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.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
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)
关键词
血管收缩
肌动蛋白类
内皮
血管
Vasoconstriction
Actins
Endothelium, vascular