机构：[1]Emergency internal medicine, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, China[2]Department of emergency, First Affiliated Hospital of Zhongshan University, Guangzhou, Guangdong, 510080, China[3]The Second Department of hepatobiliary surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650032, China昆明医科大学附属第一医院[4]Translational medicine center, The First Affiliated Hospital of Zhongshan University, Guangzhou, Guangdong, 510080, China
Neural stem cells (NSCs) transplantation is one of the most promising strategies for the treatment of CA-induced brain damage. The transplanted NSCs could differentiate into new neuron and replace the damaged one. However, the poor survival of NSCs in severe hypoxic condition is the limiting step to make the best use of this kind of therapy. In the present study, we investigated whether the overexpression of miR-26a improves the survival of NSCs in hypoxic environment in vitro and in vivo. In vitro hypoxia injury model is established in NSCs by CoCl2 treatment, and in vivo cardiac arrest (CA) model is established in Sprague-Dawley (SD) rats. Quantitative real-time polymerase chain reaction is used to detect the mRNA level and Western blot is used to examine the protein level of indicated genes. TUNEL staining and flow cytometry are applied to evaluate apoptosis. Dual-luciferase reporter assay is utilized to analyze the target gene of miR-26a. The expression of miR-26a is reduced in both in vitro and in vivo hypoxic model. MiR-26a directly targets 3'-UTR of glycogen synthase kinase 3 beta (GSK-3 beta), resulting in increased beta-catenin expression and decreased apoptosis of NSCs. Overexpression of miR-26a in transplanted NSCs improves the survival of NSCs and neurological function in CA rats. MiR-26a prevents NSCs from apoptosis by activating beta-catenin signaling pathway in CA-induced brain damage model. Modulating miR-26a expression could be a potential strategy to attenuate brain damage induced by CA.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81372023]
第一作者机构：[1]Emergency internal medicine, Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, China
通讯作者：
通讯机构：[2]Department of emergency, First Affiliated Hospital of Zhongshan University, Guangzhou, Guangdong, 510080, China[4]Translational medicine center, The First Affiliated Hospital of Zhongshan University, Guangzhou, Guangdong, 510080, China[*1]Department of emergency, First Affiliated Hospital of Zhongshan University, Guangzhou, Guangdong, 510080, China[*2]Translational medicine center, The First Affiliated Hospital of Zhongshan University, Guangzhou, Guangdong, 510080, China.
推荐引用方式(GB/T 7714)：
Li Fang,Wei Hongyan,Li Hengjie,et al.miR-26a prevents neural stem cells from apoptosis via beta-catenin signaling pathway in cardiac arrest-induced brain damage[J].BIOSCIENCE REPORTS.2019,39:doi:10.1042/BSR20181635.
APA：
Li, Fang,Wei, Hongyan,Li, Hengjie,Li, Xin,Hu, Chunlin...&Liao, Xiaoxing.(2019).miR-26a prevents neural stem cells from apoptosis via beta-catenin signaling pathway in cardiac arrest-induced brain damage.BIOSCIENCE REPORTS,39,
MLA：
Li, Fang,et al."miR-26a prevents neural stem cells from apoptosis via beta-catenin signaling pathway in cardiac arrest-induced brain damage".BIOSCIENCE REPORTS 39.(2019)
