Prostaglandin production by melanocytic cells and the effect of α-melanocyte stimulating hormone

Prostaglandins are potent mediators of the inflammatory response and are also involved in cancer development. In this study, we show that human melanocytes and FM55 melanoma cells express cyclooxygenase-1 and -2 (COX-1 and -2) and thus have the capability to produce prostaglandins. The FM55 cells pr...

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Bibliographic Details
Published in:FEBS letters 2004-07, Vol.570 (1), p.223-226
Main Authors: Nicolaou, Anna, Estdale, Sian E, Tsatmali, Marina, Herrero, Daniel Pascual, Thody, Anthony J
Format: Article
Language:English
Subjects:
alpha-MSH - metabolism
Cell Line
Cell Survival
Cells, Cultured
Chromatography, High Pressure Liquid
COX, cyclooxygenase
Cyclooxygenase
Cyclooxygenase 1
Cyclooxygenase 2
FM55
HaCaT
Humans
Inflammation
Isoenzymes - metabolism
Keratinocytes - metabolism
Melanocytes - metabolism
Melanocytic cell
Membrane Proteins
Phenotype
Prostaglandin
Prostaglandin-Endoperoxide Synthases - metabolism
Prostaglandins - biosynthesis
Prostaglandins - metabolism
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Tumor Necrosis Factor-alpha - metabolism
α-Melanocyte stimulating hormone
α-MSH, α-melanocyte stimulating hormone
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Summary:Prostaglandins are potent mediators of the inflammatory response and are also involved in cancer development. In this study, we show that human melanocytes and FM55 melanoma cells express cyclooxygenase-1 and -2 (COX-1 and -2) and thus have the capability to produce prostaglandins. The FM55 cells produced predominantly PGE 2 and PGF 2α, whereas the HaCaT keratinocyte cell line produced mainly PGE 2. The anti-inflammatory peptide, α-melanocyte stimulating hormone (α-MSH), reduced prostaglandin production in FM55 and HaCaT cells and reversed the effect of the pro-inflammatory cytokine TNF-α in the former. These results indicate that melanocytes produce prostaglandins and that α-MSH, by inhibiting this response, may play an important role in regulating inflammatory responses in the skin.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2004.06.041