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

• Published in: Science China. Life sciences 2014-10, Vol.57 (10), p.989-997
• Main Authors: Xu, JianFeng, Huang, ZheYong, Lin, Li, Fu, MingQiang, Gao, YanHua, Shen, YunLi, Zou, YunZeng, Sun, AiJun, Qian, JuYing, Ge, JunBo
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - chemistry; Apoptosis; Benzimidazoles - chemistry; Biomedical and Life Sciences; Caspase 3 - metabolism; Cell Proliferation; Cell Survival; Hydrogen Peroxide - chemistry; In Situ Nick-End Labeling; Life Sciences; Mesenchymal Stromal Cells - cytology; MicroRNAs - genetics; MicroRNAs - metabolism; Myocardium - pathology; Oxidative Stress; Proto-Oncogene Proteins c-met - metabolism; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Research Paper; Signal Transduction; Superoxide Dismutase - metabolism; 抗氧化; 氧化应激损伤; 活化; 环境; 细胞存活; 超氧化物歧化酶活性; 过表达; 间充质干细胞
• ISSN: 1674-7305; 1869-1889
• DOI: 10.1007/s11427-014-4725-z

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.