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Neuroprotective effects of Activin A on endoplasmic reticulum stress-mediated apoptotic and autophagic PC12 cell death.

Authors
  • Xue, Long-Xing1
  • Liu, Hong-Yu1
  • Cui, Yang1
  • Dong, Yue1
  • Wang, Jiao-Qi1
  • Ji, Qiu-Ye2
  • He, Jin-Ting1
  • Yao, Min1
  • Wang, Ying-Ying1
  • Shao, Yan-Kun1
  • Mang, Jing1
  • Xu, Zhong-Xin1
  • 1 Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun, Jilin Province, China. , (China)
  • 2 Research Center, China-Japan Union Hospital, Jilin University, Changchun, Jilin Province, China. , (China)
Type
Published Article
Journal
Neural Regeneration Research
Publisher
Medknow Publications
Publication Date
May 01, 2017
Volume
12
Issue
5
Pages
779–786
Identifiers
DOI: 10.4103/1673-5374.206649
PMID: 28616035
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Activin A, a member of the transforming growth factor-beta superfamily, plays a neuroprotective role in multiple neurological diseases. Endoplasmic reticulum (ER) stress-mediated apoptotic and autophagic cell death is implicated in a wide range of diseases, including cerebral ischemia and neurodegenerative diseases. Thapsigargin was used to induce PC12 cell death, and Activin A was used for intervention. Our results showed that Activin A significantly inhibited morphological changes in thapsigargin-induced apoptotic cells, and the expression of apoptosis-associated proteins [cleaved-caspase-12, C/EBP homologous protein (CHOP) and cleaved-caspase-3] and biomarkers of autophagy (Beclin-1 and light chain 3), and downregulated the expression of thapsigargin-induced ER stress-associated proteins [inositol requiring enzyme-1 (IRE1), tumor necrosis factor receptor-associated factor 2 (TRAF2), apoptosis signal-regulating kinase 1 (ASK1), c-Jun N-terminal kinase (JNK) and p38]. The inhibition of thapsigargin-induced cell death was concentration-dependent. These findings suggest that administration of Activin A protects PC12 cells against ER stress-mediated apoptotic and autophagic cell death by inhibiting the activation of the IRE1-TRAF2-ASK1-JNK/p38 cascade.

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