sort by

26 publications mentioning rno-mir-127

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-127. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 309
Other miRNAs from this paper: rno-mir-21, rno-mir-34a, rno-mir-378a, rno-mir-378b
Then we confirmed that miR-127 is strongly down-regulated and inversely correlates with the expression of the target genes Bcl6 and Setd8 during the first 24 h of LR, while the rebound of miR-127 at 120 h post-PH suggests an inhibitory role of miR-127 in the terminal phase. [score:10]
In order to verify whether this down-regulation was only occurred in rat liver cells and explore the potential significance of miR-127 in human liver disease, HCC cell line, Huh7 cells were treated by the same way, and the expression of these target genes was examined. [score:10]
Among these miRNAs, we identified 4 up-regulated and 3 down-regulated rat miRNAs, in which miR-127 had at least 3-fold difference in expression between PH and SH (Figure 1B). [score:9]
Our study also found that the artificial down-regulation of miR-127 promotes cell proliferation, while up -regulating miR-127 inhibits proliferation in rat liver cells (Figure 3B), which could be partially attributable to G2/M blockage (Figure 3A). [score:7]
We then examined the expression levels of miR-127 during the whole process of LR by qRT-PCR and found that miR-127 was down-regulated at the early stage and was especially prominent at 24 h after PH, when miR-127 expression displayed an almost 4-fold reduction compared to the SH group. [score:7]
To address the regulation of cell growth mediated by miR-127, we examined the expression of the candidate target genes Bcl6 and Setd8 in BRL-3A cells after treatment with miR-127 mimics, and found that the expression of these genes were reduced after treatment with miR-127 mimics compared to NCs at both the mRNA and protein levels (Figure 4A). [score:7]
Further studies found that CDKN1A was induced when Bcl6 was down-regulated in rat liver cells, suggesting that the miR-127-Bcl6 signaling may regulate the expression of CDKN1A during LR. [score:7]
Setd8 up-regulation in the late stage of LR implies that there may exist other regulation mo dels besides miR-127, such as the Ser-29 phosphorylation of Setd8 mediated by the Cdk1/cyclinB complex, which may stabilize Setd8 by inhibiting anaphase-promoting complex (APC) -mediated ubiquitination and proteasome -mediated degradation of Setd8 [34], and it must be further studied. [score:7]
As shown in Figure 6B, miR-127 was up-regulated 13-fold after the combination treatment with 5-Aza-CdR and PBA but showed no significant difference with either one of the two drugs alone, indicating that miR-127 can be regulated by the synergistic effects of DNA demethylation and the inhibition of histone deacetylase. [score:7]
Our data suggest that the down-regulation of miR-127 might contribute to the proliferation of hepatocytes by targeting SET domain-containing protein 8 (Setd8) and Bcl6 during the first 24 h after PH. [score:6]
To explore a mo del of miR-127 regulation in rat liver during LR, we first analyzed miR-127 expression levels in BRL-3A cells treated with 5-aza-2′-deoxycytidine (5-Aza-CdR) and 4-phenylbutyric acid (PBA), which inhibit DNA methylation and histone deacetylase, respectively. [score:6]
In contrast, miR-127 was up-regulated at the late stage (120 h), in which miR-127 exhibited a 2-fold difference in expression between PH and SH groups (Figure 1C). [score:6]
Therefore, we used a Molecular Annotation System to categorise all of the putative target genes of miR-127 that were predicted by the Targetscan, miRanda and Pictar algorithms. [score:5]
We suggest a possible epigenetic mechanism in the regulation of LR that consists of the miR-127 -mediated up-regulation of Setd8 during the first 24 h of LR. [score:5]
This conclusion is further supported by the highly induced expression of miR-127 following treatment with 5-Aza-CdR and PBA, which inhibit DNA methylation and histone deacetylase, respectively. [score:5]
Cell cycle of Huh7 cells transfected with miR-127 inhibitor or inhibitor NC were analyzed by flow cytometry. [score:5]
MiR-127 is typically expressed as part of a miRNA cluster in normal cells, but not in cancer cells, and this miRNA has a tumor-repressive function by targeting the pro-oncogene B-cell lymphoma 6 protein (Bcl6) in T24 and Ramos cells [15]. [score:5]
MiR-127 down-regulates Bcl6 and Setd8 expression. [score:5]
These data indicated an inverse correlation between the putative target genes Bcl6, Setd8, and miR-127 expression on both mRNA and protein levels during the first 24 h after PH. [score:5]
MiR-127 Down-regulates Bcl6 and Setd8 Expression. [score:5]
Cells transfected with miR-127 inhibitor or inhibitor NC were analyzed by qRT-PCR (left) and Western blotting (right), respectively. [score:5]
To evaluate the effect of miR-127 in regulating rat liver cell growth, BRL-3A immortalized rat liver cells were transfected with miR-127 mimics or a negative control (NC) to up-regulate miR-127 expression levels in liver cells. [score:5]
MiR-127 Is Significantly Down-regulated and Inversely Correlates with the Expression of Bcl6 and Setd8 during the First 24 h after PH. [score:5]
Down-regulation of miR-127 may participate in cell growth regulation through Bcl6 and Setd8 during the first 24 h after PH. [score:5]
Proliferation of Huh7 cells transfected with either miR-127 inhibitor or inhibitor NC was examined at the indicated time by methylthiazol tetrazolium. [score:5]
Bioinformatic tools for putative miR-127 target genes (TargetScan, miRanda and Pictar algorithms) were used. [score:5]
To confirm that the inverse relationship of miR-127 expression and that of its predicted target Setd8 is mediated by the 3′-UTR, we first determined the 3′-end of the full-length Setd8 transcript by 3′ rapid amplification of cDNA ends (RACE) (GenBank accession JN896763). [score:5]
In a preliminary study we found that miR-127 was down-regulated 3 h after PH using a microarray analysis, and was especially prominent at 24 h by a quantitative real-time PCR (qRT-PCR) analysis. [score:4]
Together with the observation that compared with the SH group, the PH group showed an increased proliferative activity at 24 h after liver section (Figure 5E), we speculate that down-regulation of miR-127 may participate in cell growth regulation through Bcl6 and Setd8 during LR. [score:4]
These results indicate that the down-regulation of miR-127 after PH may be due to the rapid methylation of the promoter of the miR-127 gene. [score:4]
Down-regulation of MiR-127 may Participate in Cell Growth Regulation through Bcl6 and Setd8 during LR. [score:4]
To determine how miR-127 participates in the regulation of LR, we sought to identify miR-127 target genes during LR. [score:4]
MiR-127 gene is located in the imprinted region Dlk1/Gtl2 and transcribed in an antisense orientation to a retrotransposon-like gene (Rtl1) [35], and the expression of miR-127 has been shown to undergo DNA methylation regulation in mouse embryos [36] and human cancer cells [15]. [score:4]
We selected 24 putative miR-127 target genes that could be involved in regulation of biological or cellular processes as assigned by the pathway classification analysis of these genes (Table S1) (Molecular Annotation System, MAS, http://bioinfo. [score:4]
Although a recent study showed that promoter of miR-127 was activated by estrogen related receptor gamma (ERRγ) and inhibited by small heterodimer partner (SHP) [37], further researches will be required to determine whether miR-127 is regulated by ERRγ and SHP in rat LR. [score:4]
More importantly, miR-127 is down-regulated in rat hepatocarcinomas induced by a methyl -deficient diet [17]. [score:4]
Figure S1 Down-regulation of miR-127 promotes cell proliferation in Huh7 cells. [score:4]
These findings suggest that the down-regulation of miR-127 in rat liver during the first 24 h of LR could be mediated by the DNA hypermethylation of its promoter. [score:4]
MiR-127 expression inversely correlates with the expression of Bcl6 and Setd8 during liver regeneration. [score:4]
Furthermore, by qRT-PCR and Western blot analysis, we observed a significant up-regulation of Bcl6 and Setd8 on both the mRNA and protein levels in liver tissues 24 h after PH, a time at which miR-127 is maximally decreased (Figure 2, A and B). [score:4]
As shown in Figure 4B, treatment with miR-127 mimics caused significant down-regulation of Bcl6 and Setd8 at both the mRNA and protein levels. [score:4]
In conclusion, miR-127 is down-regulated within the first 24 h after PH due to the rapid methylation of its promoter, and this event facilitates hepatocyte proliferation by releasing Bcl6 and Setd8. [score:4]
These results suggest that Setd8 is a direct target gene of miR-127 in BRL-3A cells. [score:4]
