Objective: The theory of primary venous dilatation leading to secondary valvular incompetence and varicose vein formation has received more attention nowadays. Although many studies have investigated the role of the main components of the venous wall in the development of varicose veins, the leading cause remains unknown. The present study was designed to establish the role of smooth muscle cells (SMCs) of the tunica media on the pathogenesis of varicose veins by analyzing the phenotypic and functional differences between SMCs derived from varicose veins and normal veins.
Methods: SMCs were isolated and cultured from saphenous veins of patients with varicose veins and normal veins. Cell proliferation and migration rates were compared. Expression of phenotype-dependent markers and matrix metalloproteinase-2 (MMP) production were analyzed by immunoblotting. Total collagen synthesis was evaluated by measuring the radioactivity of L-[3, 4-(3)H]proline in the media and the cell layer.
Results: SMCs derived from varicose veins demonstrated increased proliferation (2-fold, P < .01), migration (3-fold, P < .001), MMP-2 production (3-fold, P < .01), and collagen synthesis (>2-fold, P < .001), with decreased expression of phenotype-dependent markers compared with SMCs derived from normal veins (P < .05).
Conclusion: SMCs derived from varicose veins are more dedifferentiated and demonstrate increased proliferative and synthetic capacity than SMCs derived from normal veins. These properties may contribute to the remodeling of the venous wall and the weakening of its antipressure capacity.