Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (11): 1016-1024.doi: 10.3969/j.issn.1673-5374.2013.11.007

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

Guihua Xu1, 2, Jinting He1, Hongliang Guo1, Chunli Mei1, Jiaoqi Wang1, Zhongshu Li1, Han Chen1, Jing Mang1, Hong Yang1, Zhongxin Xu1   

  1. 1 Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin Province, China
    2 Department of Neurology, Changchun Central Hospital, Changchun 130051, Jilin Province, China
  • Received:2012-12-15 Revised:2013-03-14 Online:2013-04-15 Published:2013-04-15
  • Contact: Zhongxin Xu, Ph.D., Professor, Doctoral supervisor, Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130031, Jilin Province, China, xuzhongxin999@ yahoo.com.cn. Jing Mang, Ph.D., Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun 130031, Jilin Province, China, mangjing@jlu.edu.cn.
  • About author:Guihua Xu☆, Studying for doctorate.

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Abstract:

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.

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