Expression and significance of α-SMA and PCNA in the vascular adventitia of balloon-injured rat aorta

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.