To confirm that the suppression of cell proliferation by miR-127 was mediated by Bcl6, we assessed the effect of Bcl6 siRNA on hepatocyte proliferation. [score:3]
MiR-127 Is Down-regulated by Hypermethylation of a CpG Island in the Promoter Region 24 h after PH. [score:3]
MiR-127 was prominently down-regulated at 24 h after partial hepatectomy (PH). [score:3]
BRL-3A cells were treated with 5-Aza-CdR and/or PBA, and the miR-127 expression level was analyzed by qRT-PCR. [score:3]
In our study, we found that an inverse correlation between Bcl6 and miR-127 expression on both mRNA and protein levels during the first 24 h after surgery. [score:3]
Cells transfected with miR-127 mimics, miR-127 inhibitor, Bcl6 siRNA or the corresponding NCs in 6-well plates were re-seeded onto 96-well plates at a density of 1000 cells per well 24 h after transfection. [score:3]
To further illuminate the roles of miR-127 in livers, the present work sought to elucidate whether and how miR-127 and its possible target genes are involved in LR by focusing on the first 24 h after PH. [score:3]
As shown in Figure 4D, miR-127 markedly repressed the expression of the luciferase construct that contained the original miR-127 binding site (Setd8 UTR), but not the mutant binding site (Setd8 Mu-UTR). [score:3]
The protein expression of cells treated with miR-127 mimics or miRNA NC was analyzed by Western blotting. [score:3]
Another target of miR-127 that we firstly identified in rat liver cells, Setd8, is a member of a family of histone lysine methyltransferases and can monomethylate histone H4 on Lys20. [score:3]
Table S1 Candidate miR-127 target genes. [score:3]
And an in vivo study of miR-127 in rat LR mo del will be helpful to elucidate the exact mechanisms that govern the expression of CDKN1A. [score:3]
show the transfection of miR-127 mimics notably reduced H4-K20me1 expression but had no effect on histone H4 (Figure 5C). [score:3]
MiR-127 mimics, miR-127 inhibitor, or their relative negative control RNAs, Bcl6 siRNA and its negative control RNA were obtained from GenePharma (Shanghai, China). [score:3]
show that the expression levels of miR-127 in rat liver tissues, rat primary hepatocytes and BRL-3A cells were relatively higher than that in human Huh7 hepatocarcinoma cells, and there were no significant difference among rat liver tissues, primary hepatocytes and BRL-3A cells (Figure 1D). [score:3]
Furthermore, cell growth assays in Huh7 cells also indicate that down-regulation of miR-127 may play a proliferation-promoting role in human hepatocarcinoma cells (Figure S1). [score:3]
The 3′-UTR of Setd8, which contains the miR-127 response element, was cloned into the pGL4.13 luciferase reporter vector (Promega) between the XbaI and FseI restriction sites using a directional RT-PCR cloning strategy. [score:2]
Together with the observation that Bcl6 siRNA reduced proliferation in BRL-3A cells (Figure 5B), we presumed that the repression of miR-127 may contribute to the regulation of liver cell proliferation via a Bcl6 -mediated antagonism to the p53 -mediated induction of CDKN1A during the first 24 h of LR. [score:2]
These data indicate that miR-127 may regulate the progression of LR via the monomethylating modification of histone H4 mediated by Setd8. [score:2]
We proposed that the down-regulation of miR-127 may contribute to the initiation of LR and cell cycle progression during the first 24 h after PH, which is characterised by enhanced proliferation. [score:2]
0039151.g006 Figure 6 MiR-127 is induced from its promoter by DNA demethylation and histone deacetylase inhibition. [score:2]
MiR-127 is induced from its promoter by DNA demethylation and histone deacetylase inhibition. [score:2]
Our results suggest that miR-127 may have a negative regulatory effect on the cell growth of rat liver cells. [score:2]
In addition, miR-127 markedly reduced BRL-3A cell growth at 72 h (P<0.01), 96 h (P<0.05) and 120 h (P<0.01), while miR-127 inhibitor promoted BRL-3A cell growth at 96 h (P<0.01) and 120 h (P<0.01) compared with the NC groups (Figure 3B) by the MTT cell proliferation analysis. [score:2]
Our findings reveal a miRNA -mediated negative regulation pattern that occurs during the first 24 h of LR and suggest an anti-proliferative role for miR-127 in liver cells. [score:2]
Additionally, because Setd8 has a role in cell cycle regulation by monomethylating histone H4 on Lys20 (H4-K20me1) [21], [22], we measured the expression levels of H4-K20me1 and histone H4 in BRL-3A cells treated with miR-127 mimics or miRNA NC. [score:2]
To assess whether miR-127 expression is regulated by the methylation of its promoter region during the first 24 h after PH, we measured the DNA methylation levels of the promoter region of miR-127 by bisulfite sequencing. [score:2]
0039151.g004 Figure 4(A and B) BRL-3A (A) and Huh7 (B) cells transfected with miR-127 mimics or miRNA NC were analyzed by qRT-PCR (left) and Western blotting (right), respectively. [score:1]
Cells were transfected with miR-127 mimics and the negative control. [score:1]
As shown in Figure 3A, the percentage of G2/M phase cells in miR-127 and miRNA NC groups was (23.32±0.37)% and (17.65±1.28)%, respectively, and the percentage of S phase cells was (34.00±0.24)% and (38.47±0.84)%, respectively, indicating that a subpopulation of cells is arrested in the G2/M phase by transfection with miR-127 mimics. [score:1]
We then fused the 3′-UTR region of Setd8 to a luciferase reporter to validate the effects of miR-127 mimics on the wild-type and mutant plasmids. [score:1]
To elucidate the activation mechanism of miR-127 in LR, we analyzed the promoter region of the miR-127 gene in rats and found a CpG island in it, further studies show that the CpG island was highly methylated 24 h after PH by bisulfite genomic sequencing. [score:1]
BRL-3A cells were cotransfected with a luciferase reporter vector containing the 3′-UTR or the mutated 3′-UTR (Mu-UTR) of Setd8 and miR-127 mimics (miR-127) or the negative control (NC). [score:1]
The wild-type and mutated miR-127 -binding sites in the 3′-UTR of this gene were indicated (left). [score:1]
Previous studies also inferred that miR-127 has a negative effect on clonogenic survival in irradiated human endothelial cells [16]. [score:1]
To further investigate the specific role of miR-127 during LR, it is very important to identify miR-127 target genes. [score:1]
BRL-3A cells were seeded in a 24-well plate (1×10 [5] per well) and were transfected with 200 ng of the indicated luciferase reporter constructs with miR-127 mimics or miRNA NC. [score:1]
0039151.g003 Figure 3(A) Cell cycle of BRL-3A cells transfected with miR-127 mimics (miR-127) or miRNA negative control (miRNA NC) were analyzed by flow cytometry. [score:1]
[1 to 20 of 81 sentences]
2
[+] score: 217
Alteration of those miRNAs expression may in turn affect the expression of the imprinted genes, as evidenced by the down-regulation of Rtl1 by miR-127 in this study. [score:8]
Thus, the expression of human miR-127 was ∼20 times higher than human miR-433, the expression of rat miR-127 was ∼47 times higher than rat miR-433, and the expression of dog miR-127 was ∼40 times higher than dog miR-433. [score:7]
Down-Regulation of the Imprinted Gene Rtl1 by Overexpression of miR-127. [score:6]
This data suggests that miR-127 may function as a siRNA to down-regulate its host gene expression. [score:6]
Potential PCR amplification from genomic DNA contamination was eliminated by treating the total RNA with DNase I. As shown in Figures 6a–c, primary transcripts of the human (a), rat (b), or dog (c) miR-433 and miR-127 were easily detected in cells that over-expressed the recombinant expression vector, respectively. [score:5]
0007829.g005 Figure 5(a) The miR-433/127 loci expression plasmid of human, rat, or dog was expressed in mouse Hepa-1 cells (different species), and the binding of ERRγ to the endogenous promoter of miR-433 and of miR-127 of each species was detected using specific ERRγ antibodies. [score:5]
0007829.g006 Figure 6(Panels a–c) Semi-quantitative RT-PCR analysis of pri-miR-433 and pri-miR-127 expression transcribed from the human (a), rat (b), and dog (c) miR-433/127 loci expression plasmid. [score:5]
The recombinant human, rat, or dog miR-433/127 loci expression vector (designated pMIR-REPORT-NoMp-human, rat or dog) was then transfected into Hepa-1 cells and the expression of miR-433 and miR-127 primary transcripts was examined using semi-quantitative RT-PCR. [score:5]
Because miR-127 is located in an imprinted region encoding Rtl1, we determined if changes in miR-127 expression would affect the expression of Rtl1. [score:5]
