肠道病毒71型以依赖Bax的方式诱导细胞凋亡。
[Enterovirus 71 induces apoptosis in a Bax dependent manner].
作者信息
Sun Zhen-min, Xiao Yan, Ren Li-li, Lei Xiao-bo, Wang Jian-wei
机构信息
State Key Laboratory of Molecular Virology and Genetic Engineering, Institute of Pathogen Biology, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100730, China
出版信息
Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2011 Feb;25(1):49-52.
OBJECTIVE
To explore the molecular mechanism of apoptosis induced by enterovirus 71 (EV71) infection.
METHODS
The effects of EV71 on Rhabdomyosarcoma (RD) cell viability were detected by CCK8 assay. EV71-induced apoptosis on RD cells were detected by Hoechst 33342 staining and Western blot targeting Caspase 3, 8 and PARP. Bax conformational change was detected by immunoprecipitation with Bax 6A7 antibody.
RESULTS
EV71 decreased the viability of RD cells and induces the activation of Caspase 3, 8 and PARP. Bax expression increases in RD cells after EV71 infection, and Bax conformational change also can be detected after EV71 infection.
CONCLUSION
Our study reveals that EV71 induces Caspase-dependent apoptosis by Bax conformational change.
目的
探讨肠道病毒71型（EV71）感染诱导细胞凋亡的分子机制。
方法
采用CCK8法检测EV71对横纹肌肉瘤（RD）细胞活力的影响。通过Hoechst 33342染色以及针对半胱天冬酶3、8和聚（ADP-核糖）聚合酶（PARP）的蛋白质印迹法检测EV71诱导的RD细胞凋亡。用Bax 6A7抗体进行免疫沉淀检测Bax构象变化。
结果
EV71降低了RD细胞的活力，并诱导半胱天冬酶3、8和PARP的激活。EV71感染后RD细胞中Bax表达增加，且EV71感染后也能检测到Bax构象变化。
结论
我们的研究表明，EV71通过Bax构象变化诱导半胱天冬酶依赖性细胞凋亡。
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