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26 publications mentioning rno-mir-106b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-106b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 198
INH also decreased the expression of miR-122, which corresponded to the increase of two gene targets: Cyclin G1 and CAT-1. Finally, the aberrant downregulation of miR-125b and miR-106b upregulated the STAT3 expression to stimulate the secretion of inflammatory factors during INH -induced liver injury. [score:13]
Taking these experimental data into consideration, we can conclude that aberrant downregulation of miR-125b and miR-106b can upregulate STAT3 expression to stimulate the secretion of inflammatory factors involved in INH -induced liver injury. [score:9]
The above results suggested that the aberrantly downregulated miR-125b and miR-106b upregulated the STAT3 expression to stimulate the secretion of inflammatory factors during INH -induced liver injury. [score:9]
Our results suggested that DNA methylation probably regulates the expression of miRNA genes (miR-122, miR-125b, and miR-106b), affecting the expression of their gene targets (Cyclin G1, CAT-1, and STAT3) and participating in the process of INH -induced liver injury. [score:8]
In the present study, the expression levels of hepatic miR-122, miR-106b and miR-125b were downregulated and correlated with liver pathology scores and serum AST and ALT activities, suggesting that the dynamic change in the expression levels of miR-122, miR-106b and miR-125b were related to INH -induced liver injury. [score:8]
Our results suggested that DNA methylation likely regulated the expression of miRNA genes (miR-122, miR-125b and miR-106b), thereby affecting the expression of their target genes (Cyclin G1, CAT-1 and STAT3) and participating in the process of INH -induced liver injury. [score:8]
Finally, we detected the expression levels of their target genes cell cycle protein G1 (Cyclin G1), cationic amino acid transporter-1 (CAT-1) and signal transducer and activator of transcription 3 (STAT3)) and explored the possible regulation mechanisms of miR-122, miR-125b and miR-106b during INH -induced liver injury. [score:6]
These results suggested that methylation was responsible for the downregulation of miR-122, miR-106b and miR-125b expression during INH -induced liver injury. [score:6]
Methylated levels of miR-122, miR-106b and miR-125b were upregulated in INH -induced liver injury and correlated with their expression levels. [score:6]
The amount of methylated miR-122, miR-125b and miR-106b in the liver increased after INH administration and correlated with their expression levels, suggesting the role of methylation in regulating miRNA gene expression. [score:6]
Signal transducer and activator of transcription 3 (STAT3) was a common target gene of miR-125b and miR-106b, and its expression levels of mRNA and protein increased after INH administration. [score:5]
We analysed the methylation and expression levels of miR-122, miR-125b and miR-106b and their potential gene targets in livers. [score:5]
Hepatic miR-122, miR-125b and miR-106b expression levels dramatically decreased after INH administration for 3, 7 and 7 days (* p < 0.05 versus control group) The analysis of Pearson correlation coefficients demonstrated that the expression levels of miR-122, miR-125b and miR-106b were negatively correlated with liver scores (r = − 0.591, − 0.654 and − 0.701, p < 0.001, see Additional file 5: Figure S3) and serum ALT and AST activities (ALT, r = − 0.672, − 0.771 and − 0.695, p < 0.001, see Additional file 5: Figure S1; AST, r = − 0.462, − 0.584 and − 0.606, p < 0.001, see Additional file 5: Figure S2). [score:5]
Furthermore, the expression of miR-125b and miR-106b has a causal role in enhanced STAT3 mRNA and protein expression during INH -induced liver injury. [score:5]