Artificial Expression of miR-433 and miR-127 In Vitro in CellsOur previous studies showed that the mouse miR-433 and miR-127 genes overlapped and the expression of mouse miR-433 and miR-127 was controlled by independent promoters [3], [4]. [score:5]
0007829.g007 Figure 7 The expression vector of miR-127 was transfected in human Hela and mouse Hepa-1 cells and the expression of Rtl1 was determined by a modified strand-specific q-PCR. [score:5]
Similarly, the rat miR-433 and miR-127 was ∼210 fold and ∼10000 fold ovexpressed (Figure 6f) and the dog miR-433 and miR-127 was ∼4 fold and ∼160 fold ovexpressed (Figure 6g), respectively. [score:5]
The expression vector of miR-127 was transfected in human Hela and mouse Hepa-1 cells and the expression of Rtl1 was determined by a modified strand-specific q-PCR. [score:5]
We overexpressed miR-127 in human Hela and mouse Hepa-1 cells using an expression vector of miR-127 and the level of Rtl1 was assessed using a strand specific q-PCR analysis. [score:5]
For instance, if mutations occurred in the region between pre-miR-433 and pre-miR-127, it would be likely to affect both the processing of mature miR-433 and the regulation of miR-127 expression. [score:5]
We next determined expression levels of the mature miR-433 and miR-127 in Hepa-1 cells after recombinant vector over -expression. [score:5]
Interestingly, ectopic expression of miR-127 resulted in a significant reduction in Rtl1 expression in both cells (Figure 7). [score:5]
Based on this information, we made a direct comparison between the expression level of miR-433 and miR-127. [score:4]
Compared with non-vector transfected cells, the human miR-433 was ∼100 fold over-expressed whereas the human miR-127 was ∼2000 fold over-expressed (Figure 6e). [score:4]
The imprinted expression of miR-127 has been shown to undergo DNA methylation regulation in mouse embryos [26] and cancer cells [27]. [score:4]
Our studies provide evidence for a conserved gene structure and ERR/SHP dependent regulation of miR-433 and miR-127 gene expression in mammals. [score:4]
We recently have shown that gene expression of miR-433 and miR-127 in mice was regulated via a nuclear receptor ERRγ/SHP dependent mechanism [4]. [score:4]
Based on the identification of the same binding motifs, we predicted that a common regulatory mechanism of miR-433 and miR-127 expression may exist among different mammalian species. [score:4]
Artificial Expression of miR-433 and miR-127 In Vitro in Cells. [score:3]
Due to high expression of primary transcript of miR-433 and mIR-127, different PCR cycles were used (see Figure 6). [score:3]
This would allow us to determine if the transcriptional expression of miR-433 or miR-127 could be driven by its own promoter from the endogenous miR-433/127 loci. [score:3]
The mouse cell line Hepa1 and human cell line Hela were transfected with miR-127 expression vector. [score:3]
On the other hand, we observed a common transcriptional mechanism governing the expression of miR-433 and miR-127 in mammals, which involved ERR family members and orphan receptor SHP. [score:3]
As expected, ERRγ dose -dependently activated promoters of miR-433 and miR-127 of human (Figure 4a), rat (Figure 4b), and dog (Figure 4c), which was repressed by co -expression of SHP. [score:3]
Transcriptional expression of miR-433 and miR-127 from the miR-433/127 loci in human, rat, and dog. [score:3]
In addition, the expression level of pri-miR-433 was markedly lower than that of pri-miR-127 (Figure 6d) in all three species, suggesting pri-miR-433 and pri-miR-127 were transcribed differentially from an independent transcription unit. [score:3]
These differential expression results provided further evidence that miR-433 and miR-127 produced from the miR-433-127 loci were transcribed from two separate promoters in human, rat, and dog. [score:3]
Our previous studies showed that the mouse miR-433 and miR-127 genes overlapped and the expression of mouse miR-433 and miR-127 was controlled by independent promoters [3], [4]. [score:3]
In order to avoid the effect of endogenous miR-127 and miR-433 primary transcripts in Hela cells, we overexpressed the pMIR-Report human433/127 loci, pMIR-Report rat433/127 loci, and pMIR-Report dog433/127 loci in Hepa1 cells. [score:3]
The expression level of primary transcript of miR-433 and miR-127 was determined by semi-quantitative PCR using primers listed in Supplementary Material Table S3. [score:2]
We recently have reported that the full length primary transcripts of mouse miR-433 and miR-127 overlapped in a 5′–3′ unidirectional way [3]. [score:2]
We elucidated a common regulatory mechanism governing miR-433 and miR-127 promoter activities, which was dependent on nuclear receptor estrogen related receptor gamma (ERRγ, NR3B3) and small heterodimer partner (SHP, NR0B2) [4]. [score:2]
In this study, we used pMIR-Report-human 433/127, pMIR-Report-rat433/127, pMIR-Report-dog433/127 plasmids as the standard template to determine the PCR efficiency, then compared the expression level of miR-433 and miR-127 primary transcripts. [score:2]
The conservation of the transcriptional regulation of miR-433 and miR-127 further supports the notion that the miR-433/127 loci in mammals might be evolved from an ancient common origin. [score:2]
Primers used to determine the expression of primary transcripts of miR-433 and of miR-127 are located surrounding the precursors of miR-433 and of miR-127. [score:2]
In conclusion, our studies for the first time provide evidence for a conserved structure and transcriptional regulation of the clustered miR-433 and miR-127 genes in mammals, including humans. [score:2]
However, the question remains to be determined whether molecular details of miR-433 and miR-127 regulation by ERR/SHP are restricted to mouse or whether they apply to other species. [score:2]
Common Regulation of miR-433 and miR-127 Promoter Activity among Mammalian Species. [score:2]
Our published results showed that miR-433 and miR-127 genes are overlapped in a 5′–3′ unidirectional way in mouse [3] and these two non-coding genes have an antisense transcript, RTL1 [19]. [score:2]
Based on their overlapping gene structure and transcriptional initiation and termination sites, we subsequently cloned promoters of miR-433 and miR-127. [score:1]
ERRγ was co-immunoprecipitated on the ERRE containing the endogenous promoter regions of miR-433 and miR-127 in the liver of human and rat, and dog spleen, respectively (Figure 5b). [score:1]
Although the miR-433/127 loci were located on different chromosomes (Chr) in those species (human, Chr 14; Chimpanzee, Chr14; Horse, Chr 24; Dog, Chr 8; Monkey, Chr 7; Rat, Chr 6; Cow, Chr 21; mouse, Chr 12), multiple sequence alignment (MSA) of the precursors, pre-miR-433 and pre-miR-127, showed that the sequence similarity of pre-miR-433 hairpins was ∼95% (Figure 1a) and of pre-miR-127 was 100% (Figure 1b) among those species. [score:1]
To determine if miR-433 and miR-127 in human, rat, and dog can be independently and differentially transcribed using each miRNA's own promoter, we cloned a large (∼4.5 kb) human, rat, or dog genomic DNA fragment containing miR-433 and miR-127 and their promoter regions into pMIR-REPORT vector (Figure S2). [score:1]
Figure S1 Transient transfection assays to determine ERRα and ERRβ regulation of miR-433 and miR-127 promoter (pro. ) [score:1]
Transient transfection assays to determine ERRγ and SHP regulation of miR-433 and miR-127 promoter (pro. ) [score:1]
MatInspector of Genomatix Software Suite was used to predict the transcription factor binding sites in the promoter regions of miR-433 and miR-127 in different species, which was completely using Default parameters (http://www. [score:1]
0007829.g004 Figure 4Transient transfection assays to determine ERRγ and SHP regulation of miR-433 and miR-127 promoter (pro. ) [score:1]
The mature sequences of miR-433 and miR-127 were identical among the eight species. [score:1]
The response elements of the miR-433 and miR-127 genes from eight different species are illustrated. [score:1]
As shown in Figure 5, ERRγ was found to Co-IP on both the miR-433 and miR-127 promoters of human, rat, or dog. [score:1]
This resulted in the cloning of the gene cluster encoding mouse miR-433 and miR-127, which provided the first report for an overlapping code usage of the paired miR-433/127 gene [3]. [score:1]
The promoters of pri-miR-433 and pri-miR-127 were cloned into a pGL3-basic vector, respectively. [score:1]
ERRa, but not ERRβ, showed strong activation of miR-433 and miR-127 promoters of human, rat, and dog (Figure S1). [score:1]
The distance between miR-433 and miR-127 showed a striking similarity: 986 bp in human, chimpanzee, horse, dog, and monkey, 989 bp in rat, 988 bp in cow, and 1007 bp in mouse. [score:1]
The promoter of pri-miR-433 and of pri-miR-127 from each species was cloned into a pGL3-basic vector, respectively. [score:1]
