miR-210 over-expression enhances mesenchymal stem cell survival in an oxidative stress environment through antioxidation and c-Met pathway activation

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• 作者：JianFeng Xu (1) (2) (3)
  ZheYong Huang (1)
  Li Lin (1)
  MingQiang Fu (1)
  YanHua Gao (1)
  YunLi Shen (1)
  YunZeng Zou (1) (2)
  AiJun Sun (1) (2)
  JuYing Qian (1)
  JunBo Ge (1) (2)
  
• 关键词：microRNAs ; stem cells ; oxidative stress ; signal transduction
• 刊名：Science China Life Sciences
• 出版年：2014
• 出版时间：October 2014
• 年：2014
• 卷：57
• 期：10
• 页码：989-997
• 全文大小：1,942 KB
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• 作者单位：JianFeng Xu (1) (2) (3)
  ZheYong Huang (1)
  Li Lin (1)
  MingQiang Fu (1)
  YanHua Gao (1)
  YunLi Shen (1)
  YunZeng Zou (1) (2)
  AiJun Sun (1) (2)
  JuYing Qian (1)
  JunBo Ge (1) (2)
  
  1. Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
  2. Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China
  3. Department of Cardiology, Central Hospital of Minhang District, Shanghai, 201199, China
  
• ISSN：1869-1889

文摘

microRNA-210 (miR-210) has generally been reported to be associated with cell survival under hypoxia. However, there are few data regarding the role of miR-210 in the survival of mesenchymal stem cells (MSCs) under oxidative stress conditions. Thus, we sought to investigate whether miR-210 over-expression could protect MSCs against oxidative stress injury and what the primary mechanisms involved are. The results showed that over-expression of miR-210 significantly reduced the apoptosis of MSCs under oxidative stress, accompanied by obvious increases in cell viability and superoxide dismutase activity and remarkable decreases in malonaldehyde content and reactive oxygen species production, resulting in a noticeable reduction of apoptotic indices when compared with the control. Moreover, the above beneficial effects of miR-210 could be significantly reduced by c-Met pathway repression. Collectively, these results showed that miR-210 over-expression improved MSC survival under oxidative stress through antioxidation and c-Met pathway activation, indicating the potential development of a novel approach to enhance the efficacy of MSC-based therapy for injured myocardium.