Effect of Flightless I Expression on Epidermal Stem Cell Niche During Wound Repair

July 2019 in “ Advances in Wound Care ”

Gink N. Yang, Xanthe L. Strudwick, Claudine S. Bonder, Zlatko Kopecki, Allison J. Cowin

Flightless I epidermal stem cells wound repair proliferating cell nuclear antigen epidermal growth factor receptor 1 Wnt/β-catenin signaling Flii EpSCs PCNA EGFR1

TLDR Reducing Flightless I protein improves wound healing by activating skin stem cells.

The study investigated the role of Flightless I (Flii), a cytoskeletal protein, in the activation of epidermal stem cells (EpSCs) during wound repair. Using genetically modified mice, it was found that reducing Flii expression (Flii+/−) led to increased activation of EpSCs, as indicated by higher levels of proliferating cell nuclear antigen (PCNA) and epidermal growth factor receptor 1 (EGFR1), along with changes in Wnt/β-catenin signaling markers. The results suggested that Flii acts as an inhibitor of EpSC activation, potentially by disrupting Wnt/β-catenin signaling, and that reducing Flii could enhance EpSC activation and improve wound healing.

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