PAR(2) and Temporomandibular Joint Inflammation in the Rat

Autor(es)

Denadai-Souza, A. ^{[1, 2]} ; Cenac, N. ^{[3, 2]} ; Casatti, C. A. ^[4] ; de Souza Camara, P. R. ^[1] ; Yshii, L. M. ^[1] ; Costa, S. K. P. ^[1] ; Vergnolle, N. ^{[3, 2]} ; Muscara, M. N. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508900 Sao Paulo - Brazil

^[2] Ctr Physiopathol Toulouse Purpan, INSERM U563, F-31000 Toulouse - France

^[3] Univ Toulouse 3, F-31000 Toulouse - France

^[4] Sao Paulo State Univ UNESP, Sch Dent, Dept Basic Sci, Aracatuba, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF DENTAL RESEARCH; v. 89, n. 10, p. 1123-1128, OCT 2010.
• Citações Web of Science: 10

Resumo

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 proinflammatory 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. (AU)

• Processo FAPESP: 07/50299-1 - Papel dos receptores ativados por proteinases tipo 2 (par2) e vaniloides sub-tipo 1 (trpv1) e sua interacao funcional na modulacao da artrite e hiperalgesia da articulacao temporomandibular do rato.
• Beneficiário: Marcelo Nicolas Muscara
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 04/07853-0 - Estudo do impacto toxico da quinona 1,2-naftoquinona (1,2-nq) encontrada em particulas liberadas na exaustao do diesel (ped): consequencias nas respostas vasculares neurogenicas.
• Beneficiário: Soraia Katia Pereira Costa
• Modalidade de apoio: Auxílio à Pesquisa - Regular