Transactivation of epidermal growth factor receptor by enhanced levels of endogenous angiotensin II contributes to the overexpression of GiÎ± proteins in vascular smooth muscle cells from SHR

Article ID	Journal	Published Year	Pages	File Type
1963638	Cellular Signalling	2011	11 Pages	PDF

Abstract

âº The levels of both AngII and Gi proteins are increased in VSMC from SHR. âº We examine the relationship between the two and the underlying signaling. âº Inhibitors of AT1 receptor and EGFR attenuate the enhanced levels of Gi proteins, pEGFR and pERK1/2. âº c-Src inhibitor and antioxidant also inhibit the enhanced pEGFR. âº Enhanced endogenous AngÂ II through transactivation of EGFR and MAP kinase signaling enhances the expression of GiÎ± proteins in SHR.

Keywords

AT2 AVP forskolin AT1 GTPγS N-acetyl-l-cysteine Fsk WKY VSMC ACE NAC angiotensin II receptor type 2 Inhibitory G protein DPI EGFR ERK1/2 MAPK arginine–vasopressin Angiotensin II Angiotensin I converting enzyme Oxidative stress Spontaneously Hypertensive Rat Diphenyleneiodonium Vascular smooth muscle cells Shr Stimulatory G protein mitogen-activated protein kinase angiotensin II receptor type 1 Epidermal growth factor receptor