alexa Hair follicle stem cells: A new arena


Hair Therapy & Transplantation

Author(s): Dilip Gude

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Amongst the self-renewing compartments of mammalian epidermis, the hair follicle is an important component amongst others (the sebaceous gland and the interfollicular epidermis). The intrinsic follicular and extrinsic environmental signals dictate the cycling stages that hair follicle undergoes based on universal patterning principles. The WNT/bone morphogenetic protein activator/inhibitor pair signaling [1] through beta-catenin plays an important role. The Lgr6 stem cell (SC) gene is expressed in the earliest embryonic hair placodes and may mediate formation of new hair follicles. HMG-box-containing gene Sox9 dictates hair induction, differentiation of the outer root sheath, and is required for the formation of the hair SC compartment. The transcription factor Lhx2 maintains the growth and undifferentiated properties of hair follicle progenitors. Hair follicle dermal papilla-derived induced pluripotent SCs reprogrammed with the single transcription factor Oct4 are comparable with embryonic SCs with respect to morphology, gene expression, and pluripotency. [2] Hair follicle SCs function as a critical regulatory component of the melanocyte SC niche. Collagen XVII (COL17A1/BP180/BPAG2), a hemidesmosomal transmembrane collagen, is highly expressed in hair follicle SCs and is required for the maintenance of hair follicle and melanocyte SCs. [3] An irreversibly committed cell in an SC lineage can become an essential contributor to the niche microenvironment. When hair growth stops, early hair SC descendents (supposed to become transit-amplifying cells) preserve stemness, slow cycling properties, and home back to the bulge niche. Although these become the primary SCs for the next hair cycle, initial bulge SCs become reserves. Unlike their transit-amplifying progeny, when the descendents continue to proliferate, they irreversibly lose their stemness, although they retain many SC markers and survive. Intradermal adipocyte lineage cells also play a role in governing follicular SC activation (through PDGF expression by immature adipocyte cells). Positive markers for hair follicle bulge cells include CD200, PHLDA1, follistatin, and frizzled homolog-1. [4] Hair follicle bulge SCs, through nephronectin expression (and induction of α8 integrin-positive mesenchymal cells to upregulate smooth muscle markers), create a smooth muscle cell niche and act as tendon cells for the arrector pili muscle. Nestin, an intermediate filament protein, serves as a hair follicle and neural SC marker. Nestin expression may be a predictor of poor prognosis in malignant melanoma. Induction of GLI2 activator, a major mediator of hedgehog (Hh) signaling, selectively in SCs of resting hair follicles is known to instigate nodular basal cell carcinoma development. The cell of origin, tissue context (quiescent versus growing hair follicles), and level of oncogenic signaling can determine the phenotype of Hh/Gli-driven skin tumors. In androgenetic alopecia, there is markedly diminished CD200hiITGA6hi and CD34hi cell populations in the bald scalp samples due to defective conversion of hair follicle SCs to progenitor cells. Targeted deletion of PPARγ in hair follicular SCs causes a skin and hair phenotype similar to scarring alopecia. Hair follicle bulge-derived SCs were successfully used as autologous SC source for ocular surface reconstruction in bilateral limbal SC deficiency. [5] Hair follicle SCs are an indomitable resource, better understanding of which has far-reaching benefits in the management of a plethora of disorders.

This article was published in International Journal of Trichology and referenced in Hair Therapy & Transplantation

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