Published online before print March 25, 2004, doi: 10.1161/01.RES.0000126417.38728.F6
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Submitted on January 12, 2004
Revised on March 4, 2004
Accepted on March 11, 2004
SM22
Modulates Vascular Smooth Muscle Cell Phenotype During Atherogenesis
Susanne Feil ;
From the Institut für Pharmakologie und Toxikologie, Technische Universität, München, Germany.
* To whom correspondence should be addressed. E-mail: feil{at}ipt.med.tu-muenchen.de.
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.
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