PGE2 is a UVR-inducible autocrine factor for human melanocytes that stimulates tyrosinase activation

Please cite this paper as: PGE2 is a UVR‐inducible autocrine factor for human melanocytes that stimulates tyrosinase activation. Experimental Dermatology 2010; 19: 682–684. :  Prostaglandins activate signalling pathways involved in growth, differentiation and apoptosis. Prostaglandin E2 (PGE2) is re...

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Published inExperimental dermatology Vol. 19; no. 7; pp. 682 - 684
Main Authors Starner, Renny J., McClelland, Lindy, Abdel-Malek, Zalfa, Fricke, Alex, Scott, Glynis
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.07.2010
Blackwell
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Summary:Please cite this paper as: PGE2 is a UVR‐inducible autocrine factor for human melanocytes that stimulates tyrosinase activation. Experimental Dermatology 2010; 19: 682–684. :  Prostaglandins activate signalling pathways involved in growth, differentiation and apoptosis. Prostaglandin E2 (PGE2) is released by keratinocytes following ultraviolet irradiation (UVR) and stimulates the formation of dendrites in melanocytes. We show that multiple irradiations of human melanocytes with UVR‐activated cPLA2, the rate‐limiting enzyme in eicosanoid synthesis and stimulated PGE2 secretion. PGE2 increased cAMP production, tyrosinase activity and proliferation in melanocytes. PGE2 binds to four distinct G‐protein coupled receptors (EP1–4). We show that PGE2 stimulates EP4 receptor signalling in melanocytes, resulting in cAMP production. Conversely, PGE2 also stimulated the EP3 receptor in melanocytes, resulting in lowered basal cAMP levels. These data suggest that relative levels or activity of these receptors controls effects of PGE2 on cAMP in melanocytes. The data are the first to identify PGE2 as an UVR‐inducible autocrine factor for melanocytes. These data also show that PGE2 activates EP3 and EP4 receptor signalling, resulting in opposing effects on cAMP production, a critical signalling pathway that regulates proliferation and melanogenesis in melanocytes.
Bibliography:ark:/67375/WNG-4JS2T6XD-P
istex:F101717F8FEACE4D5B05D81CF9629BAFD5E21F3C
ArticleID:EXD1074
ISSN:0906-6705
1600-0625
DOI:10.1111/j.1600-0625.2010.01074.x