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Activation of transient receptor potential melastatin 8 reduces ultraviolet B ‐induced prostaglandin E 2 production in keratinocytes
Author(s) -
Park NokHyun,
Na YongJoo,
Choi HyangTae,
Cho JunCheol,
Lee HaeKwang
Publication year - 2013
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.12288
Subject(s) - trpm8 , capsazepine , prostaglandin e2 , chemistry , transient receptor potential channel , menthol , antagonist , pharmacology , receptor , biochemistry , trpv1 , endocrinology , biology , organic chemistry
Transient receptor potential melastatin 8 ( TRPM 8) is a member of the TRP family, and is activated at temperatures below 22°C, or by cooling compounds such as menthol. In this study, it was found that a new role of TRPM 8 activation on prostaglandin E2 ( PGE 2), an inflammatory cytokine and dendritogenesis stimulator of normal human melanocytes. Normal human keratinocytes were pretreated with menthol or incubated at 22°C for TRPM 8 activation before ultraviolet (UV)‐B irradiation. To examine the specificity between TRPM 8 activation and PGE 2 release, we inhibited TRPM 8 with the antagonist (capsazepine), or introduced TRPM 8 si RNA for a gene silencing experiment. UV‐B irradiation significantly induced PGE 2 release in normal human keratinocytes. Interestingly, activation of TRPM 8 at 22°C or with menthol inhibited UV‐B ‐induced PGE 2 release. The effect of the TRPM 8 agonist was completely blocked by pretreatment with the TRPM 8 antagonist, capsazepine. When TRPM 8 expression was suppressed by si RNA , UV‐B irradiation still upregulated PGE 2 in keratinocytes, but pretreatment of menthol or low temperature did not inhibit UV‐B ‐induced PGE 2. In conclusion, the activation of TRPM 8 inhibits UV‐B ‐induced PGE 2 production in keratinocytes, and the activation of TRPM 8 may reduce inflammatory responses in skin.