Activin A prevents neuron-like PC12 cell apoptosis after oxygen-glucose deprivation

作     者：Guihua Xu Jinting He Hongliang Guo Chunli Mei Jiaoqi Wang Zhongshu Li Han Chen Jing Mang Hong Yang Zhongxin Xu 

作者机构：Department of Neurology China-Japan Union Hospital Jilin University Department of Neurology Changchun Central Hospital 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2013年第8卷第11期

页      面：1016-1024页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：supported by the Natural Science Foundation of Jilin Province, China, No. 201015181 Jilin Province Science and Technology Development Projects, No.20120723 

主　　题：neural regeneration brain injury biological factor oxygen-glucose deprivation Activin A ActivinA/Smads signaling pathway caspase-3 apoptosis grants-supported paper neuroregeneration 

摘      要：In this study, PC12 cells were induced to differentiate into neuron-like cells using nerve growth factor, and were subjected to oxygen-glucose deprivation. Cells were treated with 0, 10, 20, 30, 50, 100 ng/mL exogenous Activin A. The 3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl tetrazolium bromide assay and Hoechst 33324 staining showed that the survival percentage of PC12 cells significantly decreased and the rate of apoptosis significantly increased after oxygen-glucose deprivation. Exogenous Activin A significantly increased the survival percentage of PC12 cells in a dose-dependent manner. Reverse transcription-PCR results revealed a significant increase in Activin receptor IIA, Smad3 and Smad4 mRNA levels, which are key sites in the Activin A/Smads signaling pathway, in neuron-like cells subjected to oxygen-glucose deprivation, while mRNA expression of the apoptosis-regulation gene caspase-3 decreased. Our experimental findings indicate that exogenous Activin A plays an anti-apoptotic role and protects neurons by means of activating the Activin A/Smads signaling pathway.