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(Circulation Research. 2001;88:352.)
© 2001 American Heart Association, Inc.

Integrative Physiology

Regional Differences in Integrin Expression

Role of ₅ß₁ in Regulating Smooth Muscle Cell Functions

Kelly L. Davenpeck, Cezary Marcinkiewicz, Dian Wang, Rodica Niculescu, Yi Shi, Jack L. Martin, Andrew Zalewski

From the Cardiovascular Research Center (K.L.D., D.W., R.N., Y.S., A.Z.), Department of Medicine (Cardiology), Thomas Jefferson University, Philadelphia; Department of Physiology (C.M.), Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia; and John S. Sharpe Research Foundation of Bryn Mawr Hospital (J.L.M.), Bryn Mawr, Pa.

Correspondence to Andrew Zalewski, MD, Division of Cardiology, Thomas Jefferson University, 1025 Walnut St, RM 410, Philadelphia, PA 19107. E-mail andrew.zalewski{at}mail.tju.edu

Abstract—There is increasing evidence to suggest that coronary smooth muscle cells (SMCs) differ from noncoronary SMCs. As integrin adhesion molecules regulate many SMC functions, we hypothesized that differences in integrin expression on coronary and noncoronary SMCs may account for cellular differences. Analysis of integrin expression on freshly isolated porcine coronary and noncoronary SMCs revealed that coronary SMCs express significantly less ₅ß₁ than noncoronary SMCs, whereas the expression of total ß₁ and that of _vß₃ are similar. Consistent with these findings, coronary SMCs demonstrated significantly less adhesion to fibronectin, compared with carotid artery SMCs. As ₅ß₁-mediated signaling has been associated with cellular proliferation, the effects of differential ₅ß₁ expression on cell proliferation were examined by comparing primary coronary and carotid artery SMC proliferation. Coronary SMC growth was significantly lower than that of carotid artery SMCs when plated on fibronectin or type I collagen. Blocking ₅ß₁ function on carotid artery SMCs produced a significant decrease in cellular proliferation, resulting in growth similar to that of coronary SMCs. Furthermore, blocking ₅ß₁, but not _vß₃, inhibited loss of -smooth muscle actin in proliferating SMCs. Proliferating coronary SMCs were found to upregulate ₅ß₁ expression, further indicating a role for ₅ß₁ in SMC growth. These results suggest that dissimilar ₅ß₁ integrin expression may mediate regional differences in phenotype of vascular SMCs.

Key Words: integrin adhesion molecules • coronary smooth muscle cells • dedifferentiation • proliferation

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