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Prostaglandin-E2 is produced by adult human epidermal melanocytes in response to UVB in a melanogenesis-independent manner
Article first published online: 17 MAR 2010
© 2010 John Wiley & Sons A/S
Pigment Cell & Melanoma Research
Volume 23, Issue 3, pages 394–403, June 2010
How to Cite
Gledhill, K., Rhodes, L. E., Brownrigg, M., Haylett, A. K., Masoodi, M., Thody, A. J., Nicolaou, A. and Tobin, D. J. (2010), Prostaglandin-E2 is produced by adult human epidermal melanocytes in response to UVB in a melanogenesis-independent manner. Pigment Cell & Melanoma Research, 23: 394–403. doi: 10.1111/j.1755-148X.2010.00696.x
- Issue published online: 12 MAY 2010
- Article first published online: 17 MAR 2010
- PUBLICATION DATA Received 16 November 2009, revised and accepted for publication 11 March 2010, published online 17 March 2010
- epidermal melanocyte;
- ultraviolet radiation;
- prostaglandin E2;
- skin phototype
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.