Our results presented in this study provide evidence that the miR-433 and miR-127 overlapping genes have a higher rate of conservation in mammalian species. [score:1]
The genomic region between the two pre-miRNAs is predicted to function as the promoter of miR-127 based on our published mouse data [4]. [score:1]
BLASTN search of genome sequences of different species was completed online and a 5 kb genomic sequence surrounding the miR-433 and miR-127 precursors in each species was extracted manually. [score:1]
ChIP analysis of ERRγ Co-immunoprecipitation (Co-IP) on the miR-433 and miR-127 promoter region containing putative ERRE in human, rat, and dog. [score:1]
The precursor sequences of miR-433 and miR-127 were downloaded from the Sanger Institute (http://microrna. [score:1]
MSA of miR-433 and miR-127 gene promoters in eight mammalian species. [score:1]
Using mouse miR-433 and miR-127 precursor hairpin structure sequences as a query, we searched the genome databases of seven other species, including human, chimpanzee, horse, dog, monkey, rat, and cow. [score:1]
The promoters of miR-433 and miR-127 from human, rat and dog were cloned into a pGL3 basic vector, respectively. [score:1]
Although the miR-433/127 gene loci was located on different chromosomes in different species, the distance between miR-433 and miR-127 is very similar, which is ∼1 kb. [score:1]
The 4.5 kb genomic sequences centered miR-433 and miR-127 were extracted. [score:1]
Representative common TF binding motifs (1°∼4°) are shown, and their positions appear to be conserved in the promoter region of miR-433 and of miR-127 among different species. [score:1]
Predicted ERRE sites on the miR-433 and miR-127 gene promoters. [score:1]
Promoter analysis of miR-433 and miR-127 luciferase reporters of human, rat and dog. [score:1]
Why is the miR-433 and miR-127 overlapping gene structure in mammalian species so conserved? [score:1]
0007829.g003 Figure 3 The response elements of the miR-433 and miR-127 genes from eight different species are illustrated. [score:1]
Conserved Transcription Factor Binding Motifs in the Upstream Region of miR-433 and of miR-127 among Mammalian Species. [score:1]
Finally, the long DNA fragments containing human, rat or dog miR-433 and miR-127 loci were inserted into Asc I and Pac I sites of pMIR-REPORT-NoMp. [score:1]
We used MatInspector of Genomatix Software Suite to identify transcription factor binding motifs and position preference in the upstream promoter regions of miR-433 and of miR-127 in eight mammalian species. [score:1]
We found that miR-433 and miR-127 had almost identical PCR amplification efficiency (Supplementary Material Table S4). [score:1]
Conserved response elements in the promoters of miR-433 and miR-127 of eight mammalian species. [score:1]
Semi-Quantitative RT-PCR for miR-433 and miR-127 Primary Transcripts. [score:1]
Based on the above gene structure analysis and sequence prediction referenced from our published mouse data [3], [4], we hypothesized that the genomic location of promoters of miR-433 and miR-127 was similar in other mammalian species as in mouse. [score:1]
In the present study, we analyzed genes encoding miR-433 and miR-127 and determined the promoter transactivation of miR-433 and miR-127 from other mammalian species, including humans. [score:1]
To further confirm this result, the direct association of ERRγ with miR-433 and miR-127 promoters of each species in vivo was assessed using ChIP assays. [score:1]
The lowest evolutionary distance between cow and other species is 0.10114 and the sequence homology is low, based on the sequence alignment of the miR-127 promoter region (Figure 2b). [score:1]
miR-127 pro. [score:1]
The sequence similarity in either the miR-433 promoter region (Figure 2a) or the genomic region between pre-miR-433 and pre-miR-127 (Figure 2b) was low among the eight species. [score:1]
We cloned the promoters of miR-433 and miR-127 into pGL3 luciferase reporters using genomic DNAs isolated from liver specimens of human, rat and dog. [score:1]
The conservation of pre-miR-433 and pre-miR-127 hairpin sequences as well as the distance between them among different mammalian species raised the possibility that miR-433 and miR-127 might be evolved from the same DNA origin during evolution. [score:1]
Multiple sequence alignment (MSA) of miR-433 and miR-127 precursor hairpin sequences in eight mammalian species. [score:1]
Despite lower sequence similarity, analysis of miR-433 and miR-127 promoters of those species predicted common nuclear receptor binding sites, including ERRE (Figure 3 and Table 1). [score:1]
Unique potential binding motifs were also identified in the promoter region of miR-433 and of miR-127 in each species. [score:1]
[1 to 20 of 92 sentences]
3
[+] score: 187
Other miRNAs from this paper: rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-210
Thus, miR-127 up-regulation observed during I/R could result in KIF3B downregulation and proximal tubule cell trafficking impairment, as observed during renal I/R injury [42]. [score:7]
miR-127 overexpression significantly reduces luciferase activity in a dose -dependent manner, demonstrating that this miRNA directly regulates KIF3B expression. [score:7]
Surprisingly, evidence in rat hepatocarcinogenesis mo dels reveals that hypomethylation of DNA, induced by a methyl -deficient diet, decreases miR-127 expression [33], indicating that although epigenetic DNA regulation can explain differences in miRNAs expression between species, miR-127 regulation by methylation is still controversial. [score:7]
Furthermore, E-cadherin function and AJ integrity could be indirectly regulated by miR-127 target KIF3B. [score:5]
Although significant changes were not found for mRNA studies, miR-127 overexpression and inhibition modulate the KIF3B protein (Figure 6B). [score:5]
NRK-52E cells at 90% confluence were transfected with 100 nM anti-miR-127 (AM17000, Anti-miR™ miRNA Inhibitor, Life Technologies, Madrid, Spain) y anti-miR-Scramble (Anti-miR™ miRNA Inhibitors -negative Control #1, Life Technologies). [score:5]
Pre-miR and Anti-miR Transfection in vitro NRK-52E cells at 90% confluence were transfected with 100 nM anti-miR-127 (AM17000, Anti-miR miRNA Inhibitor, Life Technologies, Madrid, Spain) y anti-miR-Scramble (Anti-miR™ miRNA Inhibitors -negative Control #1, Life Technologies). [score:5]
On the other hand, we observed different miR-127 expression pattern in human cells (HK-2), where its expression is increased mainly during complete medium hypoxia and along reperfusion. [score:5]
These results demonstrate that KIF3B is a target gene for rno-miR-127 in NRK-52E cells during H/R, both regulating proximal tubule cell function. [score:4]
Therefore, rno-miR-127 induction during I/R and H/R could protect cell-matrix and cell-cell adhesions trough KIF3B downregulation, among other mechanisms not yet identified, contributing to cell structure maintenance and epithelial barrier function. [score:4]
In this regard, a potential crosstalk between c-myc and HIF-1α could be suggested in this case since c-myc is a known regulator of miR-127 expression [34]. [score:4]
Moreover, we performed Pre/Anti-miR transfection experiments to determine if modulation of miR-127 could regulate KIF3B expression. [score:4]
Furthermore, our interference experiments in vitro demonstrated for the first time that HIF-1α is one of the regulators of miR-127 expression, among other mechanisms. [score:4]
Previous publications have described miR-127 as an ubiquitously expressed microRNA which can be detected in several human and rat tissues including kidney and proximal tubule cells [25], [26]. [score:3]
On the other hand, we identified here for the first time KIF3B as a real target of rno-miR-127 in rat proximal tubule cells during H/R. [score:3]
Therefore, KIF3B is a real target of miR-127 in our system. [score:3]
The human homolog of this miRNA (hsa-miR-127-3p) is also induced in HK-2 cells but showing a different expression pattern. [score:3]
miR-127 overexpression promotes cell adhesion, protects actin cytoskeleton organization and focal adhesion complexes assembly during H/R. [score:3]
In this work, rno-miR-127 blockade leads to KIF3B overexpression and endocytic activity increase. [score:3]
The rno-miR-127 was the most consistent and significantly modulated miRNA showing an increased expression during minimum medium hypoxia (mimicking ischemia) and 1 hour of reperfusion (Figure 1A). [score:3]
KIF3B is a rno-miR-127 target gene in proximal tubule cells submitted to H/R. [score:3]
rno-miR-127 overexpression by pre-miR transfection in NRK-52E cells promotes cell adhesion not only during normoxia but also after hypoxia (Figure 4A). [score:3]