Hepatic miR-122, miR-125b and miR-106b expression levels dramatically decreased after INH administration for 3, 7 and 7 days (* p < 0.05 versus control group)The analysis of Pearson correlation coefficients demonstrated that the expression levels of miR-122, miR-125b and miR-106b were negatively correlated with liver scores (r = − 0.591, − 0.654 and − 0.701, p < 0.001, see Additional file 5: Figure S3) and serum ALT and AST activities (ALT, r = − 0.672, − 0.771 and − 0.695, p < 0.001, see Additional file 5: Figure S1; AST, r = − 0.462, − 0.584 and − 0.606, p < 0.001, see Additional file 5: Figure S2). [score:5]
This investigation aimed to evaluate the role of methylation in the regulation of microRNA (miR)-122, miR-125b and miR-106b gene expression and the expression of their target genes during isoniazid (INH) -induced liver injury. [score:4]
These results demonstrate that lower levels of hepatic miR-125b and miR-106b contribute to the upregulation of STAT3 in stimulating the secretion of inflammatory factors during INH -induced liver injury. [score:4]
Thus, we hypothesise that methylation is responsible for the downregulation of miR-122, miR-125b and miR-106b in INH -induced liver injury. [score:4]
First, we searched for putative miR-125b and miR-106b targets that might regulate inflammatory immune response. [score:4]
Thus, the correlation between the expression levels and methylation of CpG islands of the miR-122, miR-125b and miR-106b genes have been revealed, indicating the possibility of epigenetic regulation of these genes during INH -induced liver injury. [score:4]
CpG island hypermethylation of miR-122, miR-125b and miR-106b genes correlate with their expression levels. [score:3]
Methylated levels of miR-122, miR-125b and miR-106b in INH-administered rat liver tissues were significantly higher than those in the control rats (* p < 0.05 versus control group)We also analysed the correlation between methylation levels and the gene expression of miR-122, miR-125b and miR-106b. [score:3]
We also found that STAT3, an important signal transduction pathway, was predicted and experimentally proven as the common gene target of miR-125b and miR-106b [25– 27]. [score:3]
Therefore, we first analysed the expression levels of hepatic miR-122, miR-125b and miR-106b after INH administration and explored their correlation with INH -induced liver injury. [score:3]
We further analysed whether the expression levels of miR-122, miR-106b and miR-125b are correlated with the ongoing liver damage according to liver histopathology and serum ALT and AST activities. [score:3]
miR-122 was one of the most abundant miRNAs in the liver, accounting for up to 72% of all hepatic miRNAs [12], while the expressions of miR-106b and miR-125b not only occur in the liver, but also in many other tissues, including the uterus, ovaries and lungs. [score:3]
Expression levels of the selected miRNAs (U6, miR-122, miR-125b and miR-106b) and selected mRNAs (β-actin, Cyclin G1, CAT-1, mitogen-activated protein kinase 14 MAPK14, STAT3, RAR-related orphan receptor gamma (RORγt), IL-17, IL-6, TNF-α, CXCL1 and MIP-2) were quantified using real-time RT-PCR analysis. [score:3]
To our knowledge, this study shows for the first time that hepatic miR-122, miR-125b and miR-106b expression levels gradually decreased during a mo del of INH -induced liver injury. [score:3]
Relative expression levels of miR-122, miR-125b and miR-106b genes in the liver decreased after INH administration and correlated with the scores of liver pathology and serum AST and ALT activities, suggesting that miR-122, miR-125b and miR-106b are associated with INH -induced liver injury. [score:3]
Our results also confirmed that both miR-125b and miR-106b expression levels dramatically decreased during INH -induced liver injury. [score:3]
miR-122, miR-106b and miR-125b expression levels are correlated with liver pathology scores and AST and ALT levels, supporting the correlation of these three miRNAs with INH -induced liver injury. [score:3]
Previous studies confirmed that MAPK14 and STAT3 were common gene targets of miR-125b and miR-106b [25– 27]. [score:3]
Methylated levels of miR-122, miR-125b and miR-106b in INH-administered rat liver tissues were significantly higher than those in the control rats (* p < 0.05 versus control group) We also analysed the correlation between methylation levels and the gene expression of miR-122, miR-125b and miR-106b. [score:3]
