Original Contributions |
From INSERM Unité 441, Atheroclérose, Pessac, France.
Correspondence to Pascale Dufourcq, INSERM Unité 441, Atheroclérose, Avenue du Haut-Lévêque, 33600 Pessac, France.
AbstractVitronectin (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,
vß3 and
vß5,
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,
vß3 and
vß5, 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.)
Key Words: vitronectin vitronectin receptors integrin smooth muscle cells atherosclerosis
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