Pirt functions as an endogenous regulator of TRPM8

Zongxiang Tang, Andrew Kim, Thorsten Masuch, Kyoungsook Park, HaoJui Weng, Christian Wetzel () and Xinzhong Dong ()
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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
Xinzhong Dong: Center for Sensory Biology, Johns Hopkins University, School of Medicine, 725 N Wolfe Street

Nature Communications, 2013, vol. 4, issue 1, 1-9

Abstract: 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.

Date: 2013
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DOI: 10.1038/ncomms3179

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