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

作　　者：Dan Wu Peirong Wang Shiyao Wang 

机构地区：[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

出　　处：《Neural Regeneration Research》2012年第17期1331-1337,共7页中国神经再生研究（英文版）

基　　金：supported by the National Natural Science Foundation of China,No. 30900802;the Research Fund for the Doctoral Program of Higher Education,No. 20070001801;the Leading Academic Discipline Project of Beijing Education Bureau;the Fund for Fostering Talents in Basic Science of the National Natural Science Foundation of China,No. J0630853/J0108

摘　　要：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.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.

关 键 词：Bax inhibitor-1 RNA interference SH-SY5Y endoplasmic reticulum stress TUNICAMYCIN apoptosis neural regeneration 

分 类 号：Q255[生物学—细胞生物学] S858[农业科学—临床兽医学]