PAR(2) and temporomandibular joint inflammation in the rat

Journal of Dental Research
A Denadai-SouzaM N Muscará

Abstract

The proteinase-activated receptor 2 (PAR(2)) is a putative therapeutic target for arthritis. We hypothesized that the early pro-inflammatory effects secondary to its activation in the temporomandibular joint (TMJ) are mediated by neurogenic mechanisms. Immunofluorescence analysis revealed a high degree of neurons expressing PAR(2) in retrogradely labeled trigeminal ganglion neurons. Furthermore, PAR(2) immunoreactivity was observed in the lining layer of the TMJ, co-localizing with the neuronal marker PGP9.5 and substance-P-containing peripheral sensory nerve fibers. The intra-articular injection of PAR(2) agonists into the TMJ triggered a dose-dependent increase in plasma extravasation, neutrophil influx, and induction of mechanical allodynia. The pharmacological blockade of natural killer 1 (NK(1)) receptors abolished PAR(2)-induced plasma extravasation and inhibited neutrophil influx and mechanical allodynia. We conclude that PAR(2) activation is pro-inflammatory in the TMJ, through a neurogenic mechanism involving NK(1) receptors. This suggests that PAR(2) is an important component of innate neuro-immune response in the rat TMJ.

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Citations

Oct 12, 2012·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·David K LamBrian L Schmidt
Mar 27, 2012·Canadian Journal of Physiology and Pharmacology·Delane Viana GondimMariana Lima Vale
Dec 21, 2011·Arthritis and Rheumatism·Alexandre Denadai-SouzaNicolas Cenac
Jun 8, 2017·Arthritis Research & Therapy·Alexandre Denadai-SouzaMaria Christina Werneck Avellar
Jul 30, 2021·Journal of Leukocyte Biology·Yating YiJun Wang

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