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.

1

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.

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].

Recently, it has been shown that inhibition of miR-142-3p specifically resulted in abnormal cardiac development in developing zebrafish embryos [38].

We speculate that endogenous miR-142-3p could have other targets that may be involved in vascular development.

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.

The negative regulation of miR-142 by the oncogene lmo2 and its co-factors has also been documented in cell culture mo dels [32].

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.

The oncogene lmo2 has been previously shown to transcriptionally regulate both VE-Cadherin and miR-142 in human cell culture mo dels [32], [33].

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.

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.

2

Furthermore, the enforced expression of miR-142-3p, a uniquely expressed miRNA, causes a significant decrease in primitive erythrocyte progenitor cells and HSCs.

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.

To study the hematopoietic phenotype caused by increased miR-142-3p signaling, we overexpressed miR-142-3p using miR-142-3p duplex overexpression.

However, the scl expression was comparable to the control embryos, suggesting that miR-142-3p is not required for early hemangioblast formation.

We further confirmed that one of the uniquely expressed miRNAs, miR-142-3p, plays a critical role during erythrocyte progenitor cell and HSC formation.

Using O-dianisidine hemoglobin staining, a significant decrease of mature erythroid cells was detected when miR-142-3p was overexpressed.

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].

Overall, these data suggest that increased miR-142-3p represses primitive erythroid progenitor cell and HSC formation.

miR-142-3p is required for primitive erythroid progenitor cell and HSC formation.

Furthermore, all of the above hematopoietic phenotypes were alleviated by co-injection of miR-142-3p mimics and MO (data not shown).

3

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].

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].

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].

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.

In zebrafish, miR-142-3p modulates neutrophil development by controlling its maturation [24].

Notably, hematoxylin and eosin staining result revealed that the cellular density of neutrophils was decreased during the loss of miR-142.

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.

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].

MiR-142 is also an essential regulator of lymphocyte ontogenesis and megakaryopoiesis [20, 25].

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.

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).

In Xenopus, miR-142-3p has an essential role in establishing the mesodermal lineage that contributes to both HSC emergence and vasculogenesis [23].

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.

Dre-miR-142* showed significantly higher expression than its mature miRNA, which was not detected during development.

Similar results were observed before for dre-mir-129*, dre-mir-142a*, dre-mir-142b* and dre-mir-214* [20].

5

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).

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.

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.

6

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].

7

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.