To go further into the biological significance of rno-miR-127 induction, we performed a bioinformatics target prediction for this miRNA using different databases available online, such as microcosm [19] (www. [score:3]
In several human tissues and in some types of cancer, DNA hypermethylation leads to repression of miR-127 expression [32]. [score:3]
KIF3B levels are decreased when miR-127 is overexpressed, particularly during Control Condition (CC) and minimum medium hypoxia (Hyp MM). [score:3]
miR-127 overexpression prevents FAC disassembly and TJ disruption and epithelial barrier impairment, all of them essential for kidney function. [score:3]
Kinesin Family Member 3B (KIF3B) is a rno-miR-127 Target in Rat Proximal Tubule Cells during H/R. [score:3]
miR-127 overexpression in vitro abrogates tight junction disruption during H/R. [score:3]
miR-127 overexpression significantly reduced endocytosis activity, whereas miR-127 blockade markedly raises Dextran-FITC internalization. [score:3]
In any case, our results indicate a great correlation between the expression of rno-miR-127 in both the in vitro and in vivo mo del in rat. [score:3]
Notably, a new target for miR-127 has been identified in this work: Kinesin Family Member 3B (KIF3B). [score:3]
miR-127 overexpression protects actin cytoskeleton from disorganization provoked by hypoxic injury (Figure 4B). [score:3]
Moreover, we have identified KIF3B, a component of kinesin II complex [23], as a real target of rno-miR-127 in proximal tubule cells, with potential implications in cell trafficking. [score:3]
Moreover, miR-127 induction and trafficking impair trough KI3FB inhibition could lead to tubular cell protection since cell trafficking requires high levels of ATP, compromised during renal I/R. [score:3]
Additionally we unveiled a new regulation of this miR-127 through HIF-1α. [score:2]
HIF-1α regulates miR-127-3p in HK-2 cells in response to Hypoxia/Reoxygenation. [score:2]
Several studies have identified miRNAs modulated during renal I/R injury [16], [24] but none have pointed miR-127 as a regulated miRNA in this context. [score:2]
Taken together, these data suggest that HIF-1α is a regulator of miR-127-3p in HK-2 cells during H/R, although HIF-1α binding site could not be successfully identified in this study. [score:2]
Knockdown of this factor by siRNA transfection successfully prevented miR-127-3p induction during complete medium hypoxia and 1 hour of reperfusion in HK-2 cells (Figure 2B). [score:2]
In summary, we identified for the first time a novel role of miR-127 as a critical regulator of cell-cell and cell-matrix adhesion in proximal tubule cells response to I/R. [score:2]
Moreover, in human cells, hsa-miR-127-3p is located in a CpG island which could be submitted to a fine tissue specific regulation by methylation. [score:2]
Our results demonstrated also for the first time that miR-127 is regulated by ischemia in vitro and in vivo. [score:2]
miR-127 regulates trafficking in rat proximal tubule cells in response to H/R. [score:2]
As HIF-1α is a key regulator of the cell response to hypoxia, we determined if this transcription factor could be involved in the modulation of miR-127 in our system. [score:2]
This could indicate that other HRE elements not predicted by the bioinformatic analysis could be responsible for miR-127 regulation in our in vitro system. [score:2]
hsa-miR-127 is Regulated During H/R by HIF-1α. [score:2]
This element is conserved among vertebrates and is located in a CpG island, making it a good candidate for miR-127 regulation. [score:2]
Bioinformatics approaches identified a Hypoxia Response Element (HRE) downstream miR-127 sequence (Figure 3A). [score:1]
Briefly, we first identified mammal or vertebrate PhastCons elements [46] within the region chr14∶100418481– 100419663 containing the mir-127 gene. [score:1]
Alignment map (upper part) shows miR-127 gene and HRE element location into human genomic DNA. [score:1]
0044305.g004 Figure 4 (A) NRK-52E cells were transfected with pre-miR-127, anti-miR-127 and their respective scramble control. [score:1]
0044305.g003 Figure 3 (A) Bioinformatics sequence alignment and conservation studies detected a consensus HRE sequence (CACGT) downstream miR-127 coding region. [score:1]
These results indicate that miR-127 could be a potential renal tissue damage biomarker and it could have a potential role in proximal tubule response to I/R as it will be further discussed. [score:1]
NRK-52E cells were transfected with pre-miR-127, anti-miR-127 and their respective scramble control. [score:1]
Although miR-127 is located in a cluster of microRNAs whose structure is conserved among mammals, miR-127 promoter sequence shows very low sequence conservation between rat and human. [score:1]
miR-127 is modulated in response to Hypoxia/Reoxygenation in vitro and during Ischemia/Reperfusión in vivo. [score:1]
A putative HRE element downstream miR-127 sequence, highly conserved among species, was predicted bioinformaticaly. [score:1]
miR-127 gene DNA region presents a putative Hypoxia Response Element. [score:1]
rno-miR-127 induction during I/R is a cytoskeleton protection mechanism which prevents actin depolimerization and promotes cell adhesion by preventing FAC disassembly and TJ disorganization. [score:1]
rno-miR-127 Modulation Leads to Changes in Cell Adhesion and Cytoskeleton Structure. [score:1]
Furthermore, rno-miR-127 blockade by anti-miR aggravates cytoskeleton and adhesion structures disorganization caused by hypoxia. [score:1]
Pre-miR-127 (AM17100, Pre-miR™ miRNA Precursor Molecule, Life Technologies) and Pre-miR-Scramble (AM17110 Pre-miR™ miRNA Precursor Molecules–Negative Control #1, Life Technologies) were transfected with a final concentration of 0.1 nM. [score:1]
Our data suggest that miR-127, controlled by HIF-1α, is induced in response to Hypoxia/Reoxygenation both in vitro and in vivo. [score:1]
For the identification of HIF binding sites within the mir-127 locus we follow the strategy described elsewhere [45]. [score:1]
rno-miR-127 is increased during hypoxia and Ischemia and at 1h and 24 hours of reperfusion respectively, time points where cellular damage or renal tissue damage is maximum in this mo del [6], [11]. [score:1]
Data are shown as percentage of luciferase activity reduction by Pre-miR-127 in comparison to scramble (Scramble = 100). [score:1]
Several microRNAs modulated by hypoxia have been identified [29] but miR-127 was not included among them. [score:1]
KIF3B mRNA was estimated by PCR in cells treated with pre-miR-127 (left panel) and anti-miR-127 (Right panel). [score:1]
In this work, we have identified rno-miR-127 and its human homologous hsa-miR-127-3p as important mediators of the proximal tubule response to I/R. [score:1]
Pre-miR-Scramble and Pre-miR-127 were simultaneously transfected with a final concentration of 0.1, 1 and 10 nMolar. [score:1]
All these data demonstrate that rno-miR-127 induction promotes cell adhesion and cytoskeleton structure maintenance during H/R. [score:1]
e. m. of three independent experiments and asterisks indicate statistical significance between Pre-miR-scramble and Pre-miR-127 transfected cells in each condition (P<0.05). [score:1]
Regarding a potential protective role of miR-127 in response to I/R, this work describes for the first time the effects of rno-miR-127 modulation in actin cytoskeleton organization and adhesive structures integrity during I/R injury. [score:1]
KIF3B mRNA is reduced during minimum medium hypoxia and 1 hour of reperfusion, when miR-127 is induced. [score:1]
Taken together, these data indicate that miR-127 is modulated in proximal tubule cells and renal tissue in response to H/R and I/R. [score:1]
In this regard, it has been described that miR-127 is involved in the response of pancreatic cells to glucose availability to produce insulin secretion [30]. [score:1]
Cells at 90% of confluence are transfected with HIF-1a siRNA, in the case of HK-2 cells, or pre/anti-miR-127 in NRK-52E cells. [score:1]
miR-127 is Induced in Response to H/R and I/R. [score:1]
Moreover, rno-miR-127 is also induced during ischemia and 24 hours of reperfusion in our in vivo rat mo del of I/R (Figure 1B). [score:1]
[1 to 20 of 79 sentences]
4
[+] score: 134
Related to this, here we demonstrated that in vivo HIF-1α interference leads to a lower expression of miR-127-3p and, consequently, increased expression of its target gene Bcl6, a transcriptional repressor involved in apoptosis 31 and survival regulation 32. [score:8]
HIF-1α inhibition lead to miR-127-3p expression decrease and Bcl6 expression enhance. [score:7]
The results shown in Fig. 10 indicate that inhibition of miR127-3p leads to a reduction in e-cadherin mRNA expression and to an increase of α-SMA and collagen I expression. [score:7]
Therefore, miR-127-3p could regulate EMT and fibrosis directly, affecting not yet validated targets, or indirectly through Bcl6, among other mechanisms. [score:6]
