基因敲除
骨骼肌
肌肉萎缩
C2C12型
心肌细胞
下调和上调
萎缩
小RNA
生物
细胞生物学
癌症研究
内科学
医学
内分泌学
肌发生
基因
遗传学
作者
Xinyi Gu,Shen Wang,Dongdong Li,Bo Jin,Zhidan Qi,Jin Deng,Chen Huang,Xiaofeng Yin
标识
DOI:10.1016/j.omtn.2023.05.023
摘要
Peripheral nerve injury can lead to progressive muscle atrophy and poor motor function recovery, which is a difficult point of treatment, and the mechanism needs to be further explored. In previous studies, we found that miR-142a-3p was significantly upregulated and persistently highly expressed in denervated mouse skeletal muscle. Here, we show that overexpression of miR-142a-3p inhibited the growth and differentiation of C2C12 myoblast, while knockdown of miR-142a-3p had a promoting effect. In vitro, knockdown of miR-142a-3p in denervated mouse skeletal muscle effectively increased proliferating muscle satellite cells and ameliorated muscle atrophy. Mechanistically, the myoregulator Mef2a was proved to be an important downstream target of miR-142a-3p, and miR-142a-3p regulates skeletal muscle differentiation and regeneration by inhibiting the expression of Mef2a. The co-knockdown of Mef2a and miR-142a-3p effectively alleviated or offset the biological effects of miR-142a-3p knockdown. In conclusion, our data revealed that miR-142a-3p regulates neurogenic skeletal muscle atrophy by targeting Mef2a.
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