Author + information
- Lu Wei and
- Lan Huang
Caveolin-1(cav-1) is the major coat protein responsible for caveolae assembly, regulating signaling via protein-protein interactions with resident caveolar proteins, but its biological mechanism in vascular smooth muscle cells (VSMCs) is still unclear. The aim of this study was to evaluate the role of cav-1 on VSMCs proliferation and the neointimal formation in balloon injured rat carotid artery.
Left common carotid arteries from Sprague-Dawley rats were injured by a balloon catheter, and the injured arteries were incubated with 30 μL solution of Ad-cav-1 adenoviral vectors, Ad-GFP adenoviral vectors or PBS for 30 min. The rats were euthanized for morphometric and immunohistochemical analysis, real-time PCR and western blot analysis at 2 weeks after balloon injury and gene transfer. The cultured rat VSMCs transduced with Ad-cav-1 or Ad-GFP adenoviral vectors were used for cell proliferation assay, real-time PCR and western blot analysis. The vascular or intracellular ROS level was also detected.
Adenoviral vectors encoding cav-1 cDNA could increase cav-1 expression both in mRNA and protein levels in balloon injured artery walls and cultured rat VSMCs. Upregulation of cav-1 significantly suppressed VSMCs proliferation and intimal formation. Over-expression of cav-1 could reduce vascular or intracellular ROS level and decrease the phosphorylation of the ERK1/2 in balloon injured artery walls and cultured rat VSMCs.
Our study suggests that over-expression of cav-1 significantly suppresses VSMCs proliferation and progression of neointimal formation after vascular injury.