During wound healing in mice, stimulating a stress hormone receptor in melanocyte stem cells (the precursor of pigment-containing cells) in hair follicles, replenishes the mature pool of melanocytes in the outer layer of the skin. These results, reported this week in Nature Medicine, give evidence of how melanocyte stem cells or activation of this pathway may be exploited to treat skin pigmentation disorders, such as vitiligo and piebaldism.
The skin and hair protect against damage caused by ultraviolet light by providing a physical barrier, while also containing melanocytes that produce a pigment that absorbs this type of radiation. Upon injury, however, the melanocytes in the skin need to be replenished, as production of new pigment from these cells helps protect the healing skin from the sun’s damaging rays.
Mayumi Ito and her colleagues show that in mice a wound caused by skin excision results in hair follicle stem cell migration to the outer layer of the skin and differentiation into melanocytes during the healing process. They further show that in both mouse skin and human skin cultures, these stem cells also migrate in response to ultraviolet type B (UVB) irradiation and this requires functional Mc1r, a stress hormone receptor.
Stress hormones are known to promote skin pigmentation, but stress has also been linked to premature greying of the hair, as well. The authors speculate that melanocyte stem cell depletion in the hair follicle, caused by their migration in response to excess stimulation of Mc1r by stress hormones, may explain this paradox.