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

Summary 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. View the pubcast on this paper at http://www.scivee.tv/node/18147