Do hair bulb melanocytes undergo apoptosis during hair follicle regression(catagen)?
|Authors:||D. J. Tobin, E. Hagen, V. A. Botchkarev, R. Paus|
|Journal:||J Invest Dermatol||Volume:||111|
The fate of the hair follicle pigmentary unit during the cyclical involution of anagen hair follicles is unknown. Using the C57BL/6 mouse model for hair research, hair follicle melanocytes were examined during the anagen-catagen transformation, comparing spontaneous and pharmacologically induced catagen development. This study shows that both spontaneous catagen and dexamethasone-induced catagen display similar changes in the pigmentary unit. Catagen hair follicles exhibited pigment incontinence in the dermal papilla and in selected outer root sheath keratinocytes. Melanocytes deleted by apoptosis were detected in spontaneous catagen and, more commonly, in dexamethasone-induced catagen, and were identified using transmission electron microscopy by the presence of free premelanosomes in affected cells lacking epithelial specializations, and by the colocalization of TUNEL positivity and tyrosinase-related protein-1 immunoreactivity. By contrast, cyclophosphamide-induced catagen was characterized by the initial retention of melanogenic and dendritic melanocytes in the presence of widespread keratinocyte apoptosis. Melanocyte incontinence and the ectopic distribution of melanin were more severe than in the other forms of catagen. Whereas much of this melanin was extruded, via the hair canal, to the skin surface, hair follicle-derived pigment was also detected within the epidermis, probably derived from pigment-carrying migrating outer root sheath keratinocytes from the proximal hair follicle. Thus, apoptosis may account, at least in part, for the loss of melanogenic melanocytes during spontaneous catagen. Although dexamethasone-induced catagen may provide a useful model for general hair pigmentation research, catagen induced by cyclophosphamide offers an interesting model for studying the response, and relative resistance, of melanocytes to chemical injury.