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) in epidermal stem cell (EpSC) activation during wound repair using genetically modified mice. It was found that reduced Flii expression (Flii+/−) led to increased activation of EpSCs, as indicated by higher levels of PCNA and EGFR1, and lower levels of Lrig1. These cells also showed increased markers of Wnt activation, such as β-Catenin and Lgr6, and decreased Axin2. Flii acted as an inhibitor of EpSC activation by disrupting Wnt/β-Catenin signaling, and reducing Flii could enhance EpSC activation and improve wound healing. The study involved 6 mice per group and suggested that Flii could be a potential target for improving wound healing processes.

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