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Prostaglandin‐E 2 is produced by adult human epidermal melanocytes in response to UVB in a melanogenesis‐independent manner
Author(s) -
Gledhill Karl,
Rhodes Lesley E.,
Brownrigg Margaret,
Haylett Ann K.,
Masoodi Mojgan,
Thody Anthony J.,
Nicolaou Anna,
Tobin Desmond J.
Publication year - 2010
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/j.1755-148x.2010.00696.x
Subject(s) - phototype , prostaglandin e2 , prostaglandin e , cyclooxygenase , endocrinology , prostaglandin d2 , prostaglandin , medicine , biology , epidermis (zoology) , dermis , arachidonic acid , chemistry , biochemistry , enzyme , dermatology , anatomy
Summary Excessive 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.