【摘要】 SM2 2α(smoothmuscle 2 2alpha,SM2 2α)是血管平滑肌细胞 (vascularsmoothmusclecells,VSMC)的标志蛋白 ,为了探讨该蛋白与VSMC表型和功能的关系 ,利用血清饥饿法诱导VSMC由合成型向收缩型转变 ,用RT PCR对不同表型VSMC的SM2 2α表达活性进行检测 ,并通过转染反义SM2 2α表达载体 ,观察SM2 2α表达对VSMC细胞骨架和收缩功能的影响。结果显示 ,在VSMC由合成型逆转为收缩型的过程中 ,SM2 2α和平滑肌α 肌动蛋白 (smoothmuscleα actin,SMα actin)的表达分别被显著诱导和轻度上调 ,与此同时 ,细胞骨架由稀疏的网格状变成均匀、致密的束状 ,VSMC重新获得收缩功能。用反义SM2 2α抑制该基因表达后 ,血清饥饿诱导的VSMC细胞骨架重构受阻 ,乙酰胆碱刺激引发的细胞收缩消失。结果提示 ,SM2 2α参与VSMC细胞骨架的构成及调节细胞的收缩功能 ,对维持VSMC处于收缩表型具有重要作用更多还原

【Abstract】 The expression pattern of SM22α gene and it’s effects on VSMC cytoskeleton and contraction were investigated during synthetic VSMC reversion to contractile phenotype induced by serum free culture. The results suggested that the expression of SM22α was induced quickly after serum starvation and maintained at higher levels, and the cytoskeletal structure was remodulated from discrete network to well arranged and dense bundles. At same time, acetylcholine (ACh) induced contractility was observed in the serum starved VSMC. However, after VSMC was transfected by antisense SM22α recombinant plasmid, reorganization of cytoskeleton by serum starvation was blocked, and ACh induced contraction was absent. The results demonstrated that SM22α was involved in VSMC cytoskeleton reorganization and played a key role for VSMC remaining contractile phenotype.更多还原