糖尿病患者伤口出现愈合不良，经常变成慢性而难以愈合的溃疡。内皮祖细胞（EPCs）具有修复伤口的作用，糖尿病存在EPCs功能受损，但目前为止受损机制尚不明了。前期结果显示在高糖培养的EPC细胞hnRNPA1表达增加，其外泌体（exosome）miR-363也增多，EPCs源性外泌体抑制成纤维细胞和微血管内皮细胞增殖和迁移，而加入anti-miR-363后逆转这一作用。故我们推测高糖环境下hnRNPA1的上调，外泌体miR-363增多，并将miR-363传递给伤口周围的效应细胞是抑制EPCs对伤口修复能力的原因之一。本项目拟探讨高糖条件下hnRNPA1组装miR-363入外泌体的分子机制及其作用。并利用小鼠全层皮肤外伤模型评估EPCs源性外泌体包裹的miR-363对伤口愈合的功效，揭示miR-363装载入外泌体的使动环节，为糖尿病伤口愈合的临床治疗提供理论依据。

The wounds of diabetes patients heal poorly and often become chronic ulcers and difficult to heal. Endothelial progenitor cells (EPC) have the function of impaired wounds while the effect disappears in diabetes. Previous results showed that the expression of hnRNPA1 was increased in EPC under high glucose environment，and miR-363 was up-regulated in EPCs exosomes. Overexpression of anti-miR-363 could reverse the inhibition roles of proliferation and migration derived from EPCs-Exo in fibroblasts and endothelial cells. Therefore, we hypothesized that high expression of hnRNPA1 selectively packaged of miR-363 into exosomes under high glucose environment, then transfer miR-363 to the adaptor cells around the wound, which was partly responsible for the decline ability of EPCs to repair wounds. This project intends to explore the molecular mechanism of hnRNPA1 promotes the packaging of miR-363 into exosomes under high glucose conditions and clarify the biological role of EPC-Exos in regulating fibroblasts and endothelial cells, and the full-thickness skin wounds of mice models were used to evaluate the efficacy of EPC-Exos-miR-363 on wound healing. The study will reveal the initial event of the packaging of miR-363 into exosomes and provide a new target for the treatment of wounds healing in diabetes.