Hong-Zhen Hu, Rui Xiao, and Chunbo Wang have contributed equally to this work.
Potentiation of TRPV3 channel function by unsaturated fatty acids†
Article first published online: 23 MAR 2006
Copyright © 2006 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 208, Issue 1, pages 201–212, July 2006
How to Cite
Hu, H.-Z., Xiao, R., Wang, C., Gao, N., Colton, C. K., Wood, J. D. and Zhu, M. X. (2006), Potentiation of TRPV3 channel function by unsaturated fatty acids. J. Cell. Physiol., 208: 201–212. doi: 10.1002/jcp.20648
- Issue published online: 21 APR 2006
- Article first published online: 23 MAR 2006
- Manuscript Accepted: 14 FEB 2006
- Manuscript Received: 29 SEP 2005
- NIH. Grant Numbers: R01-DK057075, R01-NS042183, P30-NS045758
Transient receptor potential vanilloid (TRPV) channels are polymodal detectors of multiple environmental factors, including temperature, pH, and pressure. Inflammatory mediators enhance TRPV function through multiple signaling pathways. The lipoxygenase and epoxygenase products of arachidonic acid (AA) metabolism have been shown to directly activate TRPV1 and TRPV4, respectively. TRPV3 is a thermosensitive channel with an intermediate temperature threshold of 31–39°C. We have previously shown that TRPV3 is activated by 2-aminoethoxydiphenyl borate (2APB). Here we show that AA and other unsaturated fatty acids directly potentiate 2APB-induced responses of TRPV3 expressed in HEK293 cells, Xenopus oocytes, and mouse keratinocytes. The AA-induced potentiation is observed in intracellular Ca2+ measurement, whole-cell and two-electrode voltage clamp studies, as well as single channel recordings of excised inside-out and outside-out patches. The fatty acid-induced potentiation is not blocked by inhibitors of protein kinase C and thus differs from that induced by the kinase. The potentiation does not require AA metabolism but is rather mimicked by non-metabolizable analogs of AA. These results suggest a novel mechanism regulating the TRPV3 response to inflammation, which differs from TRPV1 and TRPV4, and involves a direct action of free fatty acids on the channel. J. Cell. Physiol. © 2006 Wiley-Liss, Inc.