3 publications mentioning oar-mir-411b

Open access articles that are associated with the species Ovis aries and mention the gene name mir-411b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1

To reveal the role of these miRNAs in the muscular phenotype of myostatin knockout mice, we quantified their expression by qRT-PCR, and observed a significant increase in the expression of miR-411, miR-434-3p, miR-379, and miR-193b in myostatin knockout mice (Figure 1A).

Among these, the increased expressions of miR-411, miR-434-3p, and miR-379 were of interest because these miRNAs are expressed from the mouse chromosome 12qF1 (chr12qF1), called as the Dlk1-Dio3 locus (Figure 1B).

Quantitative RT-PCR showing the decreased expression of miR-411 (A) miR-540-3p (B) pri-miR-411 (C) and Gtl2 (D) in both wild-type and myostatin knockout mice with age.

Figure 5Quantitative RT-PCR showing the decreased expression of miR-411 (A) miR-540-3p (B) pri-miR-411 (C) and Gtl2 (D) in both wild-type and myostatin knockout mice with age.

However, the expression of the remaining 9 miRNAs (miR-411, miR-434-3p, miR-299*, miR-193, miR-146b, miR-379, miR-193b, miR-22, and miR-223) has not been verified.

Immunofluorescence staining of myotubes with an antibody specific to the myosin heavy chain, which is a terminally differentiated marker of skeletal muscle cells, demonstrated that overexpression of miR-411 and miR-540-3p significantly increased the C2C12 myotube diameter (miR-411; 100 ± 4.89 vs.

The expression level of pri-miR-411 also tended to increase (Figure 4A).

To determine whether myostatin deficiency activates the transcription of chr12qF1 miRNAs, we further quantified the expression levels of the primary transcripts of miR-127 (pri-miR-127) and miR-411 (pri-miR-411) by qRT-PCR.

Figure 1(A) A significant increase in miR-411, miR-434-3p, miR-379, and miR-193b expression in myostatin -deficient skeletal muscle at 13 weeks of age was determined by quantitative RT-PCR.

Although we demonstrated the potency of the Dlk1-Dio3 locus derived miRNAs (miR-411 and miR-540-3p) to induce myotube hypertrophy using an in vitro mo del, muscular hypertrophy phenotype observed in the callipyge mutation and myostatin deficiency would be caused by slightly different mechanism.

Myotubes were transfected with miR-411, miR-434-5p, and miR-540-3p mimics and immunostained with an anti-myosin heavy chain antibody and DAPI.

Transfection of miR-411 and miR-540-3p mimics, but not other miRNAs, significantly increased the myotube diameter.

miR-411 and miR-540-3p increase the C2C12 myotube diameters.

2

For example, the differentially expressed miRNA in the infarcted area was oar-miR-19b; the differentially expressed miRNAs in the infarct boundary area included downregulated oar-miR411b-5p, oar-miR-487a-5p, and upregulated oar-miR-26a.

Compared with control group, the differentially expressed miRNA in Infarct Zone was oar-miR-19b in the unloading group, while there were three differentially expressed miRNA in Infarct Border Zone (Figures 4(f), 4(g), and 4(h)) including downregulated oar-miR411b-5p and oar-miR-487a-5p and upregulated oar-miR-26a.

The results were consistent with the microarray, while the expression of oar-miR411b-5p and oar-miR-487a-5p showed no significant difference.

The RT-PCR was used for verification of the differentially expressed miRNAs including oar-miR-19b, oar-miR-26a, oar-miR411b-5p, and oar-miR-487a-5p, which were screened by microarray.

3

For example, both the sequencing data and the qRT-PCR results showed that oar-miR-411b-3p was expressed at a lower level in underfed males than in well-fed males (Fig. S2).