Smooth muscle 22 alpha maintains the differentiated phenotype of vascular smooth muscle cells, by inducing filamentous actin bundling
Smooth muscle 22 alpha maintains the differentiated phenotype of vascular smooth muscle cells, by inducing filamentous actin bundling
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平滑肌 22 α 通过诱导丝状肌动蛋白成束来维持血管平滑肌细胞的分化表型
DOI：
10.1016/j.lfs.2008.11.017
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发表时间：
2009-03-27
期刊：
影响因子：
6.1
通讯作者：
Cheng, Yunhui
中科院分区：
文献类型：
--
作者：
Han, Mei;Dong, Li-Hua;Cheng, Yunhui
目的：平滑肌22 α（SM22 α）不是平滑肌细胞（SMC）发育和基础稳态功能所必需的。然而，最近的一项研究表明，SM22 α在抑制血管平滑肌细胞（VSMC）从收缩细胞到合成/增殖细胞的表型调节中起作用。本研究探讨了SM22 α介导的维持VSMCs收缩表型的机制。主要方法：采用血清剥夺48 - 72 h诱导合成SMCs再分化。分别构建了含大鼠SM22 α全长cDNA的表达质粒和表达SM22 α反义转录本的载体。免疫共沉淀、共沉淀和免疫荧光分析表明，SM22 α与F-actin直接相互作用，并与F-actin共定位，参与了分化的VSMCs肌动蛋白骨架的组装。SM22 α促进肌动蛋白丝组装成束。通过SM 22 α反义RNA阻断SM 22 α表达导致肌动蛋白丝变细和分散。意义：SM22 α诱导的F-actin成束增强了VSMCs的收缩性和运动性，SM22 α的活性是维持VSMCs分化表型所必需的。(C)2008年由Elsevier Inc.出版
Aim: Smooth muscle 22 alpha (SM22 alpha) is not required for the development and basal homeostatic function of smooth muscle cells (SMCs). However, a recent study demonstrated that SM22 alpha plays a role in inhibiting the phenotypic modulation of vascular SMCs (VSMCs) from contractile to synthetic/proliferative cells. The present study investigated the mechanism underlying the SM22 alpha-mediated maintenance of the contractile phenotype of VSMCs.Main methods: The redifferentiation of synthetic SMCs was induced by serum deprivation for 48-72 h. The expression plasmids containing full-length cDNA of rat SM22 alpha and a vector expressing SM22 alpha antisense transcripts were constructed, respectively. Coimmunoprecipitation, cosedimentation assay and immunofluorescence analyses were used to detect the interaction of SM22 alpha with F-actin.Key findings: The results revealed that SM22 alpha directly interacted and colocalized with F-actin and thus participated in the organization of the actin cytoskeleton in differentiated VSMCs. SM22 alpha facilitated the assembly of actin filaments into bundles. The blockade of SM22 alpha expression by SM22 alpha antisense RNA led to the thinning and dispersion of actin filaments. Consequently, the ratio of F-actin to globular (G)-actin was reduced, and the cell contractility was lost.Significance: The SM22 alpha-induced F-actin bundling enhances the contractility and mobility of VSMCs, and the activity of SM22 alpha is necessary for maintaining the differentiated phenotype of VSMCs. (C) 2008 Published by Elsevier Inc.