I am going to type out an article in the bi-monthly magazine from the ISHRS. called “Hair Transplant Forum International”. I will type it out in sections because I am not a fast typist and I fatigue.
The article i believe is a re-print from the journal called “Nature”.
Title: Wnt-dependant de novo hair follicle regeneration in adult mouse after wounding.
"The loss of an adult follicle is considered permanent. The possibility that hair follicles develop de novo following wounding was raised in studies on rabbits and mice and even humans 50 years ago. In this study, the authors show that after wounding, hair follicles form de novo in genetically normal adult mice. Analysis demonstrated that the follicles arise from epithelial cells outside the hair follicle stem cell niche, suggesting that epidermal cells in the wound assume a hair follicle stem phenotype. Regenerative capabilities of the adult support the notion that wounding induces an embryonic phenotype of the skin.
During there studies on wound healing in mice, the authors noticed structures within the center of large healing wounds that resemble early developing hair follicles. The final rather than initial size of the wound seemed to correlate with hair follicle neogenesis
Hair follicles consist of at least 10 different epithelial and mesenchymal cell types geared toward the production of hair. They discovered that hair follicle neogenesis following wounding paralled embryonic follicle development at the molecular level"
The newly formed hair follicles also proliferated normally and generated hair as well as sebbaceous glands. They discovered that although bulge cell progeny migrated to the center of the wounds, they did not persist. Less than3% of the new hair follicles were labelled, suggesting that non-hair follicle bulge cells were the primary source of regenerated follicles. New follicles originated outside from cells outside of the hair follicle stem cell niche. The new follicles arose from cells in the epidermis and/or upper portion of the follicle(infundibulum). Both of these areas are considered to posses stem cells that normally undergo epidermal rather than follicular differentiiation. Their findings are the first to indicate that non-hair follicle stem cells in genetically normal adult mice acquire competence to form follicles in resonse to wounding.
The regenerated follicles produced hairs and cycled up to three times in 90 days after wounding, indicating the presence of funtional stem cells. The new hairs lacked pigment and associated melanocytes suggesting that the melanocyte stem cell niche was not re-established or that it could not be repopulated. In mice, melanocyte precursors localise to the bulge.
Wnt7a has been shown to maintain the hair follicle inducing capacity of cultured dermal papilla cells. The over expression of activated Beta-catenin, an intracellular Wnt effector, in epidermis induces new hair follicles, and exogenous Wnt promotes formation of cysts with hair follicle differentiation; however, to date, there has been no evidence that extracellular Wnt ligands can promote actual hair follicle neogenesis in adult skin.
Thus excess Wnt in combination with wound healing potetiates regeneration of hair follicles, perhaps by altering cell fate and increasing the number of cells competent to produce hair. Wnt signalling in epidermal keratinocytes is required for hair follicle regeneration.
The authors have demonstrated that the wound stimulus is sufficient to trigger regeneration of hair follicles from epithelial cells that do not normally form hair. In their opinion, this raises the possibility of treating acute wounds with modulators of Wnt pathway to decrease scar formation, and treating hairloss by regenerationg follicles through wounding and Wnt pathway activation."
“Nature” (17 May 2007) 447; 326-320