Human urotensin II-induced contraction and arterial smooth muscle cell proliferation are mediated by RhoA and Rho-kinase.
basic_science · Level V
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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.
Medical subject headings
- Botulinum Toxins
- Muscle, Smooth, Vascular
- Protein Serine-Threonine Kinases
- Urotensins
- Vasoconstriction
- rhoA GTP-Binding Protein