© 1994 by European Society of Cardiology
Copyright © 1994, European Society of Cardiology
Stimulation of migration of human aortic smooth muscle cells by vitronectin: implications for atherosclerosis
Cardiovascular Division, Washington University School of Medicine, 660 South Euclid Avenue, Box 8086, St Louis, MO 63110, USA: S L Brown, C H Lundgren, T Nordt, S Fujii.
Correspondence to Dr Fujii.
Objective: Migration of smooth muscle cells into the neointima has been implicated in atherogenesis. Vitronectin, a serum factor that promotes cell spreading and attachment, accumulates in atherosclerotic human tissues. The aim of this study was to determine the role of vitronectin and its receptor (integrin 
Vβ3) in migration of smooth muscle cells. Methods: Human aortic smooth muscle cell migration was studied in modified Boyden chambers. Expression of vitronectin receptor was determined by northern blotting of receptor mRNA and immunoprecipitation of receptor protein. Results: Vitronectin dose dependently increased smooth muscle cell migration by an amount comparable to that induced by platelet derived growth factor, (PDGF)-BB. Antiserum to Vβ3 diminished vitronectin driven migration. Northern blot analysis showed low constitutive expression of V and β3 mRNA by smooth muscle cell and rapid induction with transforming growth factor β (TGF-β) and thrombin. Immunoprecipitation confirmed increased synthesis of the Vβ3 vitronectin receptor complex by TGF-β or thrombin. Smooth muscle cells pretreated with TGF-β or thrombin showed increased vitronectin driven migration. cAMP suppressed induction of migration, but inhibition of protein kinase C increased it. Conclusions: These results show that vitronectin-induced human aortic smooth muscle cell migration is mediated by aVB3 vitronectin receptor and expression of the receptor is induced by TGF-β and thrombin, which in turn induce vitronectin driven, vitronectin receptor modulated smooth muscle cell migration.
Cardiovascular Research 1994;28:1815-1820
KEYWORDS integrin; atherogenesis; human aortic smooth muscle cells; vitronectin; migration
This work was supported in part by the National Heart, Lung, and Blood Institutes grant HL- 17646, SCOR in Coronary and Vascular Diseases, and a Grant-in-Aid from the American Heart Association, Missouri Affiliate. The authors wish to thank Dr Burton E Sobel for helpful discussions; Beth Engeszer for editorial assistance: Denise Nachowiak. John Botz. and Jeffrey Labuda for technical assistance; and Barbara Donnelly and Kelly Hall for secretarial assistance.
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