血管紧张素Ⅱ1型受体相关蛋白对血管平滑肌细胞的影响  

Effects of angiotensin Ⅱ type 1 receptor-associated protein on vascular smooth muscle cells

作　　者：张毅[1] 张凌 李震[1] 何惠娟[1] 

机构地区：[1]广东医学院附属医院中心实验室,广东省湛江市524001 [2]广东省湛江市第二人民医院,524001

出　　处：《实用医学杂志》2007年第7期947-949,共3页The Journal of Practical Medicine

基　　金：湛江市科技攻关项目(编号:2005)

摘　　要：目的:探讨血管紧张素Ⅱ1型受(AT1受体)体相关蛋白(ATRAP)对AT1受体介导的血管平滑肌增殖和新构建的影响。方法:采用细胞培养和转染,将[3H]胸腺嘧啶掺入测定DNA合成、动物实验和外科程序。结果:[3H]胸腺嘧啶掺入测定显示,ATRAPcDNA转染的血管平滑肌细胞(VSMCs)与pcDNA转染的VSMCs比较,过度表达的ATRAP明显抑制了AT1受体介导的VSMCs的增生,有时间依赖性。Western blotting结果显示,过量表达的ATRAP中含磷或不含磷的细胞外信号调控激酶(ERK)抗体表达均较对照组增高。组织病理学观察,过量表达的ATRAP明显抑制了AT1受体介导的VSMCs的增生。结论:过度表达的ATRAP明显抑制了AT1受体介导的VSMCs的增生,ATRAP的生长抑制作用可能是通过在VSMCs中的AT1受体介导的细胞外信号调控激酶(ERK)的后期激活。Objective To explore the effects of angiotensin Ⅱ type 1 （AT1） receptor-associated protein （ATRAP） on the proliferation of vascular smooth muscle cells （VSMCs） mediated by AT1 receptor and the neointimal formation. Methods Cell culture and transfection were conducted, DNA synthesis was assayed using[^3H] thymidine incorporation, and an animal experiment and surgical procedures were performed. Results By comparison between ATRAP cDNA-transfected VSMCs and pcDNA-transfected VSMCs, the overexpression of ATRAP markedly inhibited the proliferation of VSMCs mediated by AT1 receptor in a time-dependent manner. The expressions of phosphorylated or nonphosphorylated extracellular signal-regulated kinase （ERK） antibody in the ATRAP which was overexpressed were all enhanced as compared with those in the control group. The histopathological analysis also showed the overexpression of ATRAP significantly inhibited the proliferation of VSMCs. Conclusion The overexpression of ATRAP significantly inhibited the proliferation of VSMCs mediated by AT1 receptor, whose mechanism may be involved in the late activation of AT1 receptor-mediated ERK in VSMCs.

关 键 词：受体 血管紧张素 1型 血管平滑肌细胞 新构建 

分 类 号：R363[医药卫生—病理学]