Egg White-Derived Antihypertensive Peptide IRW (Ile-Arg-Trp) Inhibits Angiotensin II-Stimulated Migration of Vascular Smooth Muscle Cells via Angiotensin Type I Receptor

2018 ◽  
Vol 66 (20) ◽  
pp. 5133-5138 ◽  
Author(s):  
Wang Liao ◽  
Hongbing Fan ◽  
Jianping Wu
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Egg White ◽  
Type I ◽  
Angiotensin Type

Abstract 667: Angiotensin II-induced Osteopontin Expression in Vascular Smooth Muscle Cells involves G q/11 , Ras, ERK, Src and Ets-1.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Keiko Abe ◽  
Mari Ishida ◽  
Mariko Sawano ◽  
Hidekatsu Nakashima ◽  
Nwe Nwe Soe ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Promoter Activity ◽  
Critical Role ◽  
Muscle Cells ◽  
Separate Experiment ◽  
Type I

Background : Osteopontin (OPN), an extracellular matrix component produced by vascular smooth muscle cells (VSMC) and monocytes in response to biological stressors, is a regulator of cellular proliferation and migration. Recent studies revealed that OPN also plays a critical role in the progression of atherosclerotic plaques and that angiotensin II (AngII) is a potent upregulator of OPN expression. Therefore, the goal of the present study was to characterize the signaling mechanisms whereby AngII increases OPN expression. Methods and Results : YM254890, a specific inhibitor of G q/11 , potently suppressed AngII-induced OPN expression and ERK1/2 activation. Among DN mutants of small G proteins (Ras, Rac, Rho), only DN-Ras completely suppressed AngII-induced OPN promoter activity. Dominant negative (DN)-MEK1 inhibited AngII-induced OPN promoter activity by 54%, while DN-c-Jun N-terminal kinase (JNK) or DN-p38MAP kinase had no effect. DN-Src and Csk suppressed AngII-induced OPN promoter activity by 49% and 71%, respectively. In addition, small interfering RNA against Ets-1 (a transcriptional factor downstream of ERK1/2) suppressed AngII-induced OPN expression by 54 ± 4.3%. In a separate experiment, rats were treated with the AngII type I receptor blocker, valsartan (1 mg/kg/day), or vehicle for 2 weeks after carotid artery balloon injury. The intima/media ratio and OPN expression were significantly lower in valsartan-treated rats than in vehicle-treated rats. Conclusion : These data suggest that AngII-induced OPN expression in VSMC is mediated by signaling cascades involving G q/11 , the Ras-ERK axis, and c-Src, and by the transcription factor, Ets-1. Further, OPN may play a role in AngII-induced neointimal formation. These signaling molecules may represent therapeutic targets for the prevention of pathological vascular remodeling in patients with hypertension and atherosclerosis.

scholarly journals Angiotensin II Type I and Prostaglandin F2α Receptors Cooperatively Modulate Signaling in Vascular Smooth Muscle Cells

2014 ◽  
Vol 290 (5) ◽  
pp. 3137-3148 ◽  
Author(s):  
Eugénie Goupil ◽  
Dany Fillion ◽  
Stéphanie Clément ◽  
Xiaoyan Luo ◽  
Dominic Devost ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Prostaglandin F2α ◽  
Muscle Cells ◽  
Type I

scholarly journals Sustained diacylglycerol formation from inositol phospholipids in angiotensin II-stimulated vascular smooth muscle cells.

1986 ◽  
Vol 261 (13) ◽  
pp. 5901-5906 ◽  
Author(s):  
K K Griendling ◽  
S E Rittenhouse ◽  
T A Brock ◽  
L S Ekstein ◽  
M A Gimbrone ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Inositol Phospholipids
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