皮肤创面修复是临床亟待解决的难题之一。创面修复过程复杂，其中成纤维细胞迁移增殖对皮肤创面修复具有重要意义。bFGF促成纤维细胞迁移增殖作用已明确，但其调控机制尚不清楚。前期研究发现，bFGF能上调CK2α和α-catenin蛋白表达及α-catenin的磷酸化，而α-catenin磷酸化能抑制其自身降解。同时，抑制CK2α或干扰α-catenin都明显减缓细胞迁移。干扰α-catenin后细胞核中的β-catenin明显减少，且转录组学技术进一步证实核内β-catenin转录调控的下游基因与细胞迁移增殖息息相关。因此，本项目旨在前期研究基础上，深入探究受bFGF调控的CK2α、α-catenin和β-catenin对细胞迁移增殖和创伤愈合的影响及它们之间的相互作用关系，并确证受β-catenin转录调控的下游基因与细胞迁移增殖的关系。本项目将为开发皮肤创面修复药物提供新理论依据。

Skin wound repair is one of the difficulties in clinical therapy. Skin wound repair is a complex process in which fibroblast migration/proliferation is of great significance. Efficacy of bFGF on fibroblast migration/proliferation is well known, however, the underlying mechanism by which bFGF regulates cell migration/proliferation remains unclear. Previous studies revealed that bFGF upregulated the protein level of CK2α and α-catenin and the phosphorylation level of α-catenin, while the phosphorylated α-catenin could inhibit its degradation. Meanwhile, we had already observed that the rate of cell migration was retarded by CK2α inhibitor or α-catenin silence. And interference of α-catenin induced the decrease of nuclear β-catenin. Further through transcriptome analyses, we also had confirmed that nuclear β-catenin in transcriptional level modulate genes which were closely related to cell migration and proliferation. Thus, the objective of this project is to confirm the influence of CK2α, α-catenin and β-catenin regulated by bFGF on fibroblast migration and wound healing, to clarify the relationship between CK2α, α-catenin and β-catenin, and to confirm the connection between downstream genes of β-catenin and cell migration or proliferation. This study will provide new targets for drugs that skin repairs wound.