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JCI table of contents: June 14, 2007

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View the PDF of this article at: https://www.the-jci.org/article.php?id=30356


PHYSIOLOGY

You've got that painful feeling: How TRPA1 senses pain

Researchers have identified an interaction between the molecules transient receptor potential A1 (TRPA1) and proteinase-activated receptor 2 (PAR2) that may explain how we sense the pain caused by inflammation.

TRPA1 is present on a population of neurons and it forms channels that are important in sending signals in response to environmental irritants or other agents that cause inflammatory pain. PARs, also present on neurons, are known to play an important role in the response to tissue injury, notably in the process of inflammation and repair. Tryptase and trypsin, which are released from immune cells after injury, activate PAR2.

In their study appearing online on June 14 in advance of publication in the July print issue of the Journal of Clinical Investigation, Koichi Noguchi and colleagues from Hyogo College of Medicine, Japan, report that TRPA1 and PAR2 are significantly co-expressed in dorsal root ganglion neurons in rats and that PAR2 activation potentiates TRPA1 activity, resulting in the amplification of the pain sensation. They go on to show that this signaling pathway is dependent on the presence of the enzyme phospholipase C. The results represent a novel mechanism through which trypsin or tryptase released in response to tissue inflammation may trigger the sensation of pain through PAR2 activation. Therefore, compounds acting on TRPA1 or interfering with the interaction between TRPA1 and PAR2 may be useful in the treatment of inflammatory pain.

TITLE: Sensitization of TRPA1 by PA
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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
14-Jun-2007


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