胸主动脉夹层血管平滑肌细胞的表型转化研究

Investigation the role of phenotype transformation of vascular smooth muscle cell in thoracic aortic dissection

目的探讨血管平滑肌细胞(VSMC)表型转化及其在胸主动脉夹层(TAD)形成中的作用。方法选取TAD术中切除的升主动脉壁组织标本15例(TAD组),尸检者的正常胸主动脉壁组织标本10例作为对照(NA组),苏木精-伊红染色(H-E)和维多利亚蓝染色(VB)分别检测主动脉壁的一般情况及弹力纤维的含量。利用Western Blot技术,检测α-肌动蛋白(α-SMA)、肌动蛋白相关蛋白SM22α以及骨桥蛋白(OPN)在组织中的表达差异。结果与NA组比较,TAD组中VSMC收缩型标志物α-SMA、SM22α的表达明显下调(P<0.05);而合成型标志物OPN的表达显著上调(P<0.05)。组织学结果显示TAD组标本平滑肌弹力蛋白断裂,减少甚至部分消失,外膜胶原纤维增生。结论 TAD中VSMC以合成型为主;合成型平滑肌细胞增多可能导致了胶原分泌增加,参与了主动脉壁的损伤重塑过程,促进TAD的形成和发展。

Objective To investigate the role of the phenotype transformation of vascular smooth muscle cells (VSMC) in thoracic aortic dissection (TAD). Methods TAD specimens were taken from 15 patients with TAD during surgical intervention, and 10 control specimens were obtained from patients who were undergone the autopsy. H-E and VB trichrome staining were performed to evaluate VSMC arrangement and elastic fiber content. Western Blot was used to invalidate the expression of α-SMA、SM22 α and OPN. Results Compared with controls, the protein expression levels of α-SMA、SM22 α in TAD significantly decreased (P < 0.05), while the OPN were increased(P < 0.05). Histology and immunohistochemistry results showed degradation of elastin and disordered arrangement of VSMC in TAD. Conclusions Phenotype change of VSMC increased elastieity secretion in the media which involved aortic wall remodeling and promoted aortic dissection.