Murine miR-483-3p promotes proliferation and suppresses differentiation of C2C12 cells by targeting SRF
- Published
- Accepted
- Subject Areas
- Agricultural Science, Biochemistry, Cell Biology
- Keywords
- Mmu-miR-483-3p, C2C12, SRF, proliferation, differentiation
- Copyright
- © 2017 Huang et al.
- Licence
- This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ Preprints) and either DOI or URL of the article must be cited.
- Cite this article
- 2017. Murine miR-483-3p promotes proliferation and suppresses differentiation of C2C12 cells by targeting SRF. PeerJ Preprints 5:e3454v1 https://doi.org/10.7287/peerj.preprints.3454v1
Abstract
Myogenesis is a complicated process, which is regulated by numerous regulators. MicroRNAs (miRNAs) are conserved non-coding RNAs of ~22 nucleotides, which regulate post-transcriptional gene expression in many physiological and pathophysiological processes. Recent studies have indicated that microRNAs are critical regulators of muscle development. Here, we report miR-483-3p as a new essential regulator of muscle development, mediating myoblast proliferation and myogenic differentiation. miR-483-3p is strongly and almost exclusively expressed in muscle-related tissues such as leg muscle, back muscle, and heart. Its expression is downregulated during mouse development. Overexpression of miR-483-3p in C2C12 cells promotes proliferation and suppresses myogenic differentiation. A dual-luciferase reporter assay demonstrated miR-483-3p direct targets to the 3′-UTR of the SRF gene. Overexpression of miR-483-3p reduced SRF protein levels in C2C12 myoblasts. These results reveal a novel function of miR-483-3p as a positive regulator of C2C12 proliferation and inhibitor of myogenic differentiation via SRF downregulation.
Author Comment
This is a preprint submission to PeerJ Preprints.