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Transient receptor potential cation channel, subfamily V, member 3, also known as TRPV3, is a human gene encoding the protein of the same name.

The TRPV3 protein belongs to a family of nonselective cation channels that function in a variety of processes, including temperature sensation and vasoregulation. The thermosensitive members of this family are expressed in subsets of human sensory neurons that terminate in the skin, and are activated at distinct physiological temperatures. This channel is activated at temperatures between 22 and 40 degrees C. The gene lies in close proximity to another family member (TRPV1) gene on chromosome 17, and the two encoded proteins are thought to associate with each other to form heteromeric channels.[1]

Physiology of TRPV3 channel

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.[2] Mice lacking these protein are unable to sense elevated temperatures (>33 °C) but are able to sense cold and noxious heat.[3] 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.[4] The role of TRPV3 channels in the brain is unclear, but researchers found that they play a role in mood regulation,[5] and that a protective effects of Incensole acetate were partially mediated by TRPV3 channels.[6]


The TRPV3 channel is directly activated by various natural compounds like carvacrol, thymol and eugenol.[7] Several other monoterpenoids which cause either feeling of warmth or are skin sensitizers can also open the channel.[8] Monoterpenoids also induce agonist-specific desensitization of TRPV3 channels in a calcium-independent manner.[9]

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 is 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.[10][11][12][13][14]

See also


  1. "Entrez Gene: TRPV3 transient receptor potential cation channel, subfamily V, member 3".
  2. 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. PMID 12016205.
  3. 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. PMID 15746429.
  4. 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. PMID 17888882.
  5. "Incense on the brain, by Ran Shapira, Haaretz".
  6. 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. PMC 3294134. PMID 22284622.
  7. 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. PMID 16617338.
  8. Vogt-Eisele AK, Weber K, Sherkheli MA, et al. (2007). "Monoterpenoid agonists of TRPV3". Br. J. Pharmacol. 151 (4): 530–40. doi:10.1038/sj.bjp.0707245. PMC 2013969. PMID 17420775.
  9. Sherkheli MA, 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. doi:10.18433/j37c7k.
  10. 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. PMID 25052386.
  11. 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. PMC 4315926. PMID 25359497.
  12. Lim JY, Park CK, Hwang SW (2015). "Biological Roles of Resolvins and Related Substances in the Resolution of Pain". BioMed Research International. 2015: 830930. doi:10.1155/2015/830930. PMC 4538417. PMID 26339646.
  13. Ji RR, Xu ZZ, Strichartz G, Serhan CN (2011). "Emerging roles of resolvins in the resolution of inflammation and pain". Trends in Neurosciences. 34 (11): 599–609. doi:10.1016/j.tins.2011.08.005. PMC 3200462. PMID 21963090.
  14. Serhan CN, Chiang N, Dalli J (2015). "The resolution code of acute inflammation: Novel pro-resolving lipid mediators in resolution". Seminars in Immunology. 27 (3): 200–15. doi:10.1016/j.smim.2015.03.004. PMC 4515371. PMID 25857211.

Further reading

  • Islam, Md. Shahidul (January 2011). Transient Receptor Potential Channels. Advances in Experimental Medicine and Biology. 704. Berlin: Springer. p. 700. ISBN 978-94-007-0264-6.
  • Clapham DE, Julius D, Montell C, Schultz G (2006). "International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels". Pharmacol. Rev. 57 (4): 427–50. doi:10.1124/pr.57.4.6. PMID 16382100.

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.