FOSL1 promotes keratinocyte migration and wound repair by modulating the IL17 signaling pathway

作者：Haoran Mao, Xiao Jiang, Jiaji Liang, Lei Zhang, Zixian Yang, Zhijing Chen, Jinlong Qiao, Xifeng An, Xuangu Li, Guanghui Xie, Hong-wei Liu, L. Xiao · 发表于：Scientific Reports · 年份：2025 · DOI：10.1038/s41598-025-99128-z · 被引用次数：10 · 研究领域：Medicine

Keratinocytes, the most important cell type constituting the epidermis, migrate to restore the epithelial barrier during wound healing and are a crucial step in wound healing. This study utilized bioinformatics analysis of comprehensive expression datasets of aberrantly expressed genes in wound healing to identify the abnormal expression of the critical transcription factor Fos-like antigen-1 (FOSL1), which is involved in various diseases. Currently, there is limited research on the role of FOSL1 in wound healing, and its molecular mechanisms remain unclear. This study explores the role and regulatory mechanisms of FOSL1 in the wound-healing process. A comprehensive expression dataset of abnormal genes in wound repair was constructed by bioinformatics analysis. Mouse trauma models and mouse wound splint models were constructed to verify the role of FOSL1 in vivo. Real-time quantitative polymerase chain reaction (qRT-PCR), immunoblot, immunofluorescence staining, and HE staining were used to confirm the analysis, and FOSL1 was used as the target in the wound healing process. At the cellular level, using 5ʹ-ethynyl-2ʹ-deoxyuridine (EdU) assay, Transwell assay, Migration assay, western blotting and immunofluorescence, FOSL1 promoted the molecular mechanism of wound repair by regulating the proliferation and migration of keratinocytes through IL-17 signaling pathway. Bioinformatics analysis revealed differential expression of FOSL1 during wound healing. In the mouse back wound mo...