期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 13, 页码 -出版社
MDPI
DOI: 10.3390/ijms23137198
关键词
skeletal muscle; mice; AKT; mTOR; miR-29c; protein synthesis
资金
- Sao Paulo Research Foundation (FAPESP) [2015/04090-0, 2021/03066-9, 2017/09398-8, 2018/24419-4, 2019/08996-4, 2021/05827-7]
- National Council for Scientific and Technological Development (CNPq)
- DZHK partner site Heidelberg-Mannheim
miR-29c overexpression in skeletal muscle leads to hypertrophy and increased protein synthesis despite the downregulation of AKT/mTOR pathway components post-electrotransfer.
microRNAs negatively regulate gene expression by blocking translation or increasing mRNA degradation. In skeletal muscle, these molecules play important roles in adaptive responses, and ongoing investigations are necessary to understand the fine-tune regulation of skeletal muscle mass. Herein we showed that skeletal muscle overexpression of miR-29c increased fiber size and force at 7 and 30 days after electrotransfer. At both time points, AKT/mTOR pathway components were downregulated, and, surprisingly, overall protein synthesis was strongly elevated at day 7, which normalized by day 30 after pCMVmiR-29c electrotransfer. These results indicate that miR-29c expression induces skeletal muscle hypertrophy and gain of function, which involves increased overall protein synthesis in spite of the deactivation of the AKT/mTOR pathway.
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