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miR-130b inhibits proliferation and promotes differentiation in myocytes via targeting Sp1
Yu-Cheng Wang1,† , Xiaohan Yao2,† , Mei Ma2 , Huihui Zhang2 , Hui Wang2 , Lei Zhao3 , Shengnan Liu2 , Chao Sun2 , Peng Li2 , Yuting Wu2 , Xihua Li3 , Jingjing Jiang4 , Yuying Li2 , Yan Li5,* , Hao Ying2,6,*
1Shanghai Xuhui District Central Hospital, Zhongshan-Xuhui Hospital, Fudan University, Shanghai 200001, China
2CAS Key laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai 200031, China
3Department of Neuromuscular Disease, Children’s Hospital of Fudan University, Shanghai 201102, China
4Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai 200031, China
5State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China
6Key Laboratory of Food Safety Risk Assessment, Ministry of Health, Beijing 100021, China
These authors contributed equally to this work.
*Correspondence to:Yan Li , Email:liyan0520@jiangnan.edu.cn Hao Ying , Email:yinghao@sibs.ac.cn
J Mol Cell Biol, Volume 13, Issue 6, June 2021, Pages 422-432  https://doi.org/10.1093/jmcb/mjab012
Keyword: miR-130b, muscle regeneration, proliferation, differentiation, Sp1

Muscle regeneration after damage or during myopathies requires a fine cooperation between myoblast proliferation and myogenic differentiation. A growing body of evidence suggests that microRNAs play critical roles in myocyte proliferation and differentiation transcriptionally. However, the molecular mechanisms underlying the orchestration are not fully understood. Here, we showed that miR-130b is able to repress myoblast proliferation and promote myogenic differentiation via targeting Sp1 transcription factor. Importantly, overexpression of miR-130b is capable of improving the recovery of damaged muscle in a freeze injury model. Moreover, miR-130b expression is declined in the muscle of muscular dystrophy patients. Thus, these results indicated that miR-130b may play a role in skeletal muscle regeneration and myopathy progression. Together, our findings suggest that the miR-130b/Sp1 axis may serve as a potential therapeutic target for the treatment of patients with muscle damage or severe myopathies.