The TRPV3 channel is widely expressed in the human body, especially in the skin in keratinocytes, but also in the brain. It functions as a molecular sensor for innocuous warm temperatures.[5] Mice lacking these protein are unable to sense elevated temperatures (>33 °C) but are able to sense cold and noxious heat.[6] In addition to thermosensation TRPV3 channels seem to play a role in hair growth because mutations in the TRPV3 gene cause hair loss in mice.[7] The role of TRPV3 channels in the brain is unclear, but researchers found that they play a role in mood regulation,[8] and that a protective effects of Incensole acetate were partially mediated by TRPV3 channels.[9]
Modulation
The TRPV3 channel is directly activated by various natural compounds like carvacrol, thymol and eugenol.[10] Several other monoterpenoids which cause either feeling of warmth or are skin sensitizers can also open the channel.[11] Monoterpenoids also induce agonist-specific desensitization of TRPV3 channels in a calcium-independent manner.[12]
Resolvin E1 (RvE1), RvD2, and 17R-RvD1 (see resolvins) are metabolites of the omega 3 fatty acids, eicosapentaenoic acid (for RvE1) or docosahexaenoic acid (for RvD2 and 17R-RvD1). These metabolites are members of the specialized proresolving mediators (SPMs) class of metabolites that function to resolve diverse inflammatory reactions and diseases in animal models and, it its proposed, humans. These SPMs also dampen pain perception arising from various inflammation-based causes in animal models. The mechanism behind their pain-dampening effects involves the inhibition of TRPV3, probably (in at least certain cases) by an indirect effect wherein they activate other receptors located on neruons or nearby microglia or astrocytes. CMKLR1, GPR32, FPR2, and NMDA receptors have been proposed to be the receptors through which these SPMs operate to down-regulate TRPV3 and thereby pain perception.[13][14][15][16][17]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Peier AM, Reeve AJ, Andersson DA, et al. (2002). "A heat-sensitive TRP channel expressed in keratinocytes". Science. 296 (5575): 2046–9. doi:10.1126/science.1073140. PMID12016205.
^Moqrich A, Hwang SW, Earley TJ, et al. (2005). "Impaired thermosensation in mice lacking TRPV3, a heat and camphor sensor in the skin". Science. 307 (5714): 1468–72. doi:10.1126/science.1108609. PMID15746429.
^Imura K, Yoshioka T, Hikita I, et al. (2007). "Influence of TRPV3 mutation on hair growth cycle in mice". Biochem. Biophys. Res. Commun. 363 (3): 479–83. doi:10.1016/j.bbrc.2007.08.170. PMID17888882.
^Moussaieff A, Yu J, Zhu H, Gattoni-Celli S, Shohami E, Kindy MS, et al. (2012). "Protective effects of incensole acetate on cerebral ischemic injury". Brain Res. 1443: 89–97. doi:10.1016/j.brainres.2012.01.001. PMID22284622.
^Xu H, Delling M, Jun JC, Clapham DE (2006). "Oregano, thyme and clove-derived flavors and skin sensitizers activate specific TRP channels". Nat. Neurosci. 9 (5): 628–35. doi:10.1038/nn1692. PMID16617338.
^Sherkheli M.A., et al.,(2009) Monoterpenoids Induce Agonist-Specific Desensitization of Transient Receptor Potential Vanilloid-3 (TRPV3) ion Channels. J Pharm Pharm Sci, 12 (1): 116-128,
^Qu Q, Xuan W, Fan GH (2015). "Roles of resolvins in the resolution of acute inflammation". Cell Biology International. 39 (1): 3–22. doi:10.1002/cbin.10345. PMID25052386.
^Serhan CN, Chiang N, Dalli J, Levy BD (2015). "Lipid mediators in the resolution of inflammation". Cold Spring Harbor Perspectives in Biology. 7 (2): a016311. doi:10.1101/cshperspect.a016311. PMID25359497.
