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Cardiovascular Research 2002 53(4):952-962; doi:10.1016/S0008-6363(01)00547-8
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Vitronectin is up-regulated after vascular injury and vitronectin blockade prevents neointima formation

Pascale Dufourcq*, Thierry Couffinhal, Philipe Alzieu, Danièle Daret, Catherine Moreau, Cécile Duplàa and Jacques Bonnet

Institut National de la Santé et de la Recherche Médicale, INSERM Unité 441, Athéroclérose, Avenue du Haut-Lévêque, 33600 Pessac, France

* Corresponding author. Tel.: +33-5-5789-1975; fax: +33-5-5636-8979 pascale.dufourcq{at}biophar.u-bordeaux2.fr

Objective: Smooth muscle cell (SMC) migration involves interactions with extracellular matrix (ECM) and is an important process in response to arterial wall injury. We investigated the expression and the functional role of vitronectin (VN) in the response after vascular injury. Methods: VN and {alpha}vβ3/β5 integrin expressions were investigated after balloon carotid injury of Sprague–Dawley rats. Adventitial delivery of blocking antibodies to VN, {alpha}vβ5 and β3 integrins were performed to assess their roles in neointima formation. In vitro, migration assays were carried out on human SMC. Results: Immunohistochemistry and in situ hybridization for VN showed an upregulation of VN during the early time points of intima formation. {alpha}vβ3/β5 integrins expression correlated with VN expression. After 7 days, blocking antibodies to VN, {alpha}vβ5 and β3 induced a significant decrease on intimal area associated with a decrease in intimal cell counts. A slight decrease in intimal cell proliferation without any effect on apoptosis was observed after VN blockade. In vitro, migrating SMC strongly expressed VN after injury and neutralizing anti-VN antibody inhibited SMC migration. Blocking experiment with anti-{alpha}vβ5 and -{alpha}vβ3 integrin antibodies showed that not only VN–{alpha}vβ3 but also VN–{alpha}vβ5 interactions are required for SMC migration. Conclusion: This study characterizes the VN–ECM interaction in SMC and supports the role of VN in mediating SMC migration and neointimal formation in response to injury.

KEYWORDS ECM, extracellular matrix; MMP, matrix metalloproteinase; PAI-1, plasminogen activator inhibitor-1; SMC, smooth muscle cell; tPA, tissue-plasminogen activator; uPA, urokinase; VN, vitronectin


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