Regulation of angiotensin Ⅱ on Gαq/11 protein of vascular smooth muscle cell and its underlying mechanism

被引：0
|
作者：
XING Dongqi
机构：
来源：
Chinese Science Bulletin | 2002年 / 16期
基金：
中国国家自然科学基金;
关键词：
angiotensin II; vascular smooth muscle cell; G protein; hypertrophy; signal transduction;
D O I：
暂无
中图分类号：
R363 [病理生理学];
学科分类号：
摘要：
To study the regulation of angiotensin Ⅱ (Ang Ⅱ) on Gαq/11 protein of vascular smooth muscle cell (VSMC) and its underlying mechanism, the protein synthesis was detected by [3H]-leucine incorporation. Gαq/11 expression was measured by Western blot in cultured VSMC of rat aorta. The results showed that the level of Gαq/11 was down-regulated after stimulated by Ang Ⅱ for 1-6 h, while it was upregulated significantly by 12-24 h stimulation (P < 0.01) in VSMC. The [3H]-leucine incorporation of VSMC was increased after 24 h Ang Ⅱ stimulation. The biphase regulation of Ang Ⅱ on Gαq/11 protein was blocked by the Ang Ⅱ type I receptor (AT1) specific antagnist losartan or PLC inhibitor U73122, while PD98059 did not have this effect. These data indicated that Ang Ⅱ contributed to VSMC hypertrophy by regulating the level of Gαq/11, and this effect was mediated mainly through AT1 receptor-PLC signal transduction pathway.
引用
收藏
页码：1369 / 1372
页数：4
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