Moreover, expression levels of miR-122, miR-125b and miR-106b reached a nadir after 14-, 21-, and 21-day administration. [score:3]
Fig. 5Expression levels of miR-122, miR-125b and miR-106b in the liver tissue of different groups. [score:3]
The miR-122 expression was significantly lower after 3 days, while both miR-125b and miR-106b significantly decreased after 7 days. [score:3]
The results showed the negative correlation between methylation and expression levels of miR-122, miR-125b and miR-106b (miRNA-122, r = − 0.587, p < 0.001; miRNA-125b, r = − 0.536, p < 0.001; miRNA-106b, r = − 0.568, p < 0.001, see Additional file 5: Figure S4). [score:3]
Moreover, we clearly found that the expression of miR-122, miR-125b and miR-106b were significantly lower at different times. [score:3]
To verify this hypothesis, we used qMSP analysis to detect the methylation level of hepatic miR-122, miR-125b and miR-106b. [score:1]
We attempted to elucidate the underlying mechanism of miR-125b and miR-106b involved in INH -induced liver injury. [score:1]
Agarose gel electrophoresis of the PCR products of gene promoter methylation of (b), miR-122, (e) miR-125b and (h) miR-106b. [score:1]
In this study, lower hepatic levels of miR-122, miR-125b and miR-106b are associated with INH -induced liver injury. [score:1]
In addition, hepatic miR-122, miR-125b and miR-106b methylation levels significantly increased at 7 days after INH administration. [score:1]
These results suggested that miR-122, miR-125b and miR-106b participated during the early phases of INH -induced liver injury. [score:1]
Previous studies have confirmed that miR-125b and miR-106b were two important indicators that reflect inflammatory response. [score:1]
edu/) was used to obtain a 2000 bp promoter sequence in the upstream of miR-122, miR-125b and miR-106b genes. [score:1]
Fig. 6MiR-122, miR-125b and miR-106b were epigenetically silenced in INH -induced liver injury. [score:1]
MiR-125b and MiR-106b regulated STAT3 in INH -induced liver injury. [score:1]
DNA methylation at particular CG dinucleotides within the miR-122 gene promoter (c), miR-125b gene promoter (f) and miR-106b gene promoter (i) in liver tissues from INH-administered rats was determined by qMSP. [score:1]
The time of significant changes and the changing trends of miR-125b and miR-106b were all consistent. [score:1]
Changes in miRNA profiles, including lower miR-122, miR-106b and miR-125b levels, have been reported in animal mo del studies on drug -induced liver injury. [score:1]
The CpG island methylation of miR-122, miR-125b and miR-106b was analysed using SYBR Green -based quantitative methylation-specific PCR (qMSP). [score:1]
Altogether, this discovery raised the question of whether miR-125b and miR-106b were related to the inflammatory immune response in INH -induced liver injury. [score:1]
miR-125b and miR-106b are two miRNAs identified to be associated with inflammation. [score:1]
Another inflammatory miR-106b has been shown to be associated with halothane -induced liver injury [14]. [score:1]
demonstrated that the methylation levels of miR-122, miR-125b and miR-106b in rat liver tissues treated with INH were significantly higher than those in the control group (Figs.   6c– i and see Additional file  6, p < 0.05 versus control). [score:1]
For the first time, we have detected the frequent methylation of miR-122, miR-125b and miR-106b. [score:1]
The analysis of the promoter region revealed that miR-122, miR-125b and miR-106b had CpG islands within the 2000 bp upstream of the transcriptional start site (Fig.   6a– e), providing the structural basis of DNA methylation. [score:1]
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2
[+] score: 138
The expression levels of RB1 and PTEN were downregulated following miR-106b and miR-93 transfection in both BRL and RH-35 cells, while the levels of CEBPA and KAT2B were downregulated after miR-25 transfection. [score:9]
The main findings of this study can be summarized as follows: 1) Despite the lack of marked DNA replication, 1/3 PH also caused widespread changes in miRNA expression, and the number of altered-miRNAs increased after 2/3 PH but decreased after 1/3 PH; 2) More than half of the altered miRNAs were shared between 1/3 and 2/3 PHand changed with similar regulatory direction; 3) The miR-106b~25 cluster is essential for liver regeneration after 2/3 PH and influences the cell cycle by targeting KAT2B and RB1. [score:7]
