scholarly journals 183. Overexpression of Dominant Negative Insulin-Like Growth Factor Receptor Induces Apoptosis and Inhibited Cell Proliferation in Rat Vascular Smooth Muscle Cells

2002 ◽  
Vol 5 (5) ◽  
pp. S62-S63
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Growth Factor Receptor ◽  
Muscle Cells ◽  
Dominant Negative ◽  
Insulin Like Growth Factor

Involvement of insulin-like growth factor 1 receptor transactivation in endothelin-1-induced signaling in vascular smooth muscle cells

2010 ◽  
Vol 88 (5) ◽  
pp. 501-509 ◽  
Author(s):  
Ali Bouallegue ◽  
George Vardatsikos ◽  
Ashok K. Srivastava
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Growth Factor Receptor ◽  
Muscle Cells ◽  
Insulin Like Growth Factor ◽  
Endothelin 1 ◽  
Receptor Transactivation

Endothelin-1 (ET-1) is a potent vasoactive peptide that exerts hypertrophic, migratory, and mitogenic effects in vascular smooth muscle cells. ET-1-induced activation of several signaling events has been shown to mediate the cellular effects of ET-1. In the past several years, transactivation of growth factor receptor has gained much recognition in transducing the signaling responses of ET-1. Among various growth factor receptors studied, the involvement of epidermal growth factor receptor transactivation in triggering ET-1-induced responses has been studied in some detail. However, recent studies have implicated insulin-like growth factor 1 receptor transactivation in this process. There are also some suggestions for a role of the Src family of nonreceptor protein tyrosine kinases, such as c-Src, in transducing the signaling responses of vasoactive peptides. In this review, we will examine the contribution of both insulin-like growth factor 1 receptor and c-Src in mediating ET-1-induced signaling responses in vascular smooth muscle cells.

Angiotensin II-induced activation of p21-activated kinase 1 requires Ca2+ and protein kinase Cδ in vascular smooth muscle cells

2005 ◽  
Vol 289 (5) ◽  
pp. C1286-C1294 ◽  
Author(s):  
Elethia A. Woolfolk ◽  
Satoru Eguchi ◽  
Haruhiko Ohtsu ◽  
Hidekatsu Nakashima ◽  
Hikaru Ueno ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Growth Factor Receptor ◽  
Muscle Cells ◽  
Dominant Negative ◽  
Ang Ii ◽  
Signaling Mechanism ◽  
P21 Activated Kinase

ANG II promotes remodeling of vascular smooth muscle cells (VSMCs) in cardiovascular diseases. It has been shown to activate p21-activated kinase (PAK)1, a critical component of signaling pathways implicated in growth and migration. However, the detailed signaling mechanism by which ANG II induces PAK1 activation in VSMCs remains unclear. Therefore, we have examined the mechanism required for activation of PAK1 by ANG II in VSMCs. ANG II, through activation of the ANG II type 1 receptor, rapidly promotes phosphorylation of PAK1 in VSMCs via a pathway independent of transactivation of the epidermal growth factor receptor. Using selective agonists and inhibitors, we demonstrated that mobilization of intracellular Ca2+ and PKCδ activation are required for ANG II-induced PAK1 phosphorylation. Rottlerin, a PKCδ inhibitor, significantly blocked ANG II-induced PAK1 phosphorylation. Further support for this notion was provided through infection of VSMCs with adenovirus encoding a dominant-negative (dn)PKCδ, which also markedly reduced phosphorylation of PAK1 by ANG II. In this pathway, Ca2+ acts upstream of PKCδ because a Ca2+ ionophore rapidly induced PKCδ phosphorylation at Tyr311 and Ca2+-dependent PAK1 phosphorylation was blocked by rottlerin. In addition, dnPYK-2, dnRac, and antioxidants inhibited ANG II-induced PAK1 phosphorylation, suggesting that PYK-2, Rac, and reactive oxygen species are involved in the upstream signaling. Finally, dnPAK1 markedly inhibited ANG II-induced protein synthesis in VSMCs. These data provide a novel signaling pathway by which ANG II may contribute to vascular remodeling.

Expression and control of C-type natriuretic peptide in rat vascular smooth muscle cells

2002 ◽  
Vol 282 (1) ◽  
pp. R156-R165 ◽  
Author(s):  
Geoffrey E. Woodard ◽  
Juan A. Rosado ◽  
John Brown
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Natriuretic Peptide ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Natriuretic Peptide Receptors

C-type natriuretic peptide (CNP) is a member of the natriuretic peptide family mainly distributed in the central nervous system. CNP is also produced and secreted by the endothelium and inhibits vascular smooth muscle cell proliferation. We have reported that endothelial damage stimulates only transiently vascular smooth muscle cell proliferation in arteries due to the development of an autocrine neointimal system for CNP that modulates neointimal growth. The present study demonstrates the production and secretion of CNP in rat vascular smooth muscle cells in the absence of endothelium. In addition, these cells express atrial natriuretic peptide (ANP) and the natriuretic peptide receptors A, B, and C. The production and secretion of CNP in vascular smooth muscle cells is stimulated by transforming growth factor-β, whereas basic fibroblast growth factor plays an inhibitory role. These data show that ANP and mainly CNP are coexpressed with the natriuretic peptide receptors in rat vascular smooth muscle cells. This provides evidence for a vascular natriuretic peptide autocrine system of physiological relevance in these cells.

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