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

Studysummary This study found that hair follicle stem cells in the hairpoor mouse, a model for Marie-Unna hypotrichosis, lose their quiescent state, leading to a disordered hair cycle and contributing to alopecia. Our plain-language summary of this paper — not a Tressless recommendation.

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

18 / 18 results

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24 citations , June 2015 in “Journal of Investigative Dermatology”

This study observed that epidermal-specific deletion of aPKCλ in mice disrupts hair follicle stem cell quiescence, leading to altered hair follicle cycling and skin anomalies.

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53 citations , February 2015 in “Journal of Investigative Dermatology”

This study found that inactivating CerS4 in mice led to hair follicle stem cell exhaustion and hair loss, indicating its role in regulating hair regeneration through ceramide composition and signaling pathways.

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426 citations , August 2014 in “Nature Medicine”

This narrative review examines the interactions between skin stem cells and their niches, finding new insights from advancements in genetic and imaging tools but reporting no new experimental results.

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173 citations , January 2014 in “Nature Cell Biology”

This study found that Wnt signalling activates hair follicle fate in hair follicle stem cells by relieving TCF3/4–TLE-mediated repression, with β-catenin being crucial for this process.

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156 citations , October 2012 in “Seminars in Cell & Developmental Biology”

This study found that hair follicle stem cells initially contribute to wound re-epithelialization, but long-lasting epidermal cells are primarily derived from a stem cell population in the isthmus portion of hair follicles.

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68 citations , April 2012 in “Journal of Investigative Dermatology”

The study reports that Fgf18 and Tgf-β2 signaling pathways in hair follicle stem cells have opposing effects on the timing of hair cycle transitions, influencing the shift from telogen to anagen phases.

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158 citations , February 2012 in “Journal of Investigative Dermatology”

FGF18 helps keep hair in its resting phase, affecting hair growth cycles.

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21 citations , June 2009 in “Mammalian genome”

This study describes a mouse model for Marie Unna Hereditary Hypotrichosis, identifying mutations in the hairless gene that result in sparse or absent hair and cyst-like hair follicles.

Loss-Of-Function Mutations of an Inhibitory Upstream ORF in the Human Hairless Transcript Cause Marie Unna Hereditary Hypotrichosis

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181 citations , January 2009 in “Nature Genetics”

In this study, researchers linked defects in U2HR, an inhibitory region in the HR gene, to Marie Unna hereditary hypotrichosis, suggesting a mechanism for controlling hair growth and addressing hair loss.

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43 citations , December 2008 in “Molecular biology of the cell”

This study found that disrupting Smad4 signaling in young mice led to overactivation of follicle stem cells, causing hyperplasia and depletion of the stem cell niche.

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415 citations , January 2008 in “Cell”

NFATc1 controls hair stem cell activity, affecting hair growth and could be a target for hair loss treatments.

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141 citations , May 2007 in “Cancer Research”

This study found that CD34 is necessary for TPA-induced activation of hair follicle stem cells and tumor formation in mice, with CD34 knockout mice showing delayed and reduced tumor development compared to wild-types.

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74 citations , September 2006 in “Cell Cycle”

This review examines the role of Hairless, a nuclear receptor corepressor, in regulating Wnt signaling during hair cycling and reports no new clinical results.

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18 citations , February 2006 in “Genomics”

A new genetic mutation in mice causes permanent hair loss and skin wrinkling.

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137 citations , September 2005 in “Proceedings of the National Academy of Sciences of the United States of America”

In this study, researchers found that transgenic expression of the Hairless gene in keratinocytes can restore hair follicle regeneration in Hr-deficient mice by repressing Wise, a modulator of Wnt signaling.

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215 citations , September 2003 in “Journal of Biological Chemistry”

This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.

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561 citations , April 2003 in “Journal of Investigative Dermatology”

CD34 is a marker for isolating stem-like cells in mouse hair follicles.

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This study found that the mammalian hairless gene encodes a corepressor protein that interacts with thyroid hormone receptors, providing insights into hair loss syndromes in humans and mice.