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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampBonet, Ivan José Magayewski-
dc.contributor.authorunicampTambeli, Cláudia Herrera-
dc.typeArtigopt_BR
dc.titleThe contribution of transient receptor potential ankyrin 1 (TRPA1) to the in vivo nociceptive effects of prostaglandin E2pt_BR
dc.contributor.authorDall'Acqua, Marcelo C.-
dc.contributor.authorBonet, Ivan J. M.-
dc.contributor.authorZampronio, Aleksander R.-
dc.contributor.authorTambeli, Cláudia H.-
dc.contributor.authorParada, Carlos A.-
dc.contributor.authorFischer, Luana-
dc.subjectDinoprostonept_BR
dc.subject.otherlanguageDinoprostonapt_BR
dc.description.abstractAims Although evidence suggest that TRPA1 mediates some effects of prostaglandins, it is not known whether TRPA1 contributes to the in vivo nociceptive effects of prostaglandin E2 (PGE2), a key mediator of inflammatory pain. Main methods To address this issue, the effect of the pharmacological blockade of TRPA1 or of its gene silencing on the hyperalgesia induced in the rat paw by PGE2 or its downstream signaling molecules, protein kinase A (PKA) or protein kinase C-epsilon (PKCε), was evaluated. TRPA1 expression on dorsal root ganglia cells was assessed by western blot. Key findings The pharmacological blockade of local TRPA1 by its selective antagonist, HC 030031 decreased and reversed PGE2-induced hyperalgesia. The TRPA1 gene silencing induced by intrathecal pre-treatment with antisense oligodeoxynucleotide blocked PGE2-induced hyperalgesia and strongly reduced TRPA1 expression in dorsal root ganglia cells (L5 and L6). PGE2 injection into the hind paw did not significantly increase TRPA1 expression in dorsal root ganglia cells. Treatment with either HC 030031 or antisense oligodeoxynucleotide significantly decreased the hyperalgesia induced by PKA or PKCε. Since both kinases are the major components of PGE2-induced intracellular signal transduction, the modulation of TRPA1 function by PGE