在深II°烧伤创面愈合中皮肤成纤维细胞起主要作用。前期发现Lin28A可促进热损伤后HSF的增殖、迁移及细胞外基质（ECM）合成，加速创面愈合。鉴于TGF-β是HSF增殖、迁移、合成ECM等作用发挥的强效趋化因子，故推测Lin28A与TGF-β信号通路之间存在内在联系。结合非编码RNA芯片、生物信息学预测和实验佐证，发现长链非编码RNA-HAGLR（HOXD-AS1）在热损伤HSF中的时空表达及促进作用与Lin28A呈现相同趋势，且HAGLR可与miR-19a竞争性结合从而影响TGF-β通路及其下游靶基因的表达。故本项目拟以热损伤HSF模型和SD大鼠深II°损伤模型为研究对象，采用慢病毒包装转染、荧光素酶报告实验、WB、PCR、RNA结合免疫沉淀等方法明确Lin28A/lncRNA-HAGLR/miR-19a介导TGF-β在促进热损伤HSF转归的机制，为烧伤临床治疗提供新的潜在靶点和方向。

Human skin fibroblasts (HSF) are the main cells involved in wound repair and denatured dermis could be treated with HSF cells function getting recovery. Our previous studies showed that Lin28A was involved in the regulation of proliferation, migration and ECM synthesis of HSF cells after thermal denatured. However, the mechanism of Lin28A is still not clear. For TGF-β signaling pathway plays an important role in cells proliferation, migration, differentiation and apoptosis, it provides a new way to elucidate the mechanism of wound healing in thermal injury for the connection between Lin28A and TGF-β. Combined with high-throughput chip, bioinformatics analysis and experimental evidence, lncRNA-HAGLR （HOXD-AS1）exhibited similar effects on wound healing as well as Lin28A, and affected TGF-βR2 expression through interacting with miR-19a-3p as a competitive endogenous RNA (ceRNA). As a result, we hypothesis that lncRNA-HAGLR（HOXD-AS1） can directly bind to Lin28A and serve as a competitive endogenous RNA (ceRNA) for miR-19a-3p to inhibit its expression and up-regulate downstream target TGF-βR2 expression, finally modulating the recovery of HSF cells after thermal denatured. In this study, we are firstly intended to develop a thermal denatured cells model and SD rat burns model, and then attempted to investigate the potential mechanism of Lin28A and lncRNA-HAGLR mediated TGF-β signaling pathway in thermal injury. It provides new potential targets and ideas for burns treatment.