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Pirt functions as an endogenous regulator of TRPM8

Author

Listed:
  • Zongxiang Tang

    (Nanjing University of Chinese Medicine)

  • Andrew Kim

    (Center for Sensory Biology, Johns Hopkins University, School of Medicine, 725 N Wolfe Street)

  • Thorsten Masuch

    (Ruhr University Bochum)

  • Kyoungsook Park

    (Center for Sensory Biology, Johns Hopkins University, School of Medicine, 725 N Wolfe Street)

  • HaoJui Weng

    (Center for Sensory Biology, Johns Hopkins University, School of Medicine, 725 N Wolfe Street)

  • Christian Wetzel

    (Ruhr University Bochum
    Molecular Neurosciences, University of Regensburg)

  • Xinzhong Dong

    (Center for Sensory Biology, Johns Hopkins University, School of Medicine, 725 N Wolfe Street
    Howard Hughes Medical Institute)

Abstract

Pirt is a membrane protein that is specifically expressed in the peripheral nervous system, where it has been shown to increase the sensitivity of the transient receptor potential vanilloid 1 channel and modulate its role in heat pain. The broad expression of Pirt among dorsal root ganglion neurons suggests it may modulate other transient receptor potentials, such as the menthol and cooling sensor TRPM8. The discrepancies in the channel properties of TRPM8 in native neurons versus heterologous cells indicate the existence of endogenous modulators of the channel. Here we show that Pirt regulates the function of TRPM8 and its role in detecting cold. Pirt−/− mice exhibit decreased behavioural responses to cold and cool temperatures, and Pirt increases the sensitivity of TRPM8 to menthol and cool temperature. Our data suggest Pirt is an endogenous regulator of TRPM8.

Suggested Citation

  • Zongxiang Tang & Andrew Kim & Thorsten Masuch & Kyoungsook Park & HaoJui Weng & Christian Wetzel & Xinzhong Dong, 2013. "Pirt functions as an endogenous regulator of TRPM8," Nature Communications, Nature, vol. 4(1), pages 1-9, October.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3179
    DOI: 10.1038/ncomms3179
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