In details, miR-101a was down-regulated, and it decreased cell number in the G2-M phase with consistently increases in cell number in the G1 or S phases; meanwhile, miR-92a, miR-25, miR-93, and miR-106b were up-regulated, and they decreased the G1 cell population while concomitantly increasing the accumulation of cells in the S and G2 phases. [score:7]
As we expected, miR-106b, miR-93, miR-25 and miR-92a were significantly up-regulated at 24 and 36 hours after 2/3 PH, and miR-101a was down-regulated at 12, 24 and 36 hours after 2/3 PH (Supplementary Figure 5). [score:7]
This lack of significance may be explained by 2/3 PH itself triggering the upregulation of miR-106b~25, so that endogenously produced miR-106b~25 may mask the effect of exogenous miR-106b~25 overexpression. [score:6]
Based on our functional data for miR-106b, -93, and -25, which were associated with the cell cycle (Fig. 5), we searched in our target candidate list for targets involved in cell cycle regulation. [score:6]
RB1 was up-regulated by the spong for miR-106~25, and inhibited by miR-106~25. [score:6]
As a cluster, miR-106b~25 induces an epithelial-to-mesenchymal transition and a tumor-initiating cell phenotype in human breast cancer by targeting Smad7 26, and it increases the expression of Snail and enhances cell migration and invasion in non-small cell lung cancer 25. miR-106b~25 cluster is also essential for neovascularization after hindlimb ischaemia in mice 21. [score:5]
The miR-106b~25 cluster is reportedly overexpressed in human cancer, and it acts as an oncogene by targeting p21 and Bim 18 19. [score:5]
As shown in Fig. 8C, miR-106b and miR-93 expression significantly reduced the luciferase activities of RB1 reporters by 48% and 44%, respectively, and miR-25 reduced luciferase expression of KAT2B reporters by 41%. [score:5]
Thus, it is conceivable that up-regulation of the miR106b~25 cluster during PH is vital for the reentry of quiescent hepatocytes into the cell cycle for regrowth. [score:4]
We identified RB1 and KAT2B as novel targets of miR-106b/93 and miR-25, respectively. [score:3]
However, overexpression of the miR-106b~25 cluster revealed a trend toward acceleration of liver growth, despite not reaching statistical significance. [score:3]
Taken together, these results show that RB1 and KAT2B are targets of miR-106b/93 and miR-25, respectively. [score:3]
Furthermore, miR-106b~25 promotes liver regeneration after PH, stimulating the rapid S-phase entry of hepatocytes by targeting KAT2B and RB1. [score:3]
To assess whether the AAV9-miR-106b~25 sponge vectors were functional, we used an expression vector containing a gene encoding green fluorescent protein (GFP) with the miR-106b~25 sponge sequence added in the 3′ UTR of the gene encoding GFP (pAOV-GFP-sponges; Fig. 6D) and confirmed the effective binding of the miRNAs to the sponges. [score:3]
Gain- or loss-of function studies were performed in the rat liver using AAV9 vectors expressing the miR-106b~25 cluster or sponges for this cluster, respectively. [score:3]
In 293 T cells cotransfected with pAOV-GFP-sponges and pAOV-mCherry-cluster or pAOV-mCherry-control, the intensity of the GFP with the sponges decreased relative to the control with overexpression of the miR-106b~25 cluster (Fig. 6E). [score:3]
We found that miR-106~25 can affect the expression of Ccnb1 and Cdc25 at 24 hours after PH (Supplementary Figure 9). [score:3]
Notably, we did not find any spontaneous proliferation of hepatocytes in miR-106b~25 -overexpressing rats at 0 hours. [score:3]
Inhibition of miR-106b~25 hindered liver regrowth. [score:3]
The miR-106b~25 cluster and its targets. [score:3]
The expression of miR-106b~25 was analyzed in the livers of rats that were injected with miR-cluster using real time-PCR. [score:3]
Of them, PTEN was confirmed as a target of miR-93 and miR-106. [score:3]
