Published online before print August 7, 2003, doi: 10.1161/01.ATV.0000090130.85752.ED
© 2003 American Heart Association, Inc.
Brief Reviews |
Arterial Smooth Muscle Cell Heterogeneity
Implications for Atherosclerosis and Restenosis Development
From the Department of Pathology, University of Geneva–CMU, Geneva, Switzerland.
Correspondence to Dr Marie-Luce Bochaton-Piallat, University of Geneva–CMU, Department of Pathology, 1 rue Michel-Servet, 1211 Geneva 4, Switzerland. E-mail Marie-Luce.Piallat{at}medecine.unige.ch
Series Editor:: Giulio Gabbiani
ATVB in Focus Smooth Muscle Cells
Previous Brief Reviews in this Series:
•Hillebrands J-L, Klatter FA, Rozing J. Origin of vascular smooth muscle cells and the role of circulating stem cells in transplant arteriosclerosis. 2003;23:380–387.
•Iso T, Hamamori Y, Kedes L. Notch signaling in vascular development. 2003;23:543–553.
•Kumar MS, Owens GK. Combinatorial control of smooth muscle-specific gene expression. 2003;23:737–747.
•Schaper W, Scholz D. Factors regulating arteriogenesis. 2003;23:1143–1151.
During atheromatous plaque formation or restenosis after angioplasty, smooth muscle cells (SMCs) migrate from the media toward the intima, where they proliferate and undergo phenotypic changes. The mechanisms that regulate these phenomena and, in particular, the phenotypic modulation of intimal SMCs have been the subject of numerous studies and much debate during recent years. One view is that any SMCs present in the media could undergo phenotypic modulation. Alternatively, the seminal observation of Benditt and Benditt that human atheromatous plaques have the features of a monoclonal or an oligoclonal lesion has led to the hypothesis that a predisposed, medial SMC subpopulation could play a crucial role in the production of intimal thickening. The presence of a distinct SMC population in the arterial wall implies that under normal conditions, SMCs are phenotypically heterogeneous. The concept of SMC heterogeneity is gaining wider acceptance, as shown by the increasing number of publications on this subject. In this review, we discuss the in vitro studies that demonstrate the presence of distinct SMC subpopulations in arteries of various species, including humans. Their specific features and their regulation will be highlighted. Finally, the relevance of an atheroma-prone phenotype to intimal thickening formation will be discussed.
Key Words: smooth muscle cell • heterogeneity
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