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7 publications mentioning dre-mir-142b

Open access articles that are associated with the species Danio rerio and mention the gene name mir-142b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 30
So we hypothesized that, if lmo2 gene regulates expression of cdh5/miR-142 transcriptionally and miR-142a-3p regulates cdh5 gene post-transcriptionally, then lmo2, cdh5 and miR-142a-3p may be part of an interacting network that could regulate angiogenesis and vasculature remo deling in zebrafish embryos. [score:6]
Studies conducted on human cancers by other groups from have indicated that LMO2, a transcription factor expressed in blood and vasculature acts as a transcriptional suppressor of miR-142 [32]. [score:5]
Recently, it has been shown that inhibition of miR-142-3p specifically resulted in abnormal cardiac development in developing zebrafish embryos [38]. [score:4]
We speculate that endogenous miR-142-3p could have other targets that may be involved in vascular development. [score:4]
Taken together we speculate that lmo2, in addition to its known role as a transcriptional regulator of CDH5 and miR-142, may also regulates cdh5 post-transcriptionally through miR-142a-3p in zebrafish embryos. [score:3]
The negative regulation of miR-142 by the oncogene lmo2 and its co-factors has also been documented in cell culture mo dels [32]. [score:2]
Based on our study, we suggest a potential new function of miR-142-3p in regulating the levels of cdh5 required for normal angiogenesis and vascular remo deling in zebrafish embryos. [score:2]
The oncogene lmo2 has been previously shown to transcriptionally regulate both VE-Cadherin and miR-142 in human cell culture mo dels [32], [33]. [score:2]
To rule out the possibility of non-specific effect generated by the action of any one of single strand of the miRNA we also conducted separate microinjections of the sense and antisense strand of miR-142-3p. [score:1]
B – Synteny analysis of human miR-142 on chromosome 17 with zebrafish miR-142a on chromosome 5. Arrow in genes indicates strand information on chromosome. [score:1]
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[+] score: 30
Furthermore, the enforced expression of miR-142-3p, a uniquely expressed miRNA, causes a significant decrease in primitive erythrocyte progenitor cells and HSCs. [score:5]
Interestingly, the gata1, cmyb and runx1 expression were all markedly decreased when miR-142-3p was ectopically expressed (Figure 7), indicating that miR-142-3p affects HSC formation in zebrafish. [score:5]
To study the hematopoietic phenotype caused by increased miR-142-3p signaling, we overexpressed miR-142-3p using miR-142-3p duplex overexpression. [score:5]
However, the scl expression was comparable to the control embryos, suggesting that miR-142-3p is not required for early hemangioblast formation. [score:3]
We further confirmed that one of the uniquely expressed miRNAs, miR-142-3p, plays a critical role during erythrocyte progenitor cell and HSC formation. [score:3]
Using O-dianisidine hemoglobin staining, a significant decrease of mature erythroid cells was detected when miR-142-3p was overexpressed. [score:3]
In addition, several hematopoietic miRNA signatures are uniquely expressed in RPS24 MO such as miR-142-3p and miR-29a, which have been previously reported to be required for the formation and differentiation of hematopoietic stem cells [19, 20]. [score:3]
Overall, these data suggest that increased miR-142-3p represses primitive erythroid progenitor cell and HSC formation. [score:1]
miR-142-3p is required for primitive erythroid progenitor cell and HSC formation. [score:1]
Furthermore, all of the above hematopoietic phenotypes were alleviated by co-injection of miR-142-3p mimics and MO (data not shown). [score:1]
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[+] score: 22
It was reported that ectopic expression of the miR-142-3p duplex (concentration of 20 μmol l [−1]) suppresses the primitive erythrocyte progenitors (gata1 [+]) and HSC formation (cmyb [+]) [27]. [score:5]
Recently, by targeting two miR-142 genes including miR-142a and miR-142b, the mutants of miR-142 by zinc-finger nucleases (ZFN) method are generated, and these miR-142-3p mutants display neutrophil defects but with relatively normal HSPCs [24]. [score:3]
Another group has reported that ectopic expression of miR-142-3p leads to the reduction of primitive erythrocyte progenitor cells and HSCs in zebrafish [27]. [score:3]
