血管内皮损伤后平滑肌细胞增殖和迁移是新生内膜增生发生发展的重要过程。p300/CBP相关因子（PCAF）是一种转录辅激活子，具有组蛋白乙酰基转移酶活性，参与细胞分化、凋亡和肿瘤发生等过程。目前对于PCAF是否参与血管损伤后新生内膜增生和再内皮化尚无报道。本课题组前期实验表明，PCAF与血管平滑肌细胞增殖和迁移以及血管损伤后新生内膜增生有关。在此基础上，本项目拟通过上调和下调PCAF表达，采用组织化学和分子生物学等技术，在离体细胞和整体动物两个水平探讨：（1）PCAF对血管平滑肌细胞增殖、迁移及表型转化的作用及其分子机制；（2）PCAF对内皮细胞生物学功能的影响及其分子机制；（3）PCAF对血管新生内膜增生和血管损伤后再内皮化的影响及其机制。力图阐明PCAF对血管损伤后内膜新生和再内皮化的根本机制，为防治内膜增生相关疾病提供新的分子靶点。

The proliferation and migration of vascular smooth muscle cells after endothelial injury are the pivotal process for the initiation and development of vascular neointimal hyperplasia. p300/CBP-associated factor (PCAF), a transcriptional coactivator with histone acetyltransferase activity, is involved in the cell differentiation, apoptosis and tumorigenesis. However, the roles of PCAF in vascular neointimal hyperplasia and re-endothelialization post injury are unknown. Our previous data showed that PCAF participated in the proliferation and migration of vascular smooth muscle cells and neointimal hyperplasia after vascular injury. Hence, the present project will up-regulate and down-regulate the expression of PCAF, with immunohistochemistry and molecular biological technologies, to explore (1) the effect and related molecular mechanism of PCAF on proliferation, migration and phenotypic switching of vascular smooth muscle cells in vitro; (2) the effect and related molecular mechanism of PCAF on biological function of vascular endothelial cells in vitro; (3) the effect and related molecular mechanism of PCAF on vascular neointimal formation and re-endothelialization post injury in an animal model. The project will further elucidate the molecular mechanism of PCAF on vascular neointimal formation and re-endothelialization after vascular injury, and PCAF could be a therapeutic target for the prevention and treatment of neointimal hyperplasia-related vascular disease.