皮肤创面修复是临床上亟需解决的难题之一。皮肤创面修复过程需要多种活动细胞的参与，其中成纤维细胞的迁移对皮肤创面修复具有重要意义。bFGF促成纤维细胞迁移的作用已经明确，但其调控机制尚不清楚。前期RNA深度测序及生物信息学分析结果表明，Wnt信号通路关键基因在bFGF刺激下有显著性变化。细胞迁移实验结果显示，LiCl刺激 (GSK3β抑制剂，激活Wnt信号通路) 促细胞迁移，相反IWR-1刺激 (Wnt信号通路抑制剂) 抑制细胞迁移。而且bFGF处理上调GSK3β磷酸化及核内的β-catenin水平，提示bFGF可能通过调节GSK3β磷酸化水平，抑制GSK3β活性，降低β-catenin降解，促细胞迁移。本课题旨在前期研究基础上进一步探索bFGF调控GSK3β磷酸化的机制及β-catenin在细胞迁移过程中的作用。本项研究结果不仅能在理论上指导临床，而且可以为开发皮肤创面修复药物提供新靶点。

Skin wound healing has become one of the difficulties in clinical therapy. Skin wound healing is a complex process that requires action of many cell types, and fibroblast cell migration plays important role in skin wound closure. Efficacy of bFGF on fibroblast cell migration is well known, however, the underlying mechanism by which bFGF regulates cell migration remains unclear. RNA-deep sequencing and bioinformatics analyses against the bFGF-stimulated human foreskin fibroblast cells identified that the Wnt canonical pathway genes are significantly altered upon bFGF stimulation. In addition, application of LiCl and IWR-1, typical inhibitors of GSK3β and Wnt pathway respectively, promoted and inhibited cell migration. Also, bFGF treatment accumulated more phospho-GSK3β and nuclear β-catenin. Therefore, it suggests that bFGF may modulate GSK3β phosphorylation to reduce the GSK3β activity, which may results in reduction of β-catenin degradation. The objective of this project is to understand the regulatory mechanism of bFGF-mediated GSK3β phosphorylation and the role of β-catenin in cell migration process. This study will provide a theoretical basis for bFGF medication and new targets for drug that skin repairs wound.