Although developmental defects in HSPCs were not examined in miR-142 [−/−] mice, we speculate that a similar HSPC phenotype would be expected at the onset of definitive hematopoiesis. [score:2]
In zebrafish, miR-142-3p modulates neutrophil development by controlling its maturation [24]. [score:2]
Notably, hematoxylin and eosin staining result revealed that the cellular density of neutrophils was decreased during the loss of miR-142. [score:1]
Whole-mount in situ hybridization (WISH) result demonstrated that miR-142-3p was absent in both the thymus and caudal hematopoietic tissue region in 142 [C−/−] embryos (Supplementary Figure S1e), suggesting a loss-of-function of miR-142a-3p. [score:1]
In vitro, mouse fibroblasts were reprogrammed into hemogenic endothelial cells that differentiated into CD45 [+] cKit [+] cells (HSPCs) between day-20 and day-35 culture; in these HSPCs, the highest enrichment of microRNAs including miR-142 was observed [22]. [score:1]
MiR-142 is also an essential regulator of lymphocyte ontogenesis and megakaryopoiesis [20, 25]. [score:1]
On the basis of the deficiency of miR -142a and miR-142b genes, there is a possibility that the reported neutrophil hypermaturation in miR-142a/b mutants might be due to the deletion of miR-142b. [score:1]
Wild-type or mutated pGL3- p53 CDS co -transfected with negative control or the miR-142-3p duplex (Invitrogen, Shanghai, China) were transfected into HEK293T cells using Lipofectamine2000 (Invitrogen). [score:1]
In Xenopus, miR-142-3p has an essential role in establishing the mesodermal lineage that contributes to both HSC emergence and vasculogenesis [23]. [score:1]
[1 to 20 of 12 sentences]
[+] score: 11
Other miRNAs from this paper: dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-210, dre-mir-214, dre-mir-219-1, dre-mir-219-2, dre-mir-221, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-21-1, dre-mir-21-2, dre-mir-25, dre-mir-30e-2, dre-mir-101a, dre-mir-103, dre-mir-107a, dre-mir-122, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-126a, dre-mir-129-2, dre-mir-129-1, dre-mir-130b, dre-mir-130c-1, dre-mir-130c-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-135c-1, dre-mir-135c-2, dre-mir-140, dre-mir-142a, dre-mir-150, dre-mir-152, dre-mir-462, dre-mir-196a-2, dre-mir-196b, dre-mir-202, dre-mir-203b, dre-mir-219-3, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-mir-455-1, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-135b, dre-mir-135a, dre-mir-499, dre-mir-738, dre-mir-429b, dre-mir-1788, dre-mir-196c, dre-mir-107b, dre-mir-455-2, dre-mir-222b, dre-mir-126b, dre-mir-196d, dre-mir-129-3, dre-mir-129-4
Quantification of miRNA and miRNA* expression by qRT-PCR (Figure 5C) confirmed the higher relative abundance of miR-140* and miR-142a* and showed that dre-miR-142* was expressed during development while its mature miRNA was not detected. [score:6]
Dre-miR-142* showed significantly higher expression than its mature miRNA, which was not detected during development. [score:4]
Similar results were observed before for dre-mir-129*, dre-mir-142a*, dre-mir-142b* and dre-mir-214* [20]. [score:1]
[1 to 20 of 3 sentences]
[+] score: 9
Totally, the final results included 9 downregulated miRNAs (dre-miR-142a-3p, dre-miR-142b-5p, dre-miR-144-3p, dre-miR-146a, dre-miR-190a, dre-miR-219-5p, dre-miR-301b-3p, dre-miR-459-5p and rno-miR-33-5p) and 3 upregulated miRNAs (dre-miR-735-3p, dre-miR-735-5p and mmu-miR-6240). [score:7]
0169599.g003 Fig 3 The asterisk indicated only for dre-miR-142b-5p in low concentration BDE47 treatment, the result of statistical significance by RT-PCR determination was inconsistent with miRNA sequencing. [score:1]
The asterisk indicated only for dre-miR-142b-5p in low concentration BDE47 treatment, the result of statistical significance by RT-PCR determination was inconsistent with miRNA sequencing. [score:1]
[1 to 20 of 3 sentences]
[+] score: 3
Additionally, several miRNAs are known to regulate cardiogenesis 4– 7. For example, during the early stages of mesoderm formation, miR-142-3p plays a crucial regulatory role in cardiogenesis, hematopoiesis and somitogenesis [6]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 1
Other miRNAs from this paper: dre-mir-142a
Nishiyama T. Kaneda R. Ono T. Tohyama S. Hashimoto H. Endo J. Tsuruta H. Yuasa S. Ieda M. Makino S. miR-142–3p is essential for hematopoiesis and affects cardiac cell fate in zebrafish Biochem. [score:1]
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