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

作　　者：XU JianFeng HUANG ZheYong LIN Li FU MingQiang GAO YanHua SHEN YunLi ZOU YunZeng SUN AiJun QIAN JuYing GE JunBo 

机构地区：[1]Department of Cardiology, Zhongshan Hospital, Fudan University [2]Institutes of Biomedical Sciences, Fudan University [3]Department of Cardiology, Central Hospital of Minhang District

出　　处：《Science China(Life Sciences)》2014年第10期989-997,共9页中国科学（生命科学英文版）

基　　金：supported by the National Natural Science Foundation of China(81100145,81370003,81300082,81370322);the China Postdoctoral Science Foundation funded project(2013M531124,2014T70391);the Cardiovascular Research Fund supported by Chinese Association of Physicians(DFCMDA201259,DFCMDA201255);the Key Specialty Construction of Medical Program in Shanghai(ZK2012A24)

摘　　要：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.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.

关 键 词：microRNAs stem cells oxidative stress signal transduction 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]