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腺病毒介导AMP激活的蛋白激酶的过表达诱导肝星状细胞株LX2凋亡
引用本文:张婧,谭丽,林骏,徐爱民,罗深秋. 腺病毒介导AMP激活的蛋白激酶的过表达诱导肝星状细胞株LX2凋亡[J]. 南方医科大学学报, 2007, 27(6): 821-823
作者姓名:张婧  谭丽  林骏  徐爱民  罗深秋
作者单位:南方医科大学细胞生物教研室,广东,广州,510515;香港大学医学院
摘    要:目的 探讨在肝星状细胞株LX2中,用腺病毒介导AMP激活的蛋白激酶(AMPK)过表达对细胞凋亡的影响.方法 病毒感染细胞后,用免疫印记的方法检测外源基因的表达;流式细胞仪分析细胞的凋亡;琼脂糖凝胶电泳检测DNA梯状条带,免疫印迹检测caspase-3以及Bcl-2、Bax表达的变化.结果 免疫印迹结果显示表达组成性激活的AMPK的腺病毒感染LX2细胞72 h,AMPK过表达.过表达AMPK的LX2细胞用流式细胞仪检测到有凋亡的亚二倍体峰出现;DNA断裂出现梯状条带,casepase-3被激活,Bcl-2在LX2中是低表达的,而Bax表达水平升高.结论 腺病毒介导AMPK的过表达可以诱导LX2细胞发生凋亡,其可能的机制之一是上调促凋亡基因bax的表达.

关 键 词:肝纤维化  肝星状细胞  腺病毒  凋亡
文章编号:1673-4254(2007)06-0821-03

Adenovirus-mediated overexpression of AMP-activated protein kinase induces LX2 cell apoptosis
ZHANG Jing,TAN Li,LIN Jun,XU Ai-min,LUO Shen-qiu. Adenovirus-mediated overexpression of AMP-activated protein kinase induces LX2 cell apoptosis[J]. Journal of Southern Medical University, 2007, 27(6): 821-823
Authors:ZHANG Jing  TAN Li  LIN Jun  XU Ai-min  LUO Shen-qiu
Affiliation:1 Department of Cell Biology, Southern Medical University, Guangzhou 510515, China; 2 Medical College of the University of Hong Kong
Abstract:Objective To observe the effect of adenovirus-mediated overexpression of AMP-activated protein kinase (AMPK) on apoptosis of hepatic stellate cell line LX2. Methods After adenovirus infection of the LX2 cells, the exogenous gene expression was detected by Western blotting, and cell apoptosis evaluated by flow cytometry with PI staining. Agarose gel electrophoresis was performed to detect the DNA ladder, and the expressions of caspase-3, Bcl-2 and Bax are detected by Western blotting. Result With AMPK overexpression, apoptotic peak and DNA ladder of the infected cells appeared, and pro-caspase-3 was activated to transform into caspase-3 accompanied by up-rugulated Bax expression, whereas Bcl-2 expression was hardly detectable by Western blotting. Conclusion Overexpression of AMPK mediated by the adenovirus can induce LX2 cell apoptosis, possible as a result of up-regulated Bax expression with low Bcl-2 expression.
Keywords:hepatic fibrosis   hepatic stellate cell   adenovirus   apoptosis
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