rat genome (miRDB). [score:3]
For instance, BDNF was identified as a putative target gene for miR-10a-5p, miR-26a, miR-103 and miR-495. [score:3]
0083166.g002 Figure 2 miR-10a-5p (A), miR-26a (B), miR-103 (C), and miR-495 (D) expression levels in untreated (solid line) and EtOH -treated (dashed line) pubertal male rats. [score:3]
Finally, a significant increase was observed in miR-495 expression between early and mid/peri-puberty and these levels remained high until late puberty (Fig. 2D, solid line). [score:3]
Mature miR-10a-5p, miR-26a, miR-103, and miR-495 expression levels in the ventral hippocampus of untreated male rats are age -dependent. [score:3]
Mature miR-10a-5p, miR-26a, and miR-495 expression levels in the dorsal hippocampus of untreated male rats are age dependent. [score:3]
Also, there were 5 possible binding sites on BDNF for miR-495, suggesting miR-495 might have a stronger regulatory effect on BDNF than the other miRs. [score:2]
Rats were administered our repeated binge-pattern EtOH exposure paradigm (see methods) and dorsal hippocampal miR expression of miR-10a-5p, miR-26a, miR-103 and miR-495 was compared with untreated rats/water -treated rats immediately following binge EtOH exposure and one-month post-EtOH exposure. [score:2]
There were no potential binding sites in the 3′UTR of SIRT1 for miR-10a-5p, but there was a single potential binding site for each of the other miRs tested (miR-26a, miR-103 and miR-495; Fig. 5). [score:1]
The ventral hippocampus levels of miR-103 and miR-495 had a similar profile. [score:1]
Most striking were the results of EtOH exposure on miR-495. [score:1]
Similar to miR-26a, miR-495 was significantly decreased as a result of binge EtOH exposure at mid/peri-puberty. [score:1]
Indeed, there was a significant main effect of treatment and a significant interaction between age/treatment for miR-10a-5p, miR-103, and miR-495 in the ventral hippocampus (Table 2). [score:1]
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2
[+] score: 24
We conclude that miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543 represent an FGF2 -dependent system of multiple miRNAs that target specific genes operating in pathways and processes related to the lens differentiation (via c-Maf, Med1/PBP, N-myc, and Nfat5), miRNA-regulated RNA processing (via Cpsf6 and Tnrc6b) and nuclear/chromatin -based processes (via Med1/PBP, As1l, and Kdm5b/Jarid1b/Plu1). [score:4]
Three miRNAs from this cluster, including miR-495, miR-543, and miR-381, represent a group of most highly connected miRNAs in this system (Figure 6A) and regulate together multiple genes known to regulate lens fiber cell differentiation, including c-Maf (Figure 7 and Figure 10). [score:3]
The total number of their target genes is between 114 (1st rank, “early” miR-495) and 45 (10th rank, “early” miR-31 and miR-133b) connections. [score:3]
We found that seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, target at least two “early” genes examined (i. e., c-Maf, N-Myc, and Nfib). [score:3]
We predict that several important regulatory genes of lens fiber cell differentiation, including c-Maf, Kdm5b/Jarid1b, Med1/PBP, Nfat5/OREBP, and N-Myc, are connected by multiple shared miRNAs, with four of them, including miR-381, miR-495, miR-382, and miR-543, encoded by a miRNA cluster on rat chromosome 6, a syntenic region with mouse chromosome 12, and human 14q32.2 imprinted regions. [score:2]
This gross analysis is consistent with our findings of genes regulated by miR-495, miR-543, and miR-381 in lens that belong to these similar categories (Figure 5). [score:2]
Both c-Maf and Med1/PBP are predicted to be regulated by similar miRNAs, including miR-137, miR-200c, and miR-495 (Figure 7). [score:2]
The most connected miRNA identified here through the 12 top-ranking transcripts, including miR-495, miR-200c, miR-543, miR-381, and miR-9 (Figure 6A), retained their high-connectivity positions as identified by independent analysis shown earlier in Figure 6A. [score:1]
The miR-495 and miR-543 are neighbors, and miR-381 is located ~12.7 kb from miR-495. [score:1]
Seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, and connections to specific functional groups of genes are shown. [score:1]
The miR-381, miR-495, miR-543, and miR-382 form a miRNA-gene cluster on rat chromosome 6q32. [score:1]
Notably, miR-381, miR-495, and miR-543 form a miRNA-gene cluster on rat chromosome 6, and its syntenic regions on mouse and human chromosome 12 and 14, respectively (Sewer et al. 2005). [score:1]
[1 to 20 of 12 sentences]
3
[+] score: 16
Experiment 1: Expression of E [2]-responsive mature miRNAs in the hypothalamus of ovarian intact animals changes with ageOur previous studies showed that E [2] regulated a subset of mature miRNAs (let-7i, miR-7a, miR-9, miR-9–3p, miR-125, miR-181a, and miR-495) in an age- and brain-region dependent manner [46]. [score:4]
First, we analyzed the expression levels of the primary transcripts, which demonstrated that both PPT and DPN treatment significantly decreased the expression of pri-miR-7a, pri-miR-125a, pri-miR-181a, and pri-miR-495 compared to either vehicle or E [2] treated animals (Figure 9a). [score:4]
