Circulation Research. 2001;88:1102-1104
Published online before print May 24, 2001, doi: 10.1161/hh1101.092034
Published online before print May 24, 2001, doi: 10.1161/hh1101.092034
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© 2001 American Heart Association, Inc.
Reports |
Human Urotensin II–Induced Contraction and Arterial Smooth Muscle Cell Proliferation Are Mediated by RhoA and Rho-Kinase
Presented in part at the 73rd Scientific Sessions of the American Heart Association, New Orleans, La, November 12–15, 2000, and published in abstract form (Circulation. 2000;102[suppl II]:II-315).
From INSERM U-533 (V.S., E.L.M., G.L., P.P.), Faculté des Sciences, Nantes, France; INSERM U-461 (J.B.), Chatenay-Malabry, France; and IRIS (E.S.), Courbevoie, France.
Correspondence to Gervaise Loirand, INSERM U-533, Faculté des Sciences, 2 rue de la Houssinière, BP 92208, 44322 Nantes cedex 3, France. E-mail gervaise.loirand{at}svt.univ-nantes.fr
Abstract
The aim of this work was to investigate the coupling of human urotensin II (hU-II) to RhoA activation and regulation of RhoA-dependent functions. The use of the Rho-kinase inhibitor Y-27632 and the development of a membrane-permeant RhoA inhibitor (TAT-C3) allowed us to demonstrate that hU-II induced arterial smooth muscle contraction, actin stress fiber formation, and proliferation through the activation of the small GTPase RhoA and its downstream effector Rho-kinase.
Key Words: G protein • vascular • signal transduction
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