Oral communication, CS15 / C66

Official XXIst International Pigment Cell Conference website - 21-24 Sept 2011, Bordeaux - France | updated: September 04 2011

Do epidermal melanocytes contribute to the erythema response in human skin post-UVB irradiation?

Ultraviolet B (UVB)-induced erythema is mediated in-part by prostaglandin E2 (PGE2) (Rhodes et al, 2001). In UVB-irradiated skin the sole source of this pro-inflammatory mediator was thought to be the keratinocyte (KC), however, we have recently shown that irradiated epidermal melanocytes (EM) may also make and release PGE2 (Gledhill et al, 2010). Consequently, EM may have the capacity to contribute to erythema. It is therefore important to examine the production of PGE2 by EM and KC in response to UVB, so that the potential contribution of each cell type to the erythema response can be spatio-temporally delineated. Here we assessed the production of PGE2 by ELISA in primary EM and KC derived from healthy individuals under UVB-stimulated (73 mJ/cm²) conditions. We also investigated by RT-PCR, qPCR and Western blotting the likely route for PGE2 production by examining the expression of the cyclooxygenase (COX) and prostaglandin E synthase (PGES) enzymes. Results suggested differential production of PGE2 by primary mono-cultures of EM and KC in response to UVB. Interestingly, EM responded to UVB by increasing COX-2 mRNA expression ≈ 80 fold at 1hr post-irradiation (returning to basal levels by ≈ 6 hr post-UVB) whereas matched KC responded by increasing COX-2 mRNA expression ≈ 80 fold at 3 hr post-irradiation (returning to basal levels by ≈12hr post-UVB). However, in response to UVB a statistically-significant increase in PGE2 production was observed at 1 hr post-stimulation in both primary cultures. These results may suggest that PGE2 production immediately following UVB exposure is governed by levels of pre-existing COX-1 in EM and KC. Moreover, EM-derived PGE2 may be of more consequence to erythema following subsequent UVB exposures. These results may highlight EM as a novel therapeutic target that could modify the human skin response to UVB in cases of sunburn.

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