miR-495: Ovarian intact animals had consistently higher levels of mature miR-495 expression at all ages compared to OVX animals, although both OVX+veh and OVX+E [2] groups showed significant increases after 8 and 12 weeks post-OVX (20 and 21 mo. [score:2]
Our previous studies showed that E [2] regulated a subset of mature miRNAs (let-7i, miR-7a, miR-9, miR-9–3p, miR-125, miR-181a, and miR-495) in an age- and brain-region dependent manner [46]. [score:2]
Further, both primary transcripts for miR-181a and miR-495 were significantly decreased at 4, 8, and 12 weeks post OVX (Figure 3h–3i, black line, #). [score:1]
Finally, E [2] had no effect on pri-miR-181a or pri-miR-495 at any time point (Figure 3h, 3i). [score:1]
Similarly, DPN significantly increased the precursor form of miR-495 (pre-miR-495), but not any other precursor miRNA (Figure 9b). [score:1]
One way ANOVA analyses across the deprivation time points showed that pri-mir-7a-2, pri-mir-9-1, pri-mir-125a, pri-mir-181a, and pri-mir-495 were all significantly altered by OVX alone, and in general, they were all decreased with age (Figure 3, black line, #). [score:1]
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4
[+] score: 12
Fig. 1 a Correlation graph between miR-494 and miR-495 expression levels in tumor tissue from 28 randomly selected HCC patients. [score:3]
Since miR-494 and miR-495 were shown to be the most potent cluster members influencing tumor cell proliferation [18], we also analyzed miR-495 expression in HCCs. [score:3]
a Correlation graph between miR-494 and miR-495 expression levels in tumor tissue from 28 randomly selected HCC patients. [score:3]
TaqMan MicroRNA assays (Thermo Fisher Scientific) were used for quantifying miRNA-494 (ID: 002365) and miR-495 (ID:001108) expression, as previously described [8]. [score:2]
A positive correlation between miR-494 and miR-495 was found in tumors (Pearson’s correlation; p = 0.002) but not in surrounding livers (Fig.   1a, Supplementary Fig. S2A), suggesting their possible involvement in hepatocytes malignant transformation. [score:1]
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5
[+] score: 7
However, it should be noted that although miRNAs-including miR-352 in this paper and other miRNAs found in previous studies, such as miR-100, miR-155, miR-329, and miR-495- are important factors controlling FSS -induced collateral vessel growth 15– 17, the mechanism by which miRNAs expression is regulated remains unclear. [score:4]
More recently, several studies have demonstrated that a different miRNA expression profile is induced in collateral vessels of mice following femoral artery occlusion, and several miRNAs such as miR-100, miR-155, miR-329 and miR-495 were found to be important factors that control collateral vessel growth 15– 17. [score:3]
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6
[+] score: 7
A recent study showed that inhibition of miR-495 increased neovascularization and recovery of blood flow after cardiac ischemia in mice [60], while miR-214 protected the mouse heart from ischemic injury by controlling Ca [2+] overload and cell death [61] (Table  5). [score:3]
For example, the top three miRNA-hubs in the early IR-injury regulatory network were rno-miR-495, rno-miR-214 and rno-miR-298, whereas rno-miR-873, rno-miR-223 and rno-miR-185 were hubs observed at the late phase post-IR injury. [score:2]
For example rno-miR-495 and rno-miR-207 are common between the 24 h and 7d time points, but they are rank-ordered differently between the 2 time points. [score:1]
The top three rno-miRs at 24 h were rno-miR-495* (degree of 172), followed by rno-miR-214 (degree of 170) and rno-miR-207(degree of 143). [score:1]
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7
[+] score: 6
In an attempt to discover whether the guinea pig Abcb1 isoform 1’s 3′UTR contains MREs, the reverse complement of several human ABCB1-specific miRs validated to reduce ABCB1 mRNA expression and ABCB1 activity (miR223 [24], miR508-5p [25], bta-miR145 [26], miR381 and miR-495 [27]) were searched via BLAST alignment for extrapolation to guinea pig; however, none were found. [score:3]
The human miR cluster at 14q32.31, an imprinted region, containing miR-381 and miR-495, contains over 20 miR sequences, several known to inhibit ABCB1 in human, and there is 90% homology (BLAT) between this region and a 31 kb region in the guinea pig genome, on the plus strand of scaffold 111, therefore representing a candidate region for miR discovery. [score:3]
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8
[+] score: 3
Similarly, longSAGE tags also suggest the expression of two human (mir-7-1 and mir-125a) and three mouse (mir-331, mir-351, and mir-495) miRNAs that have not been experimentally confirmed (Table 1). [score:3]
[1 to 20 of 1 sentences]
9
[+] score: 1
Finally, there is mixed support for 7 of the miRNAs we reported (mir-129-1, miR-15b-3p, mir-204, miR-29c-3p, miR-301b-3p, miR-495, and mir-9a-2), with some studies showing changes consistent with our data, and other studies showing changes opposite those of our study (15, 31– 33, 38– 47). [score:1]
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