血管紧张素II通过血管平滑肌细胞中的血管紧张素II 1型受体将其信号转导至粘着斑。

Angiotensin II transduces its signal to focal adhesions via angiotensin II type 1 receptors in vascular smooth muscle cells.

作者信息

Okuda M, Kawahara Y, Nakayama I, Hoshijima M, Yokoyama M

机构信息

Department of Internal Medicine (1st Division), Kobe University School of Medicine, Japan.

出版信息

FEBS Lett. 1995 Jul 17;368(2):343-7. doi: 10.1016/0014-5793(95)00693-4.

DOI:10.1016/0014-5793(95)00693-4

PMID:7628634

Abstract

In cultured vascular smooth muscle cells (VSMCs), angiotensin II (Ang II) stimulated tyrosine phosphorylation of several proteins including a cluster of 70-80-kDa proteins as assessed by anti-phosphotyrosine immunoblotting. These 70-80-kDa proteins were identified as a focal adhesion-associated protein, paxillin, by anti-paxillin immunoprecipitation. Ang II-stimulated tyrosine phosphorylation of paxillin was detectable within 1 min and maximal at around 10 min and was concentration dependent (half-maximal effect at around 1 nM). Ang II also stimulated tyrosine phosphorylation of focal adhesion kinase in a time- and concentration-dependent manner. The Ang II type 1 (AT1) receptor antagonist, CV-11974, but not the Ang II type 2 receptor antagonist, PD123319, inhibited these reactions. These results indicate that Ang II transduces its signal to focal adhesions via AT1 receptors in cultured VSMCs.

摘要

在培养的血管平滑肌细胞（VSMC）中，通过抗磷酸酪氨酸免疫印迹法评估，血管紧张素II（Ang II）刺激了几种蛋白质的酪氨酸磷酸化，包括一组70 - 80 kDa的蛋白质。通过抗桩蛋白免疫沉淀法，这些70 - 80 kDa的蛋白质被鉴定为一种粘着斑相关蛋白——桩蛋白。Ang II刺激的桩蛋白酪氨酸磷酸化在1分钟内即可检测到，在约10分钟时达到最大值，且呈浓度依赖性（在约1 nM时达到半数最大效应）。Ang II还以时间和浓度依赖性方式刺激粘着斑激酶的酪氨酸磷酸化。血管紧张素II 1型（AT1）受体拮抗剂CV - 11974可抑制这些反应，而血管紧张素II 2型受体拮抗剂PD123319则不能。这些结果表明，在培养的VSMC中，Ang II通过AT1受体将其信号转导至粘着斑。