SM22α Modulates Vascular Smooth Muscle Cell Phenotype During Atherogenesis

  • Susanne Feil
    From the Institut für Pharmakologie und Toxikologie, Technische Universität, München, Germany.
  • Franz Hofmann
    From the Institut für Pharmakologie und Toxikologie, Technische Universität, München, Germany.
  • Robert Feil
    From the Institut für Pharmakologie und Toxikologie, Technische Universität, München, Germany.

抄録

<jats:p>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 SM22α, an SMC-specific cytoskeletal protein of unknown function, in the development of atherosclerosis. In hypercholesterolemic ApoE-deficient mice, genetic ablation of SM22α resulted in increased atherosclerotic lesion area and a higher proportion of proliferating SMC-derived plaque cells. These results identify a role for SM22α in the regulation of SMC phenotype during atherogenesis.</jats:p>

収録刊行物

  • Circulation Research

    Circulation Research 94 (7), 863-865, 2004-04-16

    Ovid Technologies (Wolters Kluwer Health)

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