The miR-106b~25 cluster vector (pAOV-mCherry-cluster, Fig. 6D) expressed mCherry, miR-25, miR-93 and miR-106b. [score:3]
Furthermore, we identified the targets of miR-106b~25, which contributed to the pro-cell cycle activity of hepatocytes. [score:3]
BRL cells transfected with a vector harboring the AAV9-miR-106b~25 cluster expressed more miR-25, miR-93, and miR-106b than cells transfected with the AAV9 cluster control vector, as assessed using real-time PCR (Fig. 6B). [score:3]
Ingenuity Pathway Analysis (IPA) analyses were performed to identify targets of the miR-106b~25 cluster using the microarray data for the total mRNA and for the miRNAs at 24 hours after PH. [score:3]
The sponges of miR-106b~25 were designed to generate transcripts with repeated miRNA antisense sequences that could sequester miRNAs from their endogenous targets. [score:3]
These results indicated that miR-106b~25 is involved in liver regeneration, which is consistent with results suggesting that members of the miR-106b~25 cluster induce hepatocytes to enter more rapidly into S phase. [score:1]
miR-106b~25 cluster association with liver regeneration after 2/3 PH. [score:1]
How to cite this article: Xu, X. et al. miRNA profiles in livers with different mass deficits after partial hepatectomy and miR-106b~25 cluster accelerating hepatocyte proliferation in rats. [score:1]
The miR-106b~25 cluster accelerates liver regeneration after PH. [score:1]
As demonstrated above, miR-92a, miR-25, miR-93, and miR-106b are associated with faster entry into the S and/or G2 phases. [score:1]
Our findings indicate that modulation of miR-106b~25 may represent a new therapeutic approach to treat liver failure caused by hepatocyte injury. [score:1]
In control rats, we found that miR-106b, miR-93, and miR-25 levels also increased after 2/3 PH (Supplementary Figure 6). [score:1]
AAV9-miR-106b~25 sponges are transcripts with 6 repeated miRNA antisense sequences of miR-25, miR-93 and miR-106b (Fig. 6C). [score:1]
We found that miR-106b, miR-93, and miR-25 levels remained higher after PH in the livers of rats injected with miR-cluster than in the livers of control rats; and miR-106b, miR-93 and miR-25 were significantly lower in the miR-sponge -treated rats than that in the controls, especially at 24h and 36 h after 2/3PH (Supplementary Figure 6). [score:1]
Next, 2 × 10 [12] viral particles of AAV9-miR-106b~25, AAV9-miR-sponge, and their controls were separately injected into rats via the tail vein (TV) (Fig. 7A), AAV9-miR-106b~25, AAV9-miR-sponge, and their controls are hereafter referred to as miR-cluster, miR-sponge, cluster-control and sponge-control, respectively. [score:1]
This allows us to find a specific subset of miRNAs that has not been previously identified, such as miR-106b~25 cluster. [score:1]
Interestingly, miR-25, miR-93, and miR-106b are members of the miR-106b~25 cluster located within about 0.5 kb on chromosome 12 (Fig. 6A). [score:1]
The sequences of the miR-106b~25 cluster and sponges were artificially synthesized. [score:1]
These findings led us to further pursue the role of the miR-106b~25 cluster in liver regeneration. [score:1]
Additionally, T. Bil plasma concentration at 96 hours after 2/3 PH was significantly higher in the miR-sponge group, reflecting loss of miR-106b~25 could delay recovery of liver function. [score:1]
Generation of the AAV9-miR-106b~25 cluster or sponge and verification. [score:1]
A total number of 11 and 16 miRNA–mRNA pairs were identified for miR-25 and miR-93 (miR-106b), respectively. [score:1]
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3
[+] score: 27
Using these hepatocyte and non-hepatocyte cell lines and primary tissues, we performed unsupervised clustering analysis by selecting 7 down-regulated miRNAs (miR-17-5p, miR-18a, miR-93, miR-106a, miR-106b, miR-130b and miR-375) and 4 up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182). [score:7]
Both up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182) and down-regulated miRNAs (miR-17-5p, miR-18a, miR-93, miR-106a, miR-106b, miR-130b and miR-375) were chosen as a parameter for comparison. [score:7]
