血管紧张素Ⅱ调控bax、bcl-2 mRNA表达诱导血管内皮细胞凋亡  

Angiotensin Ⅱ Induced Endothelial Apoptosis by Regulation of Expression of bax and bcl-2 mRNA

作　　者：王卫忠[1] 熊先智[1] 刘纬[2] 金阳[1] 张建初[1] 白明[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院呼吸科,武汉430022 [2]华中科技大学同济医学院网络中心,武汉430030

出　　处：《华中科技大学学报（医学版）》2005年第6期727-729,共3页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：教育部留学回国人员科研启动基金资助项目(教外司留[2000]479)

摘　　要：目的研究血管紧张素Ⅱ(AngⅡ)诱导细胞凋亡的机制。方法健康胎儿脐静脉内皮细胞培养至第3代,用不同浓度AngⅡ作用18h,用TUNEL和ELISA检测AngⅡ能否诱导细胞凋亡及其量效关系;用RT-PCR检测bax和bcl-2的mRNA表达。结果AngⅡ与2型血管紧张素Ⅱ受体(AT2)激动剂CGP42112A一样可以诱导血管内皮细胞凋亡;并且凋亡强度与AngⅡ呈典型的剂量依赖关系。在AngⅡ与CGP4211A作用18h后,bax mRNA显著增加,bcl-2mRNA显著减少。结论AngⅡ通过在转录水平调节bax和bcl-2mRNA的表达,从而诱导血管内皮细胞凋亡。Objective To study human endothelial apoptosis induced by angiotensin Ⅱ （Ang Ⅱ ） and its molecular mechanism. Methods Blood endotheliocytes isolated from healthy human infant umbilical vein were cultured to the third passage and incubated with Ang Ⅱ in various concentrations for 18 h. The apoptosis was detected by TUNEL and ELISA. The expression of bax and bcl-2 mRNA was determined by RT-PCR and densitometry. Results Ang Ⅱ, like AT2 receptor agonist CGP42112A, could induce the typical endothelial apoptosis in a dose-dependent manner. Apoptotic positive cell percentage in Ang Ⅱ treatment group was significantly higher than that in normal control group. The expression of bax mRNA was higher and that of bcl-2 mRNA lower in Ang Ⅱ or CGP42112A treatment group than in normal control group. Conclusion Ang Ⅱ triggered apoptosis of human blood endotheliocytes by up-regulating the expression of proapoptotic bax mRNA and down-regulating the expression of antiapoptotic bcl-2 mRNA.

关 键 词：BAX基因 BCL-2基因 血管紧张素Ⅱ 血管内皮细胞 细胞凋亡 

分 类 号：R349.6[医药卫生—基础医学]