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Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:949-954

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:949.)
© 2001 American Heart Association, Inc.


Vascular Biology

Cultured Arterial Smooth Muscle Cells Maintain Distinct Phenotypes When Implanted Into Carotid Artery

Marie-Luce Bochaton-Piallat; Alexander W. Clowes; Monika M. Clowes1; Jens W. Fischer; Mireille Redard; Françoise Gabbiani; Giulio Gabbiani

From the Department of Pathology (M.-L.B.-P., M.R., F.G., G.G.), University of Geneva, Geneva, Switzerland, and the Department of Surgery (A.W.C., M.W.C., J.W.F.), University of Washington, Seattle.

Correspondence to Prof Giulio Gabbiani, Department of Pathology, CMU, 1, rue Michel-Servet, 1211 Geneva 4, Switzerland. E-mail Giulio.Gabbiani{at}medecine.unige.ch

Abstract—Cultured arterial smooth muscle cells (SMCs) with distinct phenotypic features have been described by several laboratories; however, it is not presently known whether this phenotypic heterogeneity can be maintained within an in vivo environment. To answer this question, we have seeded into the intima of denuded rat carotid artery 2 SMC populations with well-established distinct biological features, ie, spindle-shaped, not growing in the absence of serum, and well differentiated versus epithelioid, growing in the absence of serum, and relatively undifferentiated, derived from the aortic media of newborn rats (aged 4 days) and old rats (aged >18 months), respectively. We show that these 2 populations maintain their distinct biochemical features (ie, expression of {alpha}-smooth muscle actin, smooth muscle myosin heavy chains, and cellular retinol binding protein-1) in the in vivo environment. The old rat media–derived SMCs continue to produce cellular retinol binding protein-1 but little {alpha}-smooth muscle actin and smooth muscle myosin heavy chains, whereas the newborn rat media–derived SMCs continue to express {alpha}-smooth muscle actin and smooth muscle myosin heavy chains but no cellular retinol binding protein-1. Our results reinforce the notion of arterial SMC phenotypic heterogeneity and suggest that in our model, heterogeneity is controlled genetically and not by the local environment.


Key Words: {alpha}-smooth muscle actin • smooth muscle myosin • restenosis • intimal thickening • atherosclerosis




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