Total RNA extracted from Dex/OSM treated AR42J-B13 cells (7 Days) and mock controls were used for Northern blot analysis using antisense probes against down-regulated miRNAs (miR-93, miR-106b and miR-130b) and up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182). [score:7]
Mature miRNA of miR-93, miR-106b, miR-130b, miR-21, miR-22 and miR-182 were differentially expressed after transdifferentiation. [score:3]
The pattern of coordinated reduction in expression of miR-25, miR-93, and miR-106b (Table 1) is due to the clustering of these three miRNA genes at intron 12 of Mcm7 on chromosome 12. [score:3]
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[+] score: 21
Other miRNAs from this paper: rno-mir-25, rno-mir-93
Brett J O et al. carried out an elaborate study of the role of miR-106b∼25 in adult NSCs and noted that miR-25 knockdown decreases NSC proliferation and that miR-25 overexpression increases adult NSC proliferation [9]. [score:4]
Moreover, injection of 1 nmol of Ant-25 or Scr did not alter expression of miR-106b and miR-93 (Figure 7B, C), whereas at the higher 4.0 nmol dose, all levels of miR-106b∼25 were significantly reduced (Figure 7B, C). [score:3]
Additionally, Brett et al. 's group reported that the miR-106b∼25 cluster could promote the proliferation of adult NSCs mainly due to miR-25 [9], [10], which also appeared to be one of the strongly expressed miRNAs in the post-ischemic brain [11]. [score:3]
Although the miR-25/p57 pathway was demonstrated to play a role in the therapeutic mechanisms of rTMS for focal cerebral ischemia in the present study, there may even be crosstalk between the different pathways that are focused on miR-25 or targeted by the other two members of the miR-106b∼25 cluster. [score:3]
In fact, miR-106b and miR-93 have the same seed sequence and similar 3′-halves, whereas miR-25-lacking the same sequence-is expected to have a separate function [12]. [score:1]
To verify their efficacies and specificities, the effects of Ant-25 and Scr on the levels of other members of the miR-106b∼25 cluster were also examined. [score:1]
This cluster is located within an intronic region of the Mcm7 gene and codes for three different mature miRNA species: miR-106b, miR-93 and miR-25. [score:1]
In addition, the current study also reveals an interesting effect of different doses of antagomir-25 and its scrambled antagomir on the miRNA levels of miR-25 and the unrelated miR-93 and miR-106b. [score:1]
Emerging data have indicated that the miR-106b∼25 cluster plays a critical role in adult NSC proliferation [7], [8]. [score:1]
MiR-25 belongs to the miR-106b∼25 cluster. [score:1]
Effects of Ant-25 and Scr on miR-106b∼25 in the ipsilateral cortex 7 days after surgery. [score:1]
0109267.g007 Figure 7(A– C) A) miR-93, B) miR-106b and C) miR-25 levels in the ischemic cortex after ICV injection of 1 nmol, 2.5 nmol and 4 nmol of Ant-25 or Scr. [score:1]
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5
[+] score: 19
As depicted in Fig 8, miR-1, miR-29a, miR-106b and miR-200a was selectively inhibited by H [2]0 [2] treated Pitx2 -overexpressing cells but up-regulated in H [2]0 [2] treated Pitx2 silenced cells at both time points (12h and 24h). [score:8]
qPCR of left atrial chambers demonstrated that miR-1, miR-26b, miR-29a, miR-30e, miR-106b, miR-133 and miR-200 are up-regulated in HTD rats as compared to controls (Fig 1), demonstrating a similar microRNA expression profile as in atrial-specific Pitx2 deficient mice [14, 16]. [score:5]
0188473.g008 Fig 8Analyses of Scn5a, Kcnj2 and Cacna1c (A), miR-1, miR-29a, miR-106b and miR-200b (B) expression in Pitx2 gain and loss-of-function experiments after H [2]0 [2] administration for 12h and 24h, respectively. [score:3]
Several lines of evidence have already reported the key regulatory role of miR-1 [60– 62], miR-26 [63], miR-106b [64], miR-133 [65– 66] and miR-200 [64] in arrhythmogenesis. [score:2]
Surprisingly none of the tested microRNAs, except for miR-26b and miR-106b, which in fact were decreased, display significant differences (Fig 2). [score:1]
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[+] score: 14
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
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[+] score: 12
