| dc.contributor | Universidade Estadual Paulista (UNESP) | |
| dc.creator | Denadai-Souza, A. | |
| dc.creator | Cenac, N. | |
| dc.creator | Casatti, Cláudio Aparecido | |
| dc.creator | de Souza Camara, P. R. | |
| dc.creator | Yshii, L. M. | |
| dc.creator | Costa, S. K. P. | |
| dc.creator | Vergnolle, N. | |
| dc.creator | Muscara, M. N. | |
| dc.date | 2013-09-30T18:29:13Z | |
| dc.date | 2014-05-20T13:43:02Z | |
| dc.date | 2016-10-25T16:57:42Z | |
| dc.date | 2013-09-30T18:29:13Z | |
| dc.date | 2014-05-20T13:43:02Z | |
| dc.date | 2016-10-25T16:57:42Z | |
| dc.date | 2010-10-01 | |
| dc.date.accessioned | 2017-04-05T20:45:49Z | |
| dc.date.available | 2017-04-05T20:45:49Z | |
| dc.identifier | Journal of Dental Research. Thousand Oaks: Sage Publications Inc, v. 89, n. 10, p. 1123-1128, 2010. | |
| dc.identifier | 0022-0345 | |
| dc.identifier | http://hdl.handle.net/11449/14975 | |
| dc.identifier | http://acervodigital.unesp.br/handle/11449/14975 | |
| dc.identifier | 10.1177/0022034510375284 | |
| dc.identifier | WOS:000283535100019 | |
| dc.identifier | http://dx.doi.org/10.1177/0022034510375284 | |
| dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/862050 | |
| dc.description | 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 (NK1) 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 NK1 receptors. This suggests that PAR(2) is an important component of innate neuro-immune response in the rat TMJ. | |
| dc.description | Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) | |
| dc.description | Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) | |
| dc.description | Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) | |
| dc.language | eng | |
| dc.publisher | Sage Publications Inc | |
| dc.relation | Journal of Dental Research | |
| dc.rights | info:eu-repo/semantics/closedAccess | |
| dc.subject | proteinase-activated receptor 2 | |
| dc.subject | temporomandibular joint | |
| dc.subject | neurogenic inflammation | |
| dc.subject | mechanical allodynia | |
| dc.title | PAR(2) and Temporomandibular Joint Inflammation in the Rat | |
| dc.type | Otro | |
