收缩蛋白在血管新生内膜形成过程中的表达变化及其对血管收缩力的影响  

Changes of contractile protein expression and its effect on vessel contraction during neointimal formation

作　　者：程云会[1] 韩梅[1] 温进坤[1] 张永刚[1] 

机构地区：[1]河北医科大学基础医学研究所

出　　处：《中国病理生理杂志》2005年第11期2111-2115,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30270499;30472167);河北省自然科学基金资助项目(No.303454)

摘　　要：目的为了探讨两种收缩蛋白SMα-actin和SM22α在新生内膜形成过程中的表达变化及与血管收缩反应性之间的关系。方法在建立大鼠颈总-胸腹主动脉血管内皮剥脱后内皮增生模型的基础上,用Western blot和免疫组化检测两种收缩蛋白的动态变化,用透射电镜观察VSMC肌丝和用生物法测定血管收缩反应性。结果血管内皮剥脱后,中膜SMα-actin和SM22α的表达下降,以术后7-14d最低,VSMC内肌丝由致密变为稀疏,由束状变为网状,但是血管的收缩反应性显著高于对照组(P<0.05)。结论内皮剥脱后,VSMC的增生及新生内膜的增厚可引起受损血管收缩反应性的升高,这是内皮损伤促发动脉硬化的重要原因。AIM： To determine the relationship between the changes of SM α- actin and SM22α expression and vascular tone. METHODS： The expression of SM α- actin and SM22α during restenosis after de - endothelialization were detected by Western blotting and immunohistochemistry. The structure of myofilaments was observed by transmission electron microscopy. The vascular contraction induced by phenylephrine was measured by a force transducer. RESULTS： The levels of SM α - actin and SM22α expression in vascualar wall declined after de - endothelialization. The myofilaments in VSMC were modulated from well arranged and dense bundles to discrete network. However, the vascular tone and reactivity to agonist were much higher than that in control （ P 〈 0.05）. CONCLUSION： After de - endothelialization, the increased contractility caused by VSMC proliferation and intimal thickening plays a key role in arteriosclerosis.

关 键 词：血管收缩 肌动蛋白类 内皮 血管 

分 类 号：Q754[生物学—分子生物学]