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Circulation Research. 2005
Published online before print March 17, 2005, doi: 10.1161/01.RES.0000163018.66460.85
A more recent version of this article appeared on April 29, 2005
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Submitted on April 16, 2004
Revised on March 3, 2005
Accepted on March 9, 2005

Contractile Properties of the Cultured Vascular Smooth Muscle Cells. The Crucial Role Played by RhoA in the Regulation of Contractility

Dan Bi ; Junji Nishimura ; Naohisa Niiro ; Katsuya Hirano ; and Hideo Kanaide *

From the Division of Molecular Cardiology, Research Institute of Angiocardiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

* To whom correspondence should be addressed. E-mail: kanaide{at}molcar.med.kyushu-u.ac.jp.

Vascular smooth muscle cells (VSMCs) have a remarkable degree of plasticity and in response to vascular injury, they can change to a dedifferentiated state that can be typically seen in cell cultures. Recently, Y27632, a Rho kinase inhibitor, has been reported to preferentially correct hypertension in a hypertensive rat model. We thus tested the hypothesis that the contraction of the cultured VSMCs might be more dependent on the function of RhoA than the VSMCs in fresh tissue. For this purpose, a tissue-like ring preparation was made using the cultured porcine coronary artery SMCs (CASMCs) and collagen gel (reconstituted ring: R-ring). The R-ring developed an isometric tension on stimulation by high external K+ or various receptor agonists. The phorbol ester (a protein kinase C (PKC) activator)-induced contraction of the intact R-ring was greatly inhibited, while the GTP{gamma}S (an activator of RhoA)-induced and Ca2+-independent contraction of permeabilized R-ring was greatly enhanced, in comparison to the fresh coronary artery ring. An immunoblot analysis showed the expression levels of RhoA and myosin phosphatase subunits (MYPT1 and PP1c{delta}) to be up-regulated, while the levels of CPI-17 (PKC-potentiated protein phosphatase-1 inhibitory protein), h1-calponin and PKC isoforms were downregulated in cultured CASMCs. The knock down of RhoA by RNA interference decreased the contractility of the cultured CASMCs. It is concluded that the contractility of the cultured VSMCs thus appears to be much more dependent on the function of RhoA than VSMCs in fresh tissue. The expression level of RhoA thus plays a crucial role in regulating the contractility of cultured VSMCs.
Key words: vascular smooth muscle • contraction • RhoA • CPI-17 • RNA interference • vascular disease




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