We observed that changes in the expression of nine miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) analyzed by qRT-PCR were consistent with those by miRNA microarray at p < 0.05 (Figure 3). [score:3]
In agreement with our previous results we observed reduced expression of all three miRNAs (mir-106b, miR25 and miR-93) belonging to the miR-106b-25 cluster during conditions of UPR in H9c2 cells. [score:3]
The expression of miR-122, miR-93, miR-103, miR-107, miR-206, miR-143, miR-24, and miR-106b were reduced upon treatment with Tg and Tm in H9c2 cells. [score:3]
We found that expression of many miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) changed significantly during conditions of UPR in cardiomyoblasts. [score:3]
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[+] score: 10
miR-106b aberrantly expressed in a double transgenic mouse mo del for Alzheimer's disease targets TGF-beta type II receptor. [score:7]
Moreover, three miRNA (miRNA-7, miRNA-9, and miRNA-106b) were found to be associated with neurodegenerative diseases and only one, namely miRNA-9, with intellectual disability (Doxakis, 2010; Wang et al., 2010; Xu et al., 2011; Hu et al., 2017). [score:3]
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[+] score: 9
For example, miR-106b, miR-21, miR- 22, miR-19b and miR-25 are known to regulate PTEN and miR-27 and miR-139 repress FoxO1 translation through direct binding to the 3′-UTR [31], [32], [33], [34], [35], [36], [37], [38]. [score:5]
Among the up-regulated miRNAs, miR-106b, miR-25 and miR-19b share the same primary transcripts, and miR-24 and miR-27 share primary transcripts. [score:4]
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[+] score: 8
QRT-PCR confirmed the downregulation of the miR-17-5p seed family miRNAs (Figure 7b), along with C13orf25 and MCM7 (Figure 7c), the host genes for the miR-17~92 cluster and the miR-106b~25 cluster, respectively. [score:4]
To construct reporter vectors bearing the promoter regions containing the putative cis-acting elements for AP1 of miR-17~92, miR-106a~363, and miR-106b~25 cluster genes, we PCR synthesized (by Invitrogen) fragments of 800 bp upstream the transcription start sites of these genes. [score:1]
Effects of activating protein-1 (AP1) on transcriptional stimulation of the miR-17-5p seed miRNAs belonging to miR-17~92, miR-106a~363, and miR-106b~25 clusters in HEK293 cells. [score:1]
This cluster has two paralogs, miR-106a~363 (miR-106a, miR-18b, miR-19b-2, miR-20b, miR-92a-2 and miR-363, located on the X chromosome) and miR-106b~25 (miR-106b, miR-93, and miR-25, located on human chromosome 7), which are located on different chromosomes but contain individual miRNAs that are highly similar to those encoded by the miR-17~92 cluster [36, 37]. [score:1]
The miR-106b~25 cluster is located within the 13th intron of the MCM7 gene encoding DNA replication licensing factor. [score:1]
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[+] score: 7
The relative quantities of target miRNAs were normalized by using qubasePLUS software to the geometric means of miR-106b and let-7i which showed stable expression and thus meet the criteria of reference targets. [score:7]
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[+] score: 7
In agreement with Jess Morhayim, Sylvia Weilner and Cheng' studies[15, 27, 28], we showed miR-433-3p and miR-106b were up-regulated in OVX rat mo del. [score:4]
sham rat) Peers' studies hsa-miR-34a-3p 2.63 upUp, Jess Morhayim[15] hsa-miR-433-3p 1.24 up This study hsa-miR-106b 2.24 up This study hsa-miR-23a 0.48 downDown, Sylvia Weilner[27] hsa-miR-328-3p 0.38 down Down, Sylvia Weilner hsa-miR-29b-3p 2.1 up Up, Jess Morhayim hsa-miR-146a-5p 2.68 up Up, Jess Morhayim hsa-miR-148a-3p 1.85 upUp, Cheng[28] We noted that DKK1 played important role in the development of osteoporosis. [score:2]
We found miR-433-3p and miR-106b were not reported previously in OVX rat circulating serum. [score:1]
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[+] score: 6
ABCA1 is also targeted by miR-106b [56], which has been identified as another downregulated miRNA in FOH group in the present study. [score:6]
