SM22α modulates vascular smooth muscle cell phenotype during atherogenesis
SM22α modulates vascular smooth muscle cell phenotype during atherogenesis
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DOI：
10.1161/01.res.0000126417.38728.f6
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发表时间：
2004-04-16
影响因子：
20.1
通讯作者：
Feil, R
中科院分区：
文献类型：
--
作者：
Feil, S;Hofmann, F;Feil, R
在血管疾病中，细胞骨架蛋白在调节血管平滑肌细胞（SMC）表型中的功能知之甚少。在这份报告中，我们在小鼠中使用基因靶向和Cre/lox介导的细胞命运作图相结合的方法来研究SM 22 α（一种功能未知的SMC特异性细胞骨架蛋白）在动脉粥样硬化发展中的作用。在高胆固醇血症ApoE缺陷小鼠中，SM 22 α基因消融导致动脉粥样硬化病变面积增加和SMC衍生斑块细胞增殖比例升高。这些结果确定了SM 22 α在动脉粥样硬化形成过程中对SMC表型的调节作用。
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 SM22alpha, an SMC-specific cytoskeletal protein of unknown function, in the development of atherosclerosis. In hypercholesterolemic ApoE-deficient mice, genetic ablation of SM22alpha resulted in increased atherosclerotic lesion area and a higher proportion of proliferating SMC-derived plaque cells. These results identify a role for SM22alpha in the regulation of SMC phenotype during atherogenesis.