Bernard BA
L’Oréal Recherche, Clichy, France

Human hair pigmentation relies on the pigmentation unit synthetic activity. Melanins, once synthesized and incorporated into melanosomes, are ultimately transferred to hair shaft cortical cells. Since tissue regression and regeneration characterize human hair cycle, the hair pigmentation unit has to be renewed as well, in a cyclic manner. We showed that inactive quiescent melanocytes were located in the upper ORS, forming a reservoir of progenitor melanocytes from which a subset was recruited at the onset of a new anagen phase and transiently committed to cell division to build a new pigmentation unit (1). A similar reservoir was later described in the mouse hair follicle (2). This transient melanocyte proliferation phase probably reflected the existence of a permissive transient niche, specific of human hair anagen I to IV follicle. Then after, melanogenesis was turned on again and pigmentation unit melanocytes constitutively produced melanins all along the anagen phase. During the whitening process, we showed that both reservoir- and bulbar melanocyte population underwent a progressive decline (3) and ultimately disappeared. This process was also recently observed in the mouse (4). Finally we found that while pMel-17, Mitf-M, tyrosinase, and TRP-1 were detected in hair bulb melanocytes, in contrast and unexpectedly TRP-2 was not! The absence of detectable level of TRP-2 was probably due to transcriptional control and linked to the absence of Sox10 expression in hair bulb (5). The absence of TRP-2 expression in human hair follicle melanocytes strongly suggest that hair follicle melanogenesis does not require dopachrome tautomerase activity. Moreover, since this lack of TRP-2 expression is specifically restricted to the hair follicle, one might suspect a possible link between repressed TRP-2 expression and the progressive melanocyte decline observed during human hair whitening process.