血管内皮生长因子(VEGF)可促进内皮祖细胞（EPC）定向分化，再生内皮，是损伤血管修复的关键"效应"分子。我们及其他研究发现缝隙连接蛋白43（CX43）介导的细胞通讯与损伤血管修复关系密切，可调控EPC分化，是再生医学研究的新靶点。在预实验发现VEGF基因转染上调EPC CX43 mRNA及蛋白表达的基础上，本课题提出VEGF可通过Cx43介导的IP3/Ca2+、cAMP"直接对话"促进EPC分化，修复损伤血管的新观点。首先，我们拟评价VEGF/CX43对EPC间缝隙连接及其分化的影响；其次，评价IP3/Ca2+、cAMP在VEGF/CX43调控EPC分化中的作用及机制。最后，建立大鼠颈动脉损伤模型，局部过表达VEGF，观察归巢EPC CX43表达及其介导的缝隙连接对血管再内皮化及再狭窄的影响。本课题提出血管损伤修复的内在调控新机制，具有重要的科学研究价值。

Vascular endothelial growth factor(VEGF) is an important neovascularization factor ,which can promote endothelial progenitor cell(EPC) differentiatioin and reendothelialrization. We and others found connexin 43(CX43) could form intercellular connection and play a key role in reparing injured vessel by mediating cell differentiation. Furthermore, we detected upregulation of CX43 mRNA and protein after VEGF overexpression in EPC. Thus, VEGF might promote EPC differentiation and repair injured vessle by inter-EPC "talk" with "IP3/Ca2+,cAMP". First, we prepare to evaluate the effect of VEGF on CX43 expression and gap junction. Second, we plan to evaluate the effect and mechanism of IP3/Ca2+、cAMP flow on EPC differentiation. Third, after local overexpression of VEGF on injured carotid artery, we evaluate the effect of CX43 on EPC differentiation, gap junction, reendothelialrization and restenosis. Our study discuss the effect of CX43 on EPC differentiation which may reveal a new mechanism for repair of injured vessel.