人腹主动脉瘤平滑肌细胞表型变化

目的:研究腹主动脉瘤(AAA)中血管平滑肌细胞(VSMC)表型改变,探讨其在AAA发病中的作用。方法:选取人体AAA、动脉闭塞性疾病(AOD)和正常腹主动脉(NA)组织,采用α-肌动蛋白(α-SMA)、结蛋白(desmin)及肌球蛋白重链3种表型(SM1、SM2和SMemb)单克隆抗体,利用免疫组化及电镜技术,检测VSMC收缩型与合成型。结果:AOD及NA中VSMC以收缩表型α-SMA、desmin、SM1和SM2表达为主,SMemb在AOD的表达较低,而在NA无表达。AAA中VSMC以合成表型SMemb为主,α-SMA、SM1和SM2明显低于AOD及NA,desmin不表达;其中破裂者的SMemb和SM2低于非破裂者。结论:VSMC表型变化参与腹主动脉壁损伤重构,促进AAA形成和发展。

Phenotypic changes of vascular smooth muscle cells in human abdominal aortic aneurysms

AIM:To study phenotypic changes of vascular smooth muscle cells (VSMC) in abdominal aortic aneurysmal (AAA) pathogenesis.METHODS: Tissue samples of human infrarenal aneurysmal and normal aorta(NA), and arterial occlusive diseases(AOD) were evaluated. Monoclonic antibodies of α-smooth muscle actin(α-SMA), desmin and smooth muscle myosin heavy chain isoforms (SM1, SM2 and SMemb) were used in immunohistochemistry to determine VSMC isoforms. Immunohistochemical results were analyzed with the use of computer-generated image technique. Ultrstructures of VSMC in three tissues above were observed by electron microscope. RESULTS:In control AOD and NA, VSMC in the media were strongly immunostained for α-SMA, desmin, SM1 and SM2. Immunoreactivity for SMemb was faint or weakly positive in AOD, but negative in NA. In AAA,the balance shifts to SMemb predominance with suppressed α-SMA, SM1 and SM2 and negative desmin, while in ruptured aneurysmal walls, the expression of SM2 and SMemb were decreased compared with the non-ruptured aneurysmal walls.CONCLUSION:Phenotypic changes of VSMC are concerned with abdominal aortic structure lesion and remodeling, which contributes to AAA formation and development.