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Cardiovascular Research 2007 73(1):198-207; doi:10.1016/j.cardiores.2006.10.012
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Copyright © 2006, European Society of Cardiology

Involvement of chloride channels in IGF-I-induced proliferation of porcine arterial smooth muscle cells

Gang Chenga,b, Min-Jung Kima,b, Guanghong Jiaa,b and Devendra K. Agrawala,b,c,*

aDepartment of Biomedical Sciences, Creighton University School of Medicine, Omaha, NE, United States
bDepartment Internal Medicine, Creighton University School of Medicine, Omaha, NE, United States
cDepartment Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, NE, United States

* Corresponding author. Department of Biomedical Sciences, Creighton University School of Medicine, CRISS II Room 510, 2500 California Plaza, Omaha, NE 68178, United States. Tel.: +1 402 280 2938; fax: +1 402 280 1421. Email address: dkagr{at}creighton.edu

Objective: The existence of Cl– channels in vascular smooth muscle cells (VSMCs) has been increasingly investigated, but the biological functions are not yet clear. Insulin-like growth factor (IGF)-I affects proliferation and migration of VSMCs, and dysregulation of this axis may be involved in atherogenesis and intimal hyperplasia. We examined the effects of Cl– channel blockers on IGF-I-induced proliferation in porcine VSMCs. The siRNA approach was used to support the role of ClC-2, a member of the volume-regulated Cl– channel family, in cell proliferation of VSMCs.

Methods and results: The IGF-I-induced VSMC proliferation was significantly suppressed by the Cl– channel blockers NPPB and IAA94 but not by DIDS. IGF-I-induced cell proliferation parallels a significant increase in the endogenous expression of ClC-2 mRNA and protein. Inhibitors of PI3-kinase, LY294002 and wortmannin, significantly attenuated the IGF-I-upregulated ClC-2 expression and cell proliferation. We observed ClC-2-like Cl– current, and this current was augmented by IGF-I. SiRNA specifically targeted to ClC-2 abolished IGF-I-induced cell proliferation.

Conclusion: Our data demonstrate that ClC-2 plays a role in IGF-1-induced regulation of VSMC proliferation in cardiovascular diseases.

KEYWORDS Atherosclerosis; Voltage-gated Cl– channels; Cl– channel blocker; Proliferation; Vascular smooth muscle cells

Time for primary review 20 days


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