C2C12型
再生(生物学)
心肌细胞
微泡
巨噬细胞
细胞生物学
体内
骨骼肌
外体
生物
M2巨噬细胞
小RNA
癌症研究
肌发生
体外
解剖
生物化学
生物技术
基因
作者
Min Zhou,Bingshu Li,Cheng Liu,Ming Hu,Jianming Tang,Jie Min,Jianhong Cheng,Li Hong
标识
DOI:10.1016/j.intimp.2021.108223
摘要
Pubococcygeal muscle injury can lead to stress urinary incontinence (SUI). M2 macrophages play a crucial role in myoblast differentiation during injured muscle regeneration. However, the underlying mechanism remains unclear. Recently, exosomes have attracted increasing attention due to their mediation of cell-to-cell communication. In this study, we found that M2 macrophages extensively infiltrated the pubococcygeal muscle on day 5 after injury (VD5) in vivo. Then, C2C12 myoblasts were treated with M2 macrophage-derived exosomes (M2-EXO) and the results revealed that these exosomes could promote myotube formation. MiR-501 was identified as one of the abundant microRNAs (miRNAs) selectively loaded in M2-EXO, and subsequently confirmed to promote C2C12 myoblast differentiation by targeting YY1. Moreover, in vivo experiments showed that M2-EXO improves the inflammatory cell infiltration and have a therapeutic effect on damaged pubococcygeal muscle in SUI models. Collectively, our present results provide new insights into the promyogenic mechanism of M2 macrophages and prove that M2 macrophage exosomal miR-501 may represent a potential therapeutic to promote recovery from diseases caused by muscle injury, including SUI.
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