创面是临床常见病症，血管新生是创面修复最重要环节之一，但其机理仍不完全清楚。研究证实，血管基底膜（VBM）降解及血管内皮细胞（VEC）迁移是创面血管新生过程中最关键的步骤。在上一基金基础上，我们初步发现，P311可能在创面血管新生中起着重要作用，结合文献，我们提出“创面低氧等调节P311-P311调节基质金蛋白酶（MMPs）促进VBM降解、P311调节VEGFR2，并通过PI3K/RhoGTP酶促进VEC迁移，最终促进血管新生”的假说。本课题拟通过体内外实验，应用分子与细胞生物学、生物信息学、敲基因动物等技术与手段，从P311促进创面血管新生、 P311通过PI3K/RhoGTP酶调控MMPs、 P311调控VEGR2的机制、P311通过VEGFR2/PI3K/RhoGTPase促进VEC迁移、创面低氧等通过NF-κB调控 P311表达等方面的研究，以验证我们这一假说并丰富创面愈合理论。

Skin wound is a common but important clinical issue, till to now the mechanism of wound healing has not yet been clear completely. Angiogenesis is considered as one of the fundamental procedures in wound healing. It was proved that enzymolysis of vascular basal membrane and the migration of vascular endothelial cell are the most two crucial steps in angiogenesis. Our primary experiments found that P311 plays a vital role in angiogenesis during wound healing. Based on our own recent and other researchers’ results, we presume that the expression of P311 is increased by ischemia and other factors in the wound microenvironment initially, which enhances enzymolysis of vascular basal membrane via regulation of MMPs and facilitates the vascular endothelial cells migration via modulating VEGFR2/ PIK3/Rho GTPase pathway. Consequentially, P311 promotes angiogenesis and wound healing. This item will focus to verify the above hypothesis by in vivo and in vitro experiments through knockout animal, siRNA and other molecular and cellular biological techniques. This project will amend the theory of wound healing and provide a new clue and target to promote wound healing.