Wu Xiangjun, Lu Qinghua
Shandong University, Jinan, Shandong 250000, P.R. China.
Exp Ther Med. 2013 Jun;5(6):1671-1676. doi: 10.3892/etm.2013.1059. Epub 2013 Apr 9.
The aim of this study was to investigate changes in the expression of α-smooth muscle actin (α-SMA) and proliferating cell nuclear antigen (PCNA) in the vascular adventitia of balloon-injured rat aortas in the second and sixth postoperative weeks. A total of 32 rats were divided into a control group and a balloon-injured group. The rats underwent vascular morphometric analysis and adventitial cell counting, as well as immunohistochemical staining of α-SMA and PCNA in postoperative weeks 2 and 6 for observation of the expression of each immune parameter in the vascular adventitia and calculation of the number of PCNA-positive nuclei and the PCNA labeling index (PCNALI) in the vascular adventitia. The area and thickness of the adventitia, the number of nuclei and the PCNALI of the vascular adventitia were significantly increased in the injured group compared with the control group (P<0.05), while the external elastic lamina area (EELA), internal elastic lamina area (IELA) and lumen area (LA) were significantly decreased (P<0.05) in the second week. The area and thickness of the adventitia, the number of nuclei and the PCNALI of the vascular adventitia were significantly increased in the injured group compared with the control group (P<0.05), while the EELA, IELA and LA were significantly reduced (P<0.05) in the sixth week, and were significantly lower than those in the injured group in the second week (P<0.05). The positive expression levels of α-SMA and PCNA in the vascular adventitia were significantly reduced compared with those in the second week after injury. The vascular adventitial cells underwent proliferation and phenotypic switching and participated in vascular remodeling and vascular restenosis following balloon-induced injury. The vascular contractile remodeling in the injured group was more evident in the sixth week than in the second week, followed by a more aggravated vascular stenosis. Consequently, the vascular remodeling was one of the causes of vascular restenosis.
本研究旨在调查术后第二周和第六周时，球囊损伤大鼠主动脉血管外膜中α-平滑肌肌动蛋白（α-SMA）和增殖细胞核抗原（PCNA）表达的变化。总共32只大鼠被分为对照组和球囊损伤组。对大鼠进行血管形态计量分析和外膜细胞计数，并在术后第2周和第6周对α-SMA和PCNA进行免疫组织化学染色，以观察血管外膜中各免疫参数的表达情况，并计算血管外膜中PCNA阳性细胞核的数量和PCNA标记指数（PCNALI）。与对照组相比，损伤组外膜的面积和厚度、血管外膜细胞核数量和PCNALI显著增加（P<0.05），而在第二周时，外弹力膜面积（EELA）、内弹力膜面积（IELA）和管腔面积（LA）显著减小（P<0.05）。与对照组相比，损伤组外膜的面积和厚度、血管外膜细胞核数量和PCNALI显著增加（P<0.05），而在第六周时，EELA、IELA和LA显著减小（P<0.05），且显著低于损伤组第二周时的水平（P<0.05）。与损伤后第二周相比，血管外膜中α-SMA和PCNA的阳性表达水平显著降低。球囊损伤后，血管外膜细胞发生增殖和表型转换，参与血管重塑和血管再狭窄。损伤组血管收缩性重塑在第六周比第二周更明显，随后血管狭窄更严重。因此，血管重塑是血管再狭窄的原因之一。
