皮肤通过自修复使创面愈合是深二度皮肤烧伤临床救治的主要途径之一。业已表明，真皮层汗腺细胞在表皮层损伤自修复中具有重要作用，但其具体的作用机制尚待研究。我们前期研究证明汗腺细胞能在体外迅速分化为表皮角质细胞，并通过汗腺细胞和角质细胞RNA-Seq高通量分析以及损伤信号诱导汗腺细胞迁移实验，发现尿激酶型纤溶酶原激活剂受体（PLAUR）可能是汗腺细胞迁移的关键分子。据此推测汗腺细胞参与表皮损伤修复的过程可能是：损伤信号诱导汗腺细胞迁移至表皮层、汗腺细胞增殖、分化为角质细胞。本项目旨在通过建立体外和体内表皮损伤模型，从而验证汗腺细胞的迁移、增殖和修复能力，进一步明确PLAUR在汗腺细胞向表皮损伤部位迁移、修复中的作用及机制，同时分析PLAUR重组蛋白对小鼠表皮损伤的促进作用。综上所述，本项目所获的研究结果将为阐明自体细胞治疗表皮损伤的调控机制提供重要的理论依据，为皮肤损伤的救治提供新方法。

During the skin wound healing of deep second degree burns, self-repair is one of the main ways among all the clinical treatments. It has been shown that the sweat gland cells in the dermis plays an important role during self-healing of the epidermal regeneration, but the specific mechanism is not clear. Our previous studies have shown that sweat gland cells can rapidly differentiate into epidermal keratinocytes in vitro. RNA-Seq high-throughput analysis of sweat gland cells and epidermal keratinocytes together with results of damage signal inducing sweat gland cell migration experiment have shown plasminogen activator, urokinase receptor (PLAUR) may be the key molecule of sweat gland cell migration. Thus we assumed that the damage signal inducing sweat gland cells migrate to the skin epidermis where they proliferate and differentiate to keratinocytes. In this project, we are trying to establish damage model both in vitro and in vivo to confirm the migration, proliferation and repair ability of sweat gland cells, reveal the effect and mechanism of PLAUR on the sweat gland cells during their migration and participating in the skin repair, and analysis the effects of PLAUR recombinant protein in mice skin injury. The results of this project will clarify the regulatory mechanism of somatic treatment in skin damage providing important theoretical basis and new treatment method in skin regeneration.