G protein-coupled receptors control vascular smooth muscle cell proliferation via pp60c-src and p21ras.
G protein-coupled receptors control vascular smooth muscle cell proliferation via pp60c-src and p21ras.
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G 蛋白偶联受体通过 pp60c-src 和 p21ras 控制血管平滑肌细胞增殖。
DOI：
10.1152/ajpcell.1997.272.6.c2019
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Marrero,MB
中科院分区：
文献类型：
--
作者：
Schieffer,B;Drexler,H;Ling,BN;Marrero,MB
The binding of vasoactive peptides to their respective G protein-coupled receptors has been implicated in the pathogenesis of vascular smooth muscle cell proliferation, leading to the development of hypertension, arteriosclerosis, and restenosis after vascular injury. We previously showed that the cytosolic tyrosine kinase pp60c-src is crucial for angiotensin II (ANG II)-induced activation of the protooncogene p21ras. Therefore, we investigated the role of pp60c-src and p21ras in rat aortic smooth muscle cell proliferation induced by several G protein-coupled receptors. ANG II, endothelin-1, or thrombin increased cell proliferation and DNA synthesis. Electroporation of anti-pp60c-src antibodies into cells abolished proliferation in response to these G protein-coupled receptor ligands but not in response to platelet-derived growth factor-BB (PDGF-BB). In contrast, electroporation of anti-p21ras antibody completely blocked DNA synthesis and cell proliferation in response to ANG II, endothelin-1, thrombin, and PDGF-BB. Our data indicate that the pp60c-src tyrosine kinase is necessary and specific for vascular smooth muscle cell proliferation and DNA synthesis in response to G protein-coupled receptors but not classic growth factor receptors.
