毛囊黑素干细胞是毛囊和表皮黑素细胞的干细胞来源，也是白癜风治疗的黑素细胞库。激活黑素干细胞并促进其移行至脱色斑区，是白癜风治疗的重要策略之一。本研究以前期工作建立的永生化的黑素干细胞为体外模型，筛选发现Wnt3a等经典wnt蛋白具有促黑素干细胞分化的能力，而sFRP4可有效拮抗Wnt3a诱导的黑素干细胞分化，我们推测sFRP4通过阻断经典Wnt信号途径抑制黑素干细胞分化。本研究首先以永生化的黑素干细胞为体外模型，以DCT-LacZ转基因小鼠为体内模型，观察sFRP4抑制黑素干细胞分化的能力；然后，从分子水平阐明sFRP4对Wnt3a诱导黑素干细胞分化的拮抗作用及其分子机制，并在体内水平进行验证。研究结果可进一步揭开调控黑素干细胞分化的信号转导网络，为临床有效治疗各种色素减退性疾病提供重要的理论依据和治疗靶点

Hair follicle melanocyte stem cells are stem cell source of hair follicle and epidermis melanocytes, and also they are cell repository for vitiligo therapy. Activating melanocyte stem cells and promoting them to migrate into demelanized area is one of the most important strategies for vitiligo therapy. Based on our previous studies, we speculate that sFRP4 could inhibit differentiation of melanocyte stem cells through blocking canonical Wnt signaling pathway. In this study, based on our established immortalized melanocyte stem cells in vitro and DCT-LacZ transgenic mice in vivo, the capacity of sFRP4 to inhibit differentiation of melanocyte stem cells is to be determined. Then, the antagonism between sFRP4 and Wnt3a-induced melanocyte stem cells differentiation, the inhibitions of sFRP4 to Wnt3a/β-catenin signaling pathways are also to be illuminated in molecular and cellular levels. Lastly, we will also work out the antagonism between sFRP4 and Wnt3a-induced melanocyte stem cells differentiation in an in vivo level. Our potential findings would further reveal the signaling transduction network in regulating melanocyte stem cell differentiation, and provide important theoretical basis and therapeutic target for treatment of various depigmented diseases clinically.