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The tyrosine kinase inhibitor bafetinib inhibits PAR2‐induced activation of TRPV4 channels in vitro and pain in vivo

Protease‐activated receptor 2 (PAR2) is expressed on nociceptive neurons, and can sensitize transient receptor potential (TRP) ion channels to amplify neurogenic inflammation and pain. The mechanisms by which this occurs are not fully understood. PAR2 causes receptor‐operated activation of TRPV4 channels and TRPV4 null mice have attenuated PAR2‐stimulated neurogenic inflammation and mechanical hyperalgesia. Here we investigate the intracellular signalling mechanisms underlying PAR2‐induced TRPV4 channel activation and pain.