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(Circulation Research. 2004;94:863.)
© 2004 American Heart Association, Inc.

Report

SM22 Modulates Vascular Smooth Muscle Cell Phenotype During Atherogenesis

Susanne Feil, Franz Hofmann, Robert Feil

From the Institut für Pharmakologie und Toxikologie, Technische Universität, München, Germany.

Correspondence to Robert Feil, Institut für Pharmakologie und Toxikologie, Technische Universität, Biedersteiner Str. 29, 80802 München, Germany. E-mail feil{at}ipt.med.tu-muenchen.de

Abstract

The function of cytoskeletal proteins in the modulation of vascular smooth muscle cell (SMC) phenotype during vascular disease is poorly understood. In this report, we used a combination of gene targeting and Cre/lox-mediated cell fate mapping in mice to investigate the role of SM22, an SMC-specific cytoskeletal protein of unknown function, in the development of atherosclerosis. In hypercholesterolemic ApoE-deficient mice, genetic ablation of SM22 resulted in increased atherosclerotic lesion area and a higher proportion of proliferating SMC-derived plaque cells. These results identify a role for SM22 in the regulation of SMC phenotype during atherogenesis.

Key Words: mouse • vascular remodeling • phenotypic modulation • Cre recombinase • fate mapping

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