The thermosensitive TRPV3 channel contributes to rapid wound healing in oral epithelia

Reona Aijima, Bing Wang, Tomoka Takao, Hiroshi Mihara, Makiko Kashio, Yasuyoshi Ohsaki, Jing Qi Zhang, Atsuko Mizuno, Makoto Suzuki, Yoshio Yamashita, Sadahiko Masuko, Masaaki Goto, Makoto Tominaga, Mizuho A. Kido

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)

Abstract

The oral cavity provides an entrance to the alimentary tract to serve as a protective barrier against harmful environmental stimuli. The oral mucosa is susceptible to injury because of its location; nonetheless, it has faster wound healing than the skin and less scar formation. However, the molecular pathways regulating this wound healing are unclear. Here, we show that transient receptor potential vanilloid 3 (TRPV3), a thermosensitive Ca2+-permeable channel, is more highly expressed in murine oral epithelia than in the skin by quantitative RT-PCR. We found that temperatures above 33°C activated TRPV3 and promoted oral epithelial cell proliferation. The proliferation rate in the oral epithelia of TRPV3 knockout (TRPV3KO) mice was less than that of wild-type (WT) mice. We investigated the contribution of TRPV3 to wound healing using a molar tooth extraction model and found that oral wound closure was delayed in TRPV3KO mice compared with that in WT mice. TRPV3 mRNA was up-regulated in wounded tissues, suggesting that TRPV3 may contribute to oral wound repair. We identified TRPV3 as an essential receptor in heat-induced oral epithelia proliferation and wound healing. Our findings suggest that TRPV3 activation could be a potential therapeutic target for wound healing in skin and oral mucosa.

Original languageEnglish
Pages (from-to)182-192
Number of pages11
JournalFASEB Journal
Volume29
Issue number1
DOIs
Publication statusPublished - Jan 1 2015

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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