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Vitronectin Expression and Interaction With Receptors in Smooth Muscle Cells From Human Atheromatous Plaque

1998; Lippincott Williams & Wilkins; Volume: 18; Issue: 2 Linguagem: Inglês

10.1161/01.atv.18.2.168

1524-4636

Pascale Dufourcq, Huguette Louis, Catherine Moreau, Danièle Daret, M Boisseau, J.-M. D. Lamaziere, Jacques Bonnet,

Corrosion Behavior and Inhibition

Abstract —Vitronectin (VN) is a plasma glycoprotein that promotes cell attachment and induces migration of human smooth muscle cells (SMCs) in culture. VN has been observed to accumulate in human atherosclerotic plaques, although its origin and role in atherosclerosis are not yet established. In the present experiments, synthesis of VN by intimal cells and its colocalization with receptors, αvβ3 and αvβ5, were studied by in situ hybridization and immunohistochemistry on 15 human atherosclerotic plaques from carotid arteries obtained after surgery. Strong VN protein and mRNA expression was observed in the intima and in the media. In the intima, VN mRNA expression was colocalized with SMCs, indicating that these cells produce VN, which may account for its accumulation in atherosclerotic plaques. In SMCs in culture, immunoprecipitation after metabolic labeling demonstrated that human SMCs do synthesize vitronectin. Confocal microscopic examination showed that VN colocalized with its receptors, αvβ3 and αvβ5, in the atherosclerotic intima. However, the distribution of the VN receptors on SMCs in culture in contact with VN was different. These observations suggest that VN plays various parts in atherogenesis via different SMC membrane receptors. ( Arterioscler Thromb Vasc Biol. 1998;18:168-176.)