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Topical application of TRPM8 agonists accelerates skin permeability barrier recovery and reduces epidermal proliferation induced by barrier insult: role of cold‐sensitive TRP receptors in epidermal permeability barrier homoeostasis
Author(s) -
Denda Mitsuhiro,
Tsutsumi Moe,
Denda Sumiko
Publication year - 2010
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2010.01154.x
Subject(s) - trpm8 , barrier function , chemistry , homeostasis , evans blue , receptor , transient receptor potential channel , microbiology and biotechnology , biology , endocrinology , biochemistry , trpv1
Please cite this paper as : Topical application of TRPM8 agonists accelerates skin permeability barrier recovery and reduces epidermal proliferation induced by barrier insult: role of cold‐sensitive TRP receptors in epidermal permeability barrier homoeostasis. Experimental Dermatology 2010; 19 : 791–795. Abstract: TRPA1 and TRPM8 receptors are activated at low temperature (A1: below 17°C and M8: below 22°C). Recently, we observed that low temperature (below 22°C) induced elevation of intracellular calcium in keratinocytes. Moreover, we demonstrated that topical application of TRPA1 agonists accelerated the recovery of epidermal permeability barrier function after disruption. In this study, we examined the effect of topical application of TRPM8 modulators on epidermal permeability barrier homoeostasis. Immunohistochemical study and RT‐PCR confirmed the expression of TRPM8 or TRPM8‐like protein in epidermal keratinocytes. Topical application of TRPM8 agonists, menthol and WS 12 accelerated barrier recovery after tape stripping. The effect of WS12 was blocked by a non‐selective TRP antagonist, Ruthenium Red, and a TRPM8‐specific antagonist, BTCT. Topical application of WS12 also reduced epidermal proliferation associated with barrier disruption under low humidity, and this effect was blocked by BTCT. Our results indicate that TRPM8 or a closely related protein in epidermal keratinocytes plays a role in epidermal permeability barrier homoeostasis and epidermal proliferation after barrier insult.