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(Circulation Research. 2006;98:448.)
© 2006 American Heart Association, Inc.

Editorials

Smooth Muscle Cell

A Key Cell for Plaque Vulnerability Regulation?

Marie-Luce Bochaton-Piallat, Giulio Gabbiani

From the Department of Pathology and Immunology, CMU-University of Geneva.

Correspondence to Professor Giulio Gabbiani, Department of Pathology and Immunology, CMU, University of Geneva, Rue Michel-Servet 1, 1211 Geneva 4., Switzerland. E-mail Giulio.Gabbiani@medecine.unige.ch

See related article, pages 472–479

Key Words: MHC II • CIITA • collagen • -smooth muscle actin • myofibroblast

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The concept that the atheromatous plaque undergoes a complex inflammatory and fibroproliferative process, which is likely responsible for the onset of complications,¹ and the notion of vulnerable plaque² have acquired wide acceptance during the last years. The crucial participation in these events of inflammatory and immunocompetent cells has been demonstrated,¹ however the mechanisms through which these cells exert their noxious activities still remain a matter of investigation. Changes of the extracellular matrix have also been suggested to be at the origin of plaque vulnerability,³ mainly because of local production of proteolytic enzymes. Much less studied are plaque changes involving: (1) the modulation of smooth muscle cells (SMCs) toward the myofibroblastic phenotype and (2) the remodeling of extracellular matrix including tissue deformations typical of granulation tissue; these changes are a landmark of chronic inflammation in various organs undergoing fibrotic changes, where myofibroblasts represent a large proportion of the cellular population.⁴ Myofibroblasts become capable of generating contractile forces thanks to the neoexpression of -smooth muscle (SM) actin, the actin isoform typical of vascular SMCs; in addition they produce collagen and proteolytic enzymes. In general myofibroblasts originate from local fibroblasts; their more sporadic derivation from local SMCs,⁵ local epithelial cells (through epithelial/mesenchymal transition),⁶ or circulating mononuclear cells⁷ has been recently documented during several pathological settings. Fibroblast/myofibroblast modulation is essentially regulated, in addition to mechanical forces, by transforming growth factor-ß1 (TGF-ß1) produced locally by macrophages and eventually fibroblastic cells; TGF-ß1 has been shown to stimulate the synthesis of -SM actin and collagen type I . . . [Full Text of this Article]

Related Article:

Interferon- Induces Major Histocompatibility Class II Transactivator (CIITA), Which Mediates Collagen Repression and Major Histocompatibility Class II Activation by Human Aortic Smooth Muscle Cells

Giovanna Butticè, Janice Miller, Lin Wang, and Barbara D. Smith
Circ. Res. 2006 98: 472-479. [Abstract] [Full Text] [PDF]