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Through the Lens of Hair Follicle Neogenesis, a New Focus on Mechanisms of Skin Regeneration After Wounding

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Date 2019 Oct 15
PMID 31607627
Citations 24
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Abstract

Wound-induced hair follicle neogenesis (WIHN) is a phenomenon that occurs in adult mammalian skin, where fully functional hair follicles are regenerated in the center of large full-thickness excisional wounds. Although originally discovered over 50 years ago in mice and rabbits, within the last decade it has received renewed interest, as the molecular mechanism has begun to be defined. This de novo regeneration of hair follicles largely recapitulates embryonic hair development, requiring canonical Wnt signaling in the epidermis, however, important differences between the two are beginning to come to light. TLR3 mediated double stranded RNA sensing is critical for the regeneration, activating retinoic acid signaling following wounding. Inflammatory cells, including Fgf9-producing γ-δ T cells and macrophages, are also emerging as important mediators of WIHN. Additionally, while dispensable in embryonic hair follicle development, Shh signaling plays a major role in WIHN and may be able to redirect cells fated to scarring wounds into a regenerative phenotype. The cellular basis of WIHN is also becoming clearer, with increasing evidence suggesting an incredible level of cellular plasticity. Multiple stem cell populations, along with lineage switching of differentiated cells all contribute towards the regeneration present in WIHN. Further study of WIHN will uncover key steps in mammalian development and regeneration, potentially leading to new clinical treatments for hair-related disorders or fibrotic scarring.

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References
1.
Lee S, Seo S, Lee D, Pi L, Lee W, Choi K . Targeting of CXXC5 by a Competing Peptide Stimulates Hair Regrowth and Wound-Induced Hair Neogenesis. J Invest Dermatol. 2017; 137(11):2260-2269. DOI: 10.1016/j.jid.2017.04.038. View

2.
Kim D, Chen R, Sheu M, Kim N, Kim S, Islam N . Noncoding dsRNA induces retinoic acid synthesis to stimulate hair follicle regeneration via TLR3. Nat Commun. 2019; 10(1):2811. PMC: 6594970. DOI: 10.1038/s41467-019-10811-y. View

3.
Gattazzo F, Urciuolo A, Bonaldo P . Extracellular matrix: a dynamic microenvironment for stem cell niche. Biochim Biophys Acta. 2014; 1840(8):2506-19. PMC: 4081568. DOI: 10.1016/j.bbagen.2014.01.010. View

4.
Cotsarelis G, Sun T, Lavker R . Label-retaining cells reside in the bulge area of pilosebaceous unit: implications for follicular stem cells, hair cycle, and skin carcinogenesis. Cell. 1990; 61(7):1329-37. DOI: 10.1016/0092-8674(90)90696-c. View

5.
Duester G . Retinoic acid synthesis and signaling during early organogenesis. Cell. 2008; 134(6):921-31. PMC: 2632951. DOI: 10.1016/j.cell.2008.09.002. View