Abstract
BackgroundWound-induced hair follicle neogenesis (WIHN) is a phenomenon of hair neogenesis that occurs at the center of a scar when the wound area is sufficiently large. Neogenic hair follicles are separated from the pre-existing follicles at the wound edge by a hairless circular region. This WIHN study provides a unique model for developing treatments for hair loss and deciphering the mechanisms underlying organogenesis in adult mammals.MethodsThe skin of a mouse was wounded by excising a 1.5 × 1.5 cm2 square of full-thickness dorsal skin. iTRAQ technology was used to screen proteins differentially expressed between the inner and outer scar areas in a mouse model of WIHN, on post-wounding day 15, to identify the regulators of WIHN. Owing to the overexpression of interleukin-36α (IL-36α) in the de novo hair follicle growth area, the regulating effect of IL-36α overexpression in WIHN was investigated. Hair follicle stem/progenitor cells were counted by flow cytometry while the expression of hair follicle stem/progenitor cell markers (Lgr5, Lgr6, Lrig1, K15, and CD34) and that of Wnt/β-catenin and IL-6/STAT3 pathway intermediaries was detected by qPCR and western blotting.ResultsWe found that wounding induced IL-36α expression. Incorporation of recombinant murine IL-36α (mrIL-36α) into murine skin wounds resulted in a greater number of regenerated hair follicles (p < 0.005) and a faster healing rate. The expression of hair follicle stem/progenitor cell markers was upregulated in the mrIL-36α-injected site (p < 0.05). Additionally, mrIL-36α upregulated the IL-6/STAT3 pathway intermediaries.ConclusionIL-36α is upregulated in de novo hair follicle growth areas and can promote wound epithelialization and WIHN.
Highlights
Wound-induced hair follicle neogenesis (WIHN) is a phenomenon in which the skin, sebaceous glands, and hair follicles regenerate following the occurrence of large, full-thickness wound in adult mice
Macrophages regulate WIHN through the AKT/β-catenin pathway by secreting a cytokine known as tumor necrosis factor (TNF) (Wang et al, 2017)
Full-thickness healed skin from wounded mice was harvested at post-wound day (PWD) 7, 10, 12, 15, and 20, and normal skin from non-wounded mice was used for immunohistochemistry, quantitative PCR (qPCR), and western blotting to detect the spatiotemporal expression of IL-36α
Summary
Wound-induced hair follicle neogenesis (WIHN) is a phenomenon in which the skin, sebaceous glands, and hair follicles regenerate following the occurrence of large, full-thickness wound in adult mice. Studying WIHN in different species is helpful for deciphering mechanisms underlying the regeneration in mammals and may provide insights into novel approaches for hair loss treatments. Wound-induced hair follicle neogenesis (WIHN) is a phenomenon of hair neogenesis that occurs at the center of a scar when the wound area is sufficiently large. Neogenic hair follicles are separated from the pre-existing follicles at the wound edge by a hairless circular region. This WIHN study provides a unique model for developing treatments for hair loss and deciphering the mechanisms underlying organogenesis in adult mammals
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