血管紧张素Ⅱ调控bax mRNA表达诱导内皮细胞凋亡

目的　研究AngⅡ诱导凋亡细胞内机制。方法　健康胎儿脐静脉内皮细胞培养至第三代,用不同浓度AngⅡ作用不同时间,用TUNEL和ELISA检测AngⅡ能否诱导凋亡及有否剂量依赖性;用RT—PCR检测bax的mRNA表达。结果　AngⅡ同AT2 受体激动剂CGP42 1 1 2A一样可以诱导内皮细胞凋亡;并且凋亡强度与AngⅡ成典型的剂量依赖关系。在AngⅡ与CGP42 1 1A作用1 8小时后,baxmRNA显著增加。结论　AngⅡ在转录水平上诱导baxmRNA高表达,使得Bax蛋白高表达,致Bax Bcl- 2比值极显著地增加,细胞内促凋亡因素占优势地位而诱发凋亡。

Angiotensin II Induced Endothelial Apoptosis by Regulation of Expression of Bax mRNA

Objective To study human endothelial apoptosis induced by angiotensin II (Ang II) and to explore its molecular mechanism. Methods Endothelium isolated from healthy human infant umbilical vein was cultured to the third passage, then added to Ang II in various concentrations and further cultured for different time periods. The apoptosis was detected by TUNEL and ELISA. The expression of bax- mRNA was determined by RT-PCR and densitometry. Results Ang II like AT 2 receptor agonist CGP42112A induced typical the endothelial apoptosis and its degree was in dose-dependent manner, apoptotic positive cell percentage in Ang II treatment group was significantly higher than that of control. The expression of bax-mRNA was higher in Ang II or CGP42112A treatment group than that of control. Conclusion Ang II triggered apoptosis of human endothelium by up-regulating the expression of proapoptotic bax mRNA