中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (17): 1331-1337.

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

Low levels of Bax inhibitor-1 gene expression increase tunicamycin-induced apoptosis in human neuroblastoma SY5Y cells

  

  • 收稿日期:2012-02-22 修回日期:2012-05-03 出版日期:2012-06-15 发布日期:2012-06-15

Low levels of Bax inhibitor-1 gene expression increase tunicamycin-induced apoptosis in human neuroblastoma SY5Y cells

Dan Wu1, Peirong Wang1, 2, Shiyao Wang1   

  1. 1  Department of Medical Genetics, School of Basic Medical Sciences, Peking University, Beijing 100191, China
    2  Institute of Biophysics, Chinese Academy of Sciences, Beijing 100190, China
  • Received:2012-02-22 Revised:2012-05-03 Online:2012-06-15 Published:2012-06-15
  • Contact: Dan Wu, Department of Medical Genetics, School of Basic Medical Sciences, Peking University, Beijing 100191, China danw@bjmu.edu.cn
  • About author:Dan Wu☆, Ph.D., Department of Medical Genetics, School of Basic Medical Sciences, Peking University, Beijing 100191, China Corresponding author: Dan Wu, Department of Medical Genetics, School of Basic Medical Sciences, Peking University, Beijing 100191, China danw@bjmu.edu.cn

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Abstract:

A human SH-SY5Y neuroblastoma cell line with a low level of Bax inhibitor-1 expression was established by lentivirus-mediated RNA interference and fluorescence-activated cell sorting. In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment. In addition, chromatin condensation and apparent apoptotic phenomena, such as marginalization and cytoplasmic vesicles, were observed. Our findings indicate that Bax inhibitor-1 can delay apoptosis induced by endoplasmic reticulum stress.

Key words: Bax inhibitor-1, RNA interference, SH-SY5Y, endoplasmic reticulum stress, tunicamycin, apoptosis, neural regeneration