title: miR-210 over-expression enhances mesenchymal stem cell survival in an oxidative stress environment through antioxidation and c-Met pathway activation.
abstract: 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.
authors.affiliation: Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
authors.forename: JianFeng
authors.initials: J
authors.lastname: Xu
authors.forename: ZheYong
authors.initials: Z
authors.lastname: Huang
authors.forename: Li
authors.initials: L
authors.lastname: Lin
authors.forename: MingQiang
authors.initials: M
authors.lastname: Fu
authors.forename: YanHua
authors.initials: Y
authors.lastname: Gao
authors.forename: YunLi
authors.initials: Y
authors.lastname: Shen
authors.forename: YunZeng
authors.initials: Y
authors.lastname: Zou
authors.forename: AiJun
authors.initials: A
authors.lastname: Sun
authors.forename: JuYing
authors.initials: J
authors.lastname: Qian
authors.forename: JunBo
authors.initials: J
authors.lastname: Ge
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000737:chemistry*; D017209:Apoptosis; D001562:Benzimidazoles / Q000737:chemistry; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation; D002470:Cell Survival; D006861:Hydrogen Peroxide / Q000737:chemistry; D020287:In Situ Nick-End Labeling; D059630:Mesenchymal Stem Cells / Q000166:cytology*; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009206:Myocardium / Q000473:pathology; D018384:Oxidative Stress; D019859:Proto-Oncogene Proteins c-met / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species; D015398:Signal Transduction; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D001562:Benzimidazoles; C546388:MIRN210 microRNA, rat; D035683:MicroRNAs; D017382:Reactive Oxygen Species; D006861:Hydrogen Peroxide; D013482:Superoxide Dismutase; D019859:Proto-Oncogene Proteins c-met; C505410:Casp3 protein, rat; D053148:Caspase 3; C017807:bisbenzimide ethoxide trihydrochloride