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 oxidativ...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.展开更多
基金supported by the National Natural Science Foundation of China(81100145,81370003,81300082,81370322)the China Postdoctoral Science Foundation funded project(2013M531124,2014T70391)+1 种基金the Cardiovascular Research Fund supported by Chinese Association of Physicians(DFCMDA201259,DFCMDA201255)the Key Specialty Construction of Medical Program in Shanghai(ZK2012A24)
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.
