Mature adipocytes and perivascular adipose tissue stimulate vascular smooth muscle cell proliferation: effects of aging and obesity.

Adipocytes and perivascular adipose tissue are emerging as regulators of vascular function. The effects of adipocytes and perivascular adipose tissue on human smooth muscle cell (SMC) proliferation were investigated. Conditioned medium was prepared from cultured premature and differentiated 3T3-L1 adipocytes and from periaortic adipose tissue from young (3 mo) and old (24 mo) Wistar-Kyoto (WKY) rats, lean and obese Zucker rats (3 mo), and WKY rats fed normal chow or a high-fat diet for 3 mo.

Thrombin stimulates human endothelial arginase enzymatic activity via RhoA/ROCK pathway: implications for atherosclerotic endothelial dysfunction.

Background: Arginase competes with endothelial nitric oxide synthase (eNOS) for the substrate l-arginine and decreases NO production. This study investigated regulatory mechanisms of arginase activity in endothelial cells and its role in atherosclerosis.

Methods And Results: In human endothelial cells isolated from umbilical veins, thrombin concentration- and time-dependently stimulated arginase enzymatic activity, reaching a 1.

Different cell cycle regulation of vascular smooth muscle in genetic hypertension.

Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) proliferate faster than those from Wistar-Kyoto rats (WKY). Therefore regulation of cell cycle progression was examined in VSMC from both strains. Analysis of G1 progression was performed in VSMC synchronized by serum starvation.

PKC is required for activation of ROCK by RhoA in human endothelial cells.

Rho/Rho-kinase (ROCK) complex formation is the only proposed mechanism for ROCK activation. Rho/ROCK and PKC can exhibit a convergence of cellular effects such as suppression of endothelial nitric oxide synthase (eNOS) expression. We, therefore, investigated the role of PKC in RhoA/ROCK complex formation and activation linked to eNOS expression in cultured human umbilical vein endothelial cells.

Small G proteins as novel therapeutic targets in cardiovascular medicine.

Small G proteins are implicated in regulation of endothelial function, smooth muscle cell contraction, proliferation, and migration, as well as cardiomyocyte hypertrophy. Targeting small G proteins and their downstream signaling could constitute promising therapeutic approaches in cardiovascular disorders such as atherosclerosis, restenosis, hypertension, vasospasm, and cardiac hypertrophy.