The Inhibitory Effect of ATRAP, an Ati Receptor-Associated Protein,on Vascular Smooth Muscle Cell Growth and Neointimal Formation
The mechanism by which ATRAP, a novel Ati receptor-associated protein, interferes with Ati receptor-mediated signaling remains largely uncertain. Here we showed that angiotensin II (Ang II)-induced vascular smooth muscle cells (VSMC) proliferation as well as neointimal formation by balloon injury were markedly inhibited by overexpression of ATRAP.In VSMC, Ang II stimulation increased extracellular signal-regulated kinase (ERK) activity, reaching a peak around 60 min. The activation of ERK could be strongly attenuated by ATRAP. We demonstrated an association between ERK activity and VSMC growth with Ang II stimulation. These results suggest that the Ati receptor-derived activation of ERK, plays an essential role in Angll-induced VSMC growth. The growth inhibitory effects of ATRAP might be due to interfering Ati receptor-mediated activation of ERK in VSMC growth and neointimal formation.
angiotensin receptor vascular smooth muscle cell neointimal formation
李震 汪忠镐 霍小森 王雷永 季锋
Vascular Surgery, Aviation General Hospital, Beijing 100012, China Vascular Surgery, Aviation General Hospital, Beijing 100012, China Vascular Institute, Xuanwu Hospit
国内会议
第六届国际布加综合征学术大会暨汪忠镐血管论坛、首届中国布加综合征与静脉疾病介入治疗大会
郑州
英文
814-818
2010-09-03（万方平台首次上网日期，不代表论文的发表时间）