Consequently, we found an upregulation of miR-127-3p target gene Bcl6 at the same times. [score:6]
75 μg/kg body weight of siRNA mixed with Jetpei (Polyplus, Genycell) following manufacturer´s instructions was injected to animals, through the tail vein, before ischemia in sham and ischemia groups or during reperfusion in R-3d, R-5d and R-7d groups, as previously described 3. HK2 cells at 70% confluence were transfected with 100 nM anti-miR-127 (MM10400, Anti-miR 127-3p miRNA Inhibitor, Life Technologies, Madrid, Spain) y anti-miR-Scrambled (miRVana miR inhibitor Negative ControlAntimiR #1, Life Technologies). [score:5]
Expression of miR-127-3p and its target gene Bcl6 was estimated by qRT-PCR in renal tissue from I/R rats (n = 5 in each experimental group). [score:5]
75 μg/kg body weight of siRNA mixed with Jetpei (Polyplus, Genycell) following manufacturer´s instructions was injected to animals, through the tail vein, before ischemia in sham and ischemia groups or during reperfusion in R-3d, R-5d and R-7d groups, as previously described 3. Pre-miRs and Anti-miRs Transfection in vitro HK2 cells at 70% confluence were transfected with 100 nM anti-miR-127 (MM10400, Anti-miR 127-3p miRNA Inhibitor, Life Technologies, Madrid, Spain) y anti-miR-Scrambled (miRVana miR inhibitor Negative ControlAntimiR #1, Life Technologies). [score:5]
miR-127-3p inhibition in HK2 cells promotes EMT markers expression. [score:5]
By means of qRT-PCR we analysed the expression of miR-127-3p and its validated target gene Bcl6. [score:5]
To our knowledge none of these markers are validated targets of miR-127-3p even though MMP13 is a predicted target for this miRNA. [score:5]
Some of these alterations are mediated by miR-127-3p which is downregulated when HIF-1α is knocked down. [score:5]
HIF-1α inhibition affects miR-127-3p expression during I/R repair. [score:5]
miR-127-3p inhibition leads to a loss of e-cadherin and to an increase of α-SMA and collagen I expression, at 24 h of reoxygenation, in comparison to scrambled group. [score:5]
In fact, miR127 regulates IL-6 and TNF-α cytokine release by macrophages in lung inflammation since the IgG FcγRI (CD64) is a target of miR-127-3p 43. [score:4]
Indeed our in vitro results demonstrate that miR127-3p regulates the expression of EMT and fibrotic markers. [score:4]
The overexpression of miR127-3p reverses these effects. [score:3]
Our work unveils HIF-1α dependent mechanisms, including miR127-3p, responsible for adaptive processes of repair since their inhibition results in abnormal restoration. [score:3]
Accordingly, Bcl6 expression increased at the same time (Fig. 9b), indicating that miR-127-3p and Bcl6 are possible mediators of HIF-1α in the renal repair in our mo del. [score:3]
The mechanisms described here could allow designing novel and targeted therapeutic strategies, including HIF-1α and miR127-3p based strategies, in order to promote adaptive renal recovery and to minimize chronic kidney alterations after acute injury, as an outstanding aim in clinical Nephrology 47. [score:3]
Related to our results, it has been recently reported that miR-127-3p suppressed NFkB activity in HCC cells, also promoting HCC proliferation and tumor -associated inflammation 37. [score:3]
Accordingly with our results, other groups demonstrate that miR-127-3p inhibits cell proliferation 14 33, migration and invasion 34. [score:3]
Up to this moment, there are no reports validating MCP-1, IL-1b, TNF-α or VCAM-1 as miR-127-3p targets genes. [score:3]
Data are expressed as fold change using RNU6B and 5S mean and 28S levels as references in miR-127-3p and Bcl6 respectively. [score:3]
The over expresion of miR-127-3p exhibited the opposite results: increase in e-cadherin and reduction in α-SMA and collagen I expression. [score:3]
HIF-1α interference leads to miR-127-3p expression decrease during ischemia and at 3–5 days of reperfusion as compared to scrambled control. [score:2]
Thus, we studied the role of HIF-1α in the regulation of miR-127-3p as a possible mechanism contributing to the repair of renal I/R injury. [score:2]
Previous results of our lab demonstrated that miR127-3p is regulated by HIF-1α during proximal epithelial cell response to ischemia and it is a protector mechanism against renal ischemic injury 13. [score:2]
However, miR127 appears as an important miRNA for inflammatory regulation response, in particular for macrophages response 42. [score:2]
Moreover miR127-3p can also regulate macrophages polarization in lung 44. [score:2]
Moreover, trying to investigate the involvement of miR127-3p in the abnormal repair exhibited by HIF-1α interfered rats, we modulated miR127-3p using specific Pre-miR127-3p and anti-miR-127-3p in human proximal tubule cells HK2 and we estimated the expression of EMT markers including e-cadherin, α-SMA and collagen I, by qRT-PCR. [score:1]
Since HIF-1α interfered rats, where miR127-3p is reduced, exhibited EMT induction and initial fibrosis, miR127-3p also appears here as a protector mediator against renal chronic damage establishment. [score:1]
The miRNA modulation was efficient: pre-miR127-3p/pre-scrambled, 140 ± 15 folds; anti-miR-127-3p/anti-scrambled: 5 ± 0,5 folds. [score:1]
Pre-miR-127 (miRVana miRNA mimic miR-127-3p MC10400, Life Technologies) and Pre-miR-Scrambled (miRVana miRNA mimic Negative Control #1, Life Technologies) were transfected with a final concentration of 0.1 nM, using Lipofectamine 2000 according to the manufacturer’s protocol. [score:1]
Cell culture, in vitro miR-127-3p modulation, RNA extraction and qRT-PCR were performed during 2016. [score:1]
How to cite this article: Conde, E. et al. HIF-1a induction during reperfusion avoids maladaptive repair after renal ischemia/reperfusion involving miR127-3p. [score:1]
All these findings demonstrate that miR-127-3p is a HIF-1α effector during the renal tissue repair after ischemia, among others. [score:1]
Experimental chirurgic mo del, RNA extraction and qRT-PCR were performed during 2011. miR-127-3p was modulated by transfection of specific pre-miR127-3p and anti-miR127-3p and 48 h later, cells were subjected to the H/R protocol. [score:1]
We cannot discard that the absence of miR127-3p in HIF-1α interfered rats could also contribute to the abnormal renal tissue repair by modulating macrophages responses and phenotypes shift. [score:1]
Previous data from our lab described miR-127-3p as key mediator of proximal epithelial tubule cell response to I/R 13. [score:1]
[1 to 20 of 40 sentences]
5
[+] score: 111
Other miRNAs from this paper: rno-mir-16, rno-mir-217
Of note, recent study identified that miR-127 expression was aberrant in the inflammation-related pulmonary disorders [36] and further revealed that enhanced expression of miR-127 could promote the development of inflammatory macrophages and contribute to the exaggerated lung inflammation and injury [37]. [score:6]
Among the limited studies on miR-127 in human pancreatic diseases, it was transiently expressed in pancreatic duct progenitor cells during the embryonic stages [51] and deregulated in pancreatic intraepithelial neoplasia [52] and in human pancreatic cancer [53]. [score:6]
miR-127 has been reported to play a pivotal role in organic development [35, 47], ischemia/reperfusion injury [48], cancer [49], lung disease [37], and so forth. [score:4]
The upregulation of miR-127 in the AP-sLI group was significant than that in both AP-mLI and control groups at 6 and 24 h (P < 0.05). [score:4]
However, another study [37] showed that miR-127 was downregulated in lipopolysaccharide-stimulated LI, which appeared to be paradoxical to the previous study [32] and our findings. [score:4]
The levels of miR-127 were upregulated in the lung tissues of AP rats. [score:4]
miR-127 is originally found to be highly expressed in human and murine embryos and has a critical role in lung development and placental formation [34, 35]. [score:4]
3.3. miR-127 Was Significantly Upregulated in Lung Tissues of AP Rats. [score:4]
The upregulation of miR-127 in the lungs of rats was detected in the groups of AP with severe LI at 6 h and 24 h, whereas it was scarcely detectable in plasma. [score:4]
Significant downregulation of plasma miR-127 was shown in the RF group than in the HV group (P = 0.014) and the nRF group (P = 0.043). [score:4]
In the pilot study that included 18 AP patients and 5 healthy volunteers, the plasma miR-127 level was significantly downregulated in AP patients with respiratory failure compared with the healthy volunteers (P = 0.014) and those without respiratory failure (P = 0.043). [score:3]
The major findings of this study were that miR-127 correlated to the severity of LI in AP rats and differentially expressed in plasma of AP patients with RF. [score:3]
