The Stem Cell Quiescence and Niche Signaling Is Disturbed in the Hair Follicle of the Hairpoor Mouse, an MUHH Model Mouse

May 2022 in “ Stem cell research & therapy ”

Kyu-Yong Choi, Sanghee Park, Seo-Yeon Park, Sungjoo Kim

hair follicle stem cell HFSC quiescence niche signaling Fgf18 Bmp6 Wnt pathways hair follicle cycling alopecia telogen phase anagen induction stem cell quiescence fibroblast growth factor 18 bone morphogenetic protein 6 Wnt signaling hair loss resting phase growth phase

TLDR Disrupted stem cell signals in hairpoor mice cause hair loss.

The study on hairpoor mice, a model for Marie-Unna hypotrichosis (MUHH), reveals that disrupted hair follicle stem cell (HFSC) quiescence and niche signaling, particularly involving Fgf18, Bmp6, and Wnt pathways, lead to abnormal hair follicle cycling and alopecia. Hairpoor mice exhibit reduced HFSC quiescence, increased cell proliferation, and a shorter telogen phase, resulting in fewer hair follicles and premature anagen induction. These findings highlight the critical role of these signaling pathways in hair follicle biology and suggest potential therapeutic targets for hair loss disorders.

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Research cited in this study

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