Copyright © 2004, European Society of Cardiology
In vitro differences between venous and arterial-derived smooth muscle cells: potential modulatory role of decorin
Roy and Ann Foss Interventional Cardiology Research Program, Terrence Donnelly Heart Centre, St. Michael's Hospital, Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada M5B 1W8
* Corresponding author. Tel.: +1 416 864 5913; fax: +1 416 864 5978. Email address: straussb{at}smh.toronto.on.ca
Objective: We analyzed the phenotypic and functional differences between venous and arterial smooth muscle cells (SMC) and the role of decorin in modulating these differences.
Methods and results: SMC were isolated from the jugular veins and carotid arteries of male white New Zealand rabbits. Venous SMC demonstrated increased proliferation (2-fold, p<0.001), migration (1.7-fold, p<0.001), and collagen synthesis (4-fold, p<0.001), with decreased adhesion to collagen and fibronectin (1.2-fold, p<0.01) compared to arterial SMC. Higher levels of gelatinase activity (MMP-2 and MMP-9) and tissue inhibitor of metalloproteinase (TIMP) were also observed in venous SMC. Venous SMC demonstrated increased expression of SMemb and decreased expression of SM1–markers of a dedifferentiated and differentiated phenotype, respectively. Arterial SMC produced increased levels of the inhibitory proteoglycan, decorin, compared to venous SMC. Conditioned medium from arterial SMC (ASMC-CM) significantly decreased DNA synthesis, collagen synthesis, and gelatinase activity in venous SMC. Removal of decorin from ASMC-CM by immunoprecipitation significantly reversed the inhibitory effects of ASMC-CM on venous SMC proliferation and collagen synthesis but did not affect gelatinase activities.
Conclusion: Venous SMC are more dedifferentiated and demonstrate increased proliferative and synthetic capacity than arterial SMC. Differential decorin expression between arterial and venous SMC contributes to these differences in biologic behavior. Venous SMC properties may contribute to accelerated atherosclerosis in venous bypass grafts.
KEYWORDS In vitro; Smooth muscle cells; Decorin
1 Present address: Thoracic Surgery Research Laboratories, Max Bell Research Centre, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada.
Dedicated to the memory of Robyn Strauss Albert.
Time for primary review 21 days
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