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[+] score: 6
While miR-199a, miR-376b-5p, miR-539 and miR-106 were all significantly upregulated (more than 3 times compared to the control), only miR-376b-5p and miR-539 were downregulated to the level similar to the control group after treatment with choline. [score:6]
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[+] score: 5
For instance, we observed a decrease in the levels of 5 miRNA with predicted target sites in the Foxa1 3′UTR (miR-106b, miR-194, miR-30c, miR-30b-5p and miR-20a) along with increased Foxa1 mRNA expression on methamphetamine exposure. [score:5]
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[+] score: 4
Nonetheless, the authors identified a pool of dysregulated miRNAs (∼50 miRNAs) in which some of them such as miR-144, miR-106b, miR-185, miR-30e, miR-589, miR-665 and many more showed similarities in expression as observed in our study (either humans/animals or both). [score:4]
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[+] score: 4
Maimaiti A Maimaiti A Yang Y Ma Y MiR-106b exhibits an anti-angiogenic function by inhibiting STAT3 expression in endothelial cellsLipids Health Dis. [score:4]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, within the differentially expressed pool of miRNAs, 10 were identified that are intimately involved in regulating intracellular trafficking pathways, including: miR-7b-5p, miR-9-5p, miR-31-5p, miR-92a-3p, miR-106-5p, miR-126-3p, miR-150-5p, miR-204-5p, miR-222-3p, and miR-322-5p (S2 Fig). [score:4]
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[+] score: 4
Ventral combined with dorsal root avulsion resulted in a sustained upregulation of 10 miRNAs, including miR-19b-3p, miR-20b-5p, miR-21-5p, miR-27a-3p, miR-29b-3p, miR-106b-3p, miR-142-3p, miR-322-5p, miR-352, and let-7a-5p (Figure  2E). [score:4]
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[+] score: 3
Also, Kim and colleagues identified miR-106b as a regulator of Aβ metabolism, increasing Aβ production and preventing its clearance. [score:2]
In this case, the rise in miR-106 observed for the BMFC +  KOC supplemented group does not appear to be desirable, but literature is scant and additional studies are indispensable. [score:1]
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[+] 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]
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[+] score: 2
Namely, pregnant rats fed SO and FO diets during the first 12 days of pregnancy showed significant lower expression of miR-449c-5p, miR-134–5p, miR-188, miR-32, miR130a, miR-144–3p, miR-431, miR-142–5p, miR-33, miR-340–5p, miR-301a, miR-30a, miR-106b, and miR-136–5p, as compared with OO, LO, and PO diets. [score:2]
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MiR-19b is a member of miR-19 family located in the miR-106–25 cluster, which has been reported to be involved in regulating NSC proliferation and differentiation through a network related to the insulin/IGF-FoxO pathway [37]. [score:2]
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On the other hand, other miRNAs such as, let-7i, miR-143, miR-148b-3p, miR-15b, miR-17-5p, miR-24, miR-27b, miR-92a, miR-106b, miR-125b-5p, miR-181a, miR-181c, miR-181d, miR-200c, miR-375, miR-107, miR-141, and miR-370, were present at higher levels in colostrum whey than in mature milk whey (Fig. 6). [score:1]
The results for miR-15b, miR-27b, and miR-106b are in accordance with those for bovine [4]. [score:1]
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[+] score: 1
Among the spleen-specific miRNAs identified, five of them belong to the mir17 miRNA cluster, which comprise miR-17, miR-18, miR-19a, miR-19b, miR-20, miR-25, miR-92, miR-93, miR-106a, and miR-106b [59]. [score:1]
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We began by measuring the levels of several miRNAs reportedly associated with cardiovascular diseases, including mir-129, mir-106, mir-26a, mir-20, mir-197, mir-17, mir-27 and mir-30d, 24, 25, 26, 27, 28, 29 in cardiomyocytes under both normal and high-glucose conditions. [score:1]
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