Prostaglandin-E(2) is produced by adult human epidermal melanocytes in response to UVB in a melanogenesis-independent manner.

Abstract

SummaryExcessive ultraviolet radiation (UVR) exposure induces erythema, mediated in part by prostaglandin-E 2 (PGE 2 ). While keratinocytes are a major PGE 2 source, epidermal melanocytes (EM) also express PGE 2 -production machinery. It is unclear whether EM-produced PGE 2 contributes to UVR-induced skin inflammation, and whether this is correlated with melanogenesis. Epidermal melanocytes were cultured from skin phototype-1 and -4 donors, followed by assessment of PGE 2 production and melanogenesis. Epidermal melanocytes expressed cytoplasmic phospholipase-A 2 , cyclooxygenase-1, cytoplasmic prostaglandin-E synthase and microsomal prostaglandin-E synthase-1, -2. Epidermal melanocytes produced PGE 2 under basal conditions, which increased further after arachidonic acid stimulation. Epidermal melanocytes expressed cyclooxygenase-2 (COX-2) mRNA and a selective COX-2 inhibitor (NS-398) reduced PGE 2 production. Ultraviolet B-induced PGE 2 production was positively correlated with skin phototype-1, despite variability between individual EM donors.By contrast, there was no correlation between PGE 2 production by EM and their melanogenic status. Thus, EM may contribute to UVR-induced erythema, with role of donor skin phototype more important than their melanogenic status.