Prostaglandin-E2 is produced by adult human epidermal melanocytes in response to UVB in a melanogenesis-independent manner.

Abstract

Excessive ultraviolet radiation (UVR) exposure induces erythema, mediated in part by prostaglandin-E2 (PGE2). While keratinocytes are a major PGE2 source, epidermal melanocytes (EM) also express PGE2-production machinery. It is unclear whether EM-produced PGE2 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 PGE2 production and melanogenesis. Epidermal melanocytes expressed cytoplasmic phospholipase-A2, cyclooxygenase-1, cytoplasmic prostaglandin-E synthase and microsomal prostaglandin-E synthase-1, -2. Epidermal melanocytes produced PGE2 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 PGE2 production. Ultraviolet B-induced PGE2 production was positively correlated with skin phototype-1, despite variability between individual EM donors. By contrast, there was no correlation between PGE2 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.