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miR-130b 通过靶向 Sp1 抑制心肌细胞增殖并促进分化。

miR-130b inhibits proliferation and promotes differentiation in myocytes via targeting Sp1.

机构信息

Shanghai Xuhui District Central Hospital, Zhongshan-Xuhui Hospital, Fudan University, Shanghai 200001, China.

CAS Key laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai 200031, China.

出版信息

J Mol Cell Biol. 2021 Sep 11;13(6):422-432. doi: 10.1093/jmcb/mjab012.

Abstract

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.

摘要

肌肉在损伤后或肌肉疾病期间的再生需要成肌细胞增殖和肌生成分化之间的精细合作。越来越多的证据表明,microRNAs 在肌细胞增殖和分化的转录中发挥关键作用。然而,协调的分子机制尚不完全清楚。在这里,我们表明 miR-130b 通过靶向 Sp1 转录因子能够抑制成肌细胞增殖并促进肌生成分化。重要的是,miR-130b 的过表达能够改善冷冻损伤模型中受损肌肉的恢复。此外,miR-130b 的表达在肌肉疾病患者的肌肉中下降。因此,这些结果表明 miR-130b 可能在骨骼肌再生和肌肉疾病进展中发挥作用。总之,我们的研究结果表明,miR-130b/Sp1 轴可能作为治疗肌肉损伤或严重肌肉疾病患者的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1921/8436675/9aec76c4dc63/mjab012f1.jpg

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