Autor: |
Xinyi Gu, Shen Wang, Dongdong Li, Bo Jin, Zhidan Qi, Jin Deng, Chen Huang, Xiaofeng Yin |
Jazyk: |
angličtina |
Rok vydání: |
2023 |
Předmět: |
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Zdroj: |
Molecular Therapy: Nucleic Acids, Vol 33, Iss , Pp 191-204 (2023) |
Druh dokumentu: |
article |
ISSN: |
2162-2531 |
DOI: |
10.1016/j.omtn.2023.05.023 |
Popis: |
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. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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