ESCs的增殖和分化与瘢痕形成密切相关。文献和我们既往研究证实皮肤特异的miRNA203表达异常是导致ESCs增殖分化紊乱、瘢痕形成的重要原因，但调控机制不清楚。前期工作发现瘢痕形成中miRNA203可以激活Jagged1通路和下游基因Hes1的表达；采用靶基因预测和Pathway分析软件发现miRNA203的靶基因可能是Hes1，而Jagged1信号是其发挥作用的特异性通路；进一步生物信息学证实Hes1基因3’UTR存在miRNA203结合位点。因此，我们推测：创面愈合过程中miRNA203通过激活Jagged1信号通路并靶向下游Hes1基因调控ESCs增殖、分化，最终导致瘢痕形成。本课题将采用siRNA、GOF和LOF、蛋白印迹、质粒转染及构建转基因小鼠等技术，系统研究miRNA203-Jagged1-Hes1信号轴在瘢痕形成中的作用机制，为临床治疗瘢痕提供理论依据和新靶点。

The skin-specific miRNA203 regulates the proliferation and differentiation of epidermal stem cells (ESCs), which are critical for the formation of hypertrophic scar. However, the mechanism of miRNA203 in regulating hypertrophic scar formation is not clear. We previously found the miRNA203 can activate Jagged1 signaling and elevate Hes1 expression during the formation of hypertrophic scar. Moreover, Jagged1 and Hes1 are targets of miRNA203 indicated by Target Scan and Pathway bioinformatics prediction. . Thus, we proposed that the abnormal expression of miRNA203 affects Hes1 expression and Jagged1 signaling pathway, resulting in proliferation and differentiation disorders of ESCs during the formation of hypertrophic scar in wound healing. In this study, we will take some molecular biology techniques such as RT-PCR, western blotting, siRNA, immunofluorescence, GOF (gain-of-function)/LOF (loss-of-function) strategies of transfection, and transgenic mice model by microinjection to acquire evidence of miRNA203-Jagged1-Hes1 on the regulation of epidermal stem cells (ESCs) proliferation and differentiation during the formation of hypertrophic scar in vivo and vitro. The work is likely to lead to clarify the mechanism of miRNA203-Jagged1-Hes1 on ESCs proliferation and differentiation and the formation of hypertrophic scar and provide the theoretical basis and new therapeutic targets for the treatment of hypertrophic scar.