Similar expressions were detected in terms of plasma miR-127 between nRF and HV groups. [score:3]
The aim of this study was to determine the expression of microRNA-127 (miR-127) in both rat mo dels and patients of acute pancreatitis (AP) with lung injury (LI). [score:3]
Here, microRNA-127 (miR-127) is one of the miRNAs that focuses on lung diseases [31– 33]. [score:3]
No difference was observed in the expression level of miR-127 between AP-mLI and AP-sLI groups at 12 h. U6 snRNA in the lung tissues was insignificantly different in any of the groups. [score:3]
We determined the expression levels of miR-127 in serum of the rats using miR-16 as an internal control. [score:3]
Nevertheless, the expressions of miR-127 and its role in AP with LI are unknown. [score:3]
Third, pancreatitis is a complex and heterogeneous disease that evolves over time to time, and the discriminative ability of miR-127 at multiple time points should be determined in future studies. [score:3]
3.4. miR-127 Was Lowly Expressed in Serum of Rats. [score:3]
The expression of miR-127 was successfully detected in plasma of both AP patients and the HVs (Figure 5). [score:3]
In this study, we sought to determine the expressions of miR-127 in the lung tissues of sodium taurocholate -induced AP mo dels in rats and that in plasma of AP patients and to preliminarily explore the association of miR-217 levels and LI. [score:3]
Second, miR-127 was detected in a small number of sample size (n = 23) for analysis in our study, and it was still lowly expressed. [score:3]
The expression levels of miR-127 in the lung tissues of the rats in AP-mLI group were significantly higher than those in the control group at 24 h (Figure 4, P < 0.05) and were insignificantly different at 6 and 12 h (all P > 0.05). [score:3]
The levels of miR-127 in serum and lung tissues were quantified using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and the expression between different time points was compared. [score:2]
3.5. miR-127 Levels Positively Correlated with Pathological Severity in the Lung Tissues of Rats. [score:1]
Thus, miR-127 might be a potential biomarker for early identification of RF in severe AP patients. [score:1]
Therefore, these results suggested that miR-127 in the lungs might reflect pancreatic and lung tissue injuries and play a potential role in the inflammatory signaling and lung pathology. [score:1]
These results indicate the exact role of miR-127 in pulmonary inflammation, and injury is still controversial. [score:1]
This study explored the relationship between miR-127 and AP with LI from the perspective of blood and tissue. [score:1]
Recent studies demonstrated the similar result that miR-127 was prominently induced in an exaggerated pulmonary inflammation and injury [32]. [score:1]
To the best of our knowledge, it was the first study reporting plasma miR-127 in AP patients. [score:1]
The levels of lung miR-127 also demonstrated a significant positive correlation with lung edema, inflammatory infiltration, capillary congestion, and total scores (Table 2, all P < 0.05). [score:1]
The results showed that plasma miR-127 in the RF group tended to be significantly lower than those in the nRF group and the HV group. [score:1]
3.6. miR-127 in the Plasma of AP Patients and Healthy Controls. [score:1]
However, miR-127 could not be detected by qRT-PCR in serum samples of the rats even with the modifications to the methods allowed their reliable quantitation (all nearly Ct = 45). [score:1]
First, miR-127 was undetectable in serum of rats, and the correlations of serum and tissue miR-127 were not analyzed. [score:1]
miR-127 might be of help for the identification of AP with LI. [score:1]
To our best knowledge, it is the first study that integrated miR-127 and the inflammatory injuries of the pancreas and the lung. [score:1]
miR-127 might serve as a potential marker for the identification of AP with LI. [score:1]
Considering the potential role of miR-127 in the vital biological process of inflammation, we hypothesized that miR-127 may serve as a marker of AP with LI. [score:1]
The right lung was placed in liquid nitrogen immediately after removal for the detection of myeloperoxidase (MPO) activity and miR-127 levels. [score:1]
Furthermore, both miR-127 and proinflammatory cytokine (IL-1 β, IL-6, and TNF- α) were increased in AP with LI. [score:1]
Although the mechanism involved has been largely undefined, the studies indicated that miR-127 promoted lung inflammation and injury by activating the inflammatory pathway [32]. [score:1]
The levels of miR-127 in the tissues and plasma were detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). [score:1]
In this study, miR-127 levels presented a significant positive correlation with histopathological severity scores of the pancreas and the lungs. [score:1]
A Pearson's correlation coefficient analysis showed that the miR-127 levels in the lung tissues were significantly positively correlated with pancreatic edema, inflammatory infiltration, acinar cell necrosis, and total scores (Table 2, all P < 0.05). [score:1]
The levels of miR-127 in AP-mLI and AP-sLI groups at 12 h were slightly increased, but they did not significantly differ from those in the control group. [score:1]
[1 to 20 of 48 sentences]
6
[+] score: 92
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
miRNA-127-3p has been shown to be upregulated in senescent cells, and its downregulation has been shown to promote cell proliferation [40, 41]. [score:7]
In view of the previously discussed results, it seems that CD results in a cascade of interrelated activity that revolves around increased NF-κB activity and expression of BCL6, with aberrant CD -induced downregulation of miR-127 and miR-146b potentially contributing to this cascade. [score:6]
Figure 6 A. Mean relative expression of miR-127 based on Illumina sequencing, * p-adjusted < 0.1, N = 6. B. Mean Relative expression of miR-127 based on qRT-PCR data, * p < 0.05, N = 10. [score:5]
Consequently, this dynamic potentially results in the decreased expression of miR-127 through increased Tudor-SN activity, which in turn results in increased expression of the proto-oncogene BCL6. [score:5]
Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:5]
A. Mean relative expression of miR-127 based on Illumina sequencing, * p-adjusted < 0.1, N = 6. B. Mean Relative expression of miR-127 based on qRT-PCR data, * p < 0.05, N = 10. [score:5]
A target of miR-127, the BCL6 gene has been identified as a potent inhibitor of cell senescence and a contributor to oncogenesis, and the western blot data showed that BCL6 levels were significantly increased in the circadian-disrupted samples (Figure 6) [43, 44]. [score:5]
Circadian disruption causes decreased expression of miR-127, and increased expression of Tudor-SN and BCL6. [score:5]
Amongst the miRNAs influenced by Tudor-SN, is miR-127, and studies have shown that Tudor-SN triggers miR-127 downregulation in breast cancer cells [50]. [score:4]
The results also illustrated higher quantities of a verified target of miR-127 and a protein linked to cellular senescence, BCL6 (Figure 6). [score:3]
The basis of the link between miRNA activity and CD -induced breast cancer seems to be an interconnected web of increased NF-κB activity and BCL6 expression, likely linked to and promoted by the CD -induced decrease in miR-127 and miR-146b. [score:3]
Validation of sequencing results through qRT-PCR verifies miR-127 expression. [score:3]
Amongst the qRT-PCRs performed on the differentially expressed miRNAs in the two-week chronic ZT06 group, the miR-127 qPCR results validated the sequencing results. [score:3]
also showed higher quantities of Tudor-SN, a protein linked to NF-kappaB activity and lower miR-127 expression (Figure 6). [score:3]
Small RNA sequencing and validation through qRT-PCR showed that miR-127 is underexpressed in the two-week chronic ZT06 group (Figure 6A-6B). [score:3]
Amongst the proteins linked to miR-127 activity and breast cancer development, are BCL6 and Tudor-SN. [score:2]
The qPCR data illustrated a similar and consistent change in relative miR-127 expression when compared to the Illumina sequencing (Figure 6A and 6B). [score:2]
All the forward primers were miRNA-specific primers ordered from GeneCopoeia based on the target of interest, for example, rno-miR-127-3p (RmiRQP0111). [score:1]
Verification of potential circadian-relevant targets through luciferase reporter experiments, incorporation of the CD schemes into xenograft mo dels, and further investigation of the dynamic of miR-127 and miR-146b activity in cancer cells are all logical extensions of the present study. [score:1]
[1 to 20 of 21 sentences]
7
[+] score: 26
rno-miR-675-5p 4.143757751 Premature senescence of cardiac progenitor cells, G1 arrest, reduced cell proliferation, colony formation, migration and invasion rno-miR-183-3p 3.74730108 Regulates claudin-1 expression rno-miR-299a-5p 3.626723224 Anti-apoptotic role rno-miR-200c-3p 3.593610443 Targets the VEGF-VEGFR2 pathway and angiogenesis rno-miR-665 3.511737089 Negatively targets anti-apoptotic BCL2L1 rno-miR-291a-5p 3.457928187 VSMC migration rno-miR-490-5p 2.373358 Tumour suppressor rno-miR-1 2.505729 Suppresses cell growth rno-miR-133b 2.192279 Inhibits cell proliferation and invasion rno-miR-30c-1-3p 2.70761 Suppresses PXR expression rno-miR-294 2.010496 Promotes proliferation and differentiation rno-miR-127-5p 2.780488 A regulator of MMP-13 and suppresses cell growth rno-miR-503 2.327383 Inhibits cell proliferation and invasion Table 2 Twenty down-regulated miRNAs. [score:26]
[1 to 20 of 1 sentences]
8
[+] score: 24
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]
At P21, the differential expression of 5 of 10 of the miRNAs was statistically confirmed, with miR378a-5p, miR127-3p, and miR184 downregulated and miR30e-5p and miR449a-5p upregulated. [score:9]
Among the other miRNAs found deregulated in our study, miR-34c-5p, miR-128-3p miR-184, miR127-3p, miR-30e-5p, and miR-23b-5p were also previously described as “tumour suppressors”[22– 26], although many miRNA studies previously dealt with cancer or oncogenic proliferation states and the current analysis depended on previous reports. [score:4]
[1 to 20 of 3 sentences]
9
[+] score: 20
Among the 11 significantly dysregulated miRNAs, 4 miRNAs were up-regulated (miR-34c, miR-374, miR-181a, and miR-let-7c-1), and 7 miRNAs were down-regulated (miR-1188, miR-770-5p, miR-127-5p, miR-375, miR-331, miR-873-5p, and miR-328a) (differentially expressed miRNAs were defined by a fold-change >1.5, up or down-regulated; p <0.05). [score:13]
Some of the up-regulated (miR-34c, miR-374, miR-181a, and miR-let-7c-1) and down-regulated (miR-1188, miR-770-5p, miR-127-5p, miR-375, miR-331, miR-873-5p, and miR-328a) miRNAs we detected using miRNA microarray were suggested to be closely connected with memory function. [score:7]
[1 to 20 of 2 sentences]
10
[+] score: 15
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
The miR-127 family has been reported to play a role in regulating the expression of the tumor suppressor gene BCL6, in cell proliferation, and in apoptosis [32]. [score:6]
Most reads (highest expression) were from the miR-379 family; next was miR-127 family with 5,235 reads. [score:3]
By comparing with sheep miRNA sequences, we found that 5 miRNA families containing miR-127, miR-136, miR-154, miR-229 and miR-379, were conserved in all these species It is, therefore, tempting to speculated that these 5 miRNA families are critical in mammal development. [score:2]
Another study found that the miR-127 family plays an important role in fetal lung development [33]. [score:2]
We suggest that miR-127 may play a part in skin follicle cell apoptosis and proliferation. [score:1]
Most of the miRNAs were sequenced only a few times, whereas miR-127, miR-154 and miR-375 were sequenced thousands of times. [score:1]
[1 to 20 of 6 sentences]
11
[+] score: 14
The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7a, b, c, f. The up-regulated miRNAs were composed of miR-344, miR-346, miR-99a, miR-127, miR-128b, miR-135b, and miR-30a/b. [score:7]
The up-regulated miRNAs included miR-99a, miR-127, miR-128b, miR-135b, miR-30a, and miR-30b. [score:4]
miR-17, miR-92a and miR-127 have been shown to regulate lung development [11, 12]. [score:3]
[1 to 20 of 3 sentences]
12
[+] score: 14
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-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
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]
[1 to 20 of 3 sentences]
13
[+] score: 12
Treatment Group MiRNA changed Log2 (G/CT) Validated targets 80 kVp/0.1 Gy 2 Low fold change – 80 kVp/0.1 Gy Low signals – – 80 kVp/1 Gy miR-34a 1.55 E2F3, Tagln, INHBB miR-29c −1.02 Tpm1 miR-20b-5p −1.65 – miR-204 −1.39 – 30 kVp/2.5 Gy miR-34a 1.08 E2F3, Tagln, INHBB miR-20b-5p −1.55 – miR-98 −1.16 – miR-127 2.08 – The elevated expression of miR-34a was interesting to us, and we decided to proceed with identifying protein levels of its targets E2F3 and transgelin as well as p53, the key protein in DNA damage response. [score:7]
Treatment Group MiRNA changed Log2 (G/CT) Validated targets 80 kVp/0.1 Gy 2 Low fold change – 80 kVp/0.1 Gy Low signals – – 80 kVp/1 Gy miR-34a 1.55 E2F3, Tagln, INHBB miR-29c −1.02 Tpm1 miR-20b-5p −1.65 – miR-204 −1.39 – 30 kVp/2.5 Gy miR-34a 1.08 E2F3, Tagln, INHBB miR-20b-5p −1.55 – miR-98 −1.16 – miR-127 2.08 – Relative miR expression values are represented in folds in the irradiated cells in comparison to non-irradiated control cells as analyzed by miRNA microarray. [score:5]
[1 to 20 of 2 sentences]
14
[+] score: 10
Some experiments have demonstrated that miR-127 was capable of suppressing the hepatocyte proliferation, notably by inhibiting BCL6 and SETD8 [38]. [score:5]
Thus, circ137 and circ2270 might regulate the hepatocyte proliferation to control rat LR process by interacting with miR-127. [score:2]
It was also scientifically predicted that circ137 and circ2270 could regulate the hepatocyte proliferation by interacting with miR-127. [score:2]
The outcome of biomathematical prediction manifested that circ137 and circ2270 could both couple with miR-127. [score:1]
[1 to 20 of 4 sentences]
15
[+] score: 6
Other miRNAs from this paper: rno-mir-327, rno-mir-338, rno-mir-210, rno-mir-377, rno-mir-465
miR-127 is important during the later stage of fetal lung development (5); however, no statistically significant difference in miR-127 expression was identified between the hypoxic and normoxic groups in the present study. [score:4]
Furthermore, miR-127 is an important miRNA in late lung development (5, 8); thus, was selected. [score:2]
[1 to 20 of 2 sentences]
16
[+] score: 6
[26] MiR-27b and miR-127 inhibit the IL-1 β -induced upregulation of MMP-13 in human osteoarthritic chondrocytes. [score:6]
[1 to 20 of 1 sentences]
17
[+] score: 4
In agreement with their results, we observed the downregulation of miR-127, miR-181a, miR-411, miR-99a, miR-34a, miR-30b, and miR-30c, which according to Liu [6] should lead to increased inflammation. [score:4]
[1 to 20 of 1 sentences]
18
[+] score: 4
37Tryndyak VP, Ross SA, Beland FA, Pogribny IP (2009) Down-regulation of the microRNAs miR-34a, miR-127, and miR-200b in rat liver during hepatocarcinogenesis induced by a methyl -deficient diet. [score:4]
[1 to 20 of 1 sentences]
19
[+] score: 4
Down-regulation of the microRNAs miR-34a, miR-127, and miR-200b in rat liver during hepatocarcinogenesis induced by a methyl -deficient diet. [score:4]
[1 to 20 of 1 sentences]
20
[+] score: 4
MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection. [score:4]
[1 to 20 of 1 sentences]
21
[+] score: 3
Notably, 3 of the mRNAs (BCL6, PRDM1, and XBP1), all targets of miR-127, were associated with the hematological system. [score:3]
[1 to 20 of 1 sentences]
22
[+] score: 3
Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
[1 to 20 of 1 sentences]
23
[+] score: 2
Conserved microRNA signatures were identified in valves (miR-let-7c, miR-125b, miR-127, miR-199a-3p, miR-204, miR-320, miR-99b, miR-328 and miR-744) and in ventricular-specific regions of the myocardium (miR-1, miR-133b, miR-133a, miR-208b, miR-30e, miR-499-5p, miR-30e*) of Wistar rat, Beagle dog and cynomolgus monkey. [score:1]
An assessment of the degree of conservation for structure-specific distribution of microRNAs in Wistar rat, Beagle dog and cynomolgus monkey (see for relative enrichment analysis), revealed high enrichment of nine microRNAs cardiac valves (miR-let7c, mIR-125b, miR-127, mir-199a-3p, miR204, miR-320, miR-99b, miR-328 and miR-744) (Figure 3A) and seven microRNAs in the myocardium (miR-1, mir-133a, miR-133b, miR-208b, miR-30e, miR-499-5p, miR-30e*) (Figure 3A). [score:1]
[1 to 20 of 2 sentences]
24
[+] score: 1
Moreover, the level of miRNA-375, together with miRNA-127-3p and miR-184 is positively correlated to insulin mRNA levels in islets from human donors and the association between these miRNAs and β-cell function was deranged in islets from glucose intolerant donors [18]. [score:1]
[1 to 20 of 1 sentences]
25
[+] score: 1
Other miRNAs from this paper: rno-mir-21, rno-mir-27a, rno-mir-126a, rno-mir-126b
Furthermore, several studies have demonstrated that miR-21[10] and miR-127[11] are involved in mature endothelial cell EndMT induced by TGF-β1 and TGF-β2, respectively. [score:1]
[1 to 20 of 1 sentences]
26
[+] score: 1
In nine cases, i. e., miR-127-3p, −139-3p, −140-5p, 145-5p, 27a-3p, 29a-3p, −344-b1-3p, 369-5p, and −409a-5p, miRNAs and Partner-miRNAs displayed close FCEs and padj-values (= < 5.0E-2). [score:1]
[1 to 20 of 1 sentences]