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miR-130b inhibits proliferation and promotes differentiation in myocytes via targeting 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...

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Detalles Bibliográficos
Autores principales: Wang, Yu-Cheng, Yao, Xiaohan, Ma, Mei, Zhang, Huihui, Wang, Hui, Zhao, Lei, Liu, Shengnan, Sun, Chao, Li, Peng, Wu, Yuting, Li, Xihua, Jiang, Jingjing, Li, Yuying, Li, Yan, Ying, Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8436675/
https://www.ncbi.nlm.nih.gov/pubmed/33751053
http://dx.doi.org/10.1093/jmcb/mjab012
Descripción
Sumario: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.