The role of kinin B-1 receptors in the nociception produced by peripheral protein kinase C activation in mice

The role of kinin B-1 receptors in the nociception produced by peripheral protein kinase C activation in mice

Author Ferreira, Juliano Google Scholar
Triches, Karen M. Google Scholar
Medeiros, Rodrigo Google Scholar
Cabrini, Daniela A. Google Scholar
Mori, Marcelo A. S. Autor UNIFESP Google Scholar
Pesquero, Joao B. Autor UNIFESP Google Scholar
Bader, Michael Google Scholar
Calixto, Joao B. Google Scholar
Institution Universidade Federal de Santa Catarina (UFSC)
Universidade Federal de Sergipe (UFS)
Univ Fed Parana
Max Delbruck Ctr Mol Med
Universidade Federal de São Paulo (UNIFESP)
Abstract The peripheral injection of phorbol myristate acetate (PMA) into the mouse paw induces nociception mediated through activation of protein kinase C (PKC). in the present study, we examine the contribution of kinin B I receptor to PMA-induced nociception. Nociception was assessed after intraplantar injection of PMA or the B-1 receptor agonist des-Arg(9)-bradykinin in mice. Mechanisms of nociception were studied using the combination of knockout mice, selective drugs, and measurement of B-1 receptor mRNA and protein levels. Peripheral injection of PMA (50 pmol/paw) induced a nociceptive behaviour that was abolished by selective B I receptor antagonist des-Arg9-Leu8-bradykinin or by the B-1 receptor gene deletion. Moreover, PMA treatment did not alter B-1 receptor rnRNA levels, but greatly increased B-1 receptor protein levels in the mouse paw. the injection of des-Arg9-bradykinin did not cause nociception in naive mice, but produced marked nociception in animals previously treated with a low dose of PMA (0.5 nmol/paw). the co-treatment of PMA with selective PKC or protein synthesis inhibitors, but not with p38 mitogen activated protein kinase (MAPK) or transcription inhibitors significantly reduced des-Arg(9)-bradykinin-induced nociception. On the other hand, the co-administration of selective PKC or p38 MAPK inhibitors, but not of protein synthesis or transcription inhibitors, reduced des-Arg9-bradykinin-induced nociception when evaluated in PMA pre-injected animals. These results suggest that the B 1 receptor exerts a critical role in the nociception caused by PKC activation in peripheral tissues. Since the PKC pathway is downstream of several pro-inflammatory mediators, B, receptor stimulation appears to contribute to the acute inflammatory pain process. (c) 2007 Elsevier B.V. All rights reserved.
Keywords kinin B-1 receptor
protein kinase c
pain
MAPK
Language English
Date 2008-03-01
Published in Neuropharmacology. Oxford: Pergamon-Elsevier B.V., v. 54, n. 3, p. 597-604, 2008.
ISSN 0028-3908 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 597-604
Origin http://dx.doi.org/110.1016/j.neuropharm.2007.11.008
Access rights Closed access
Type Article
Web of Science ID WOS:000254151200013
URI http://repositorio.unifesp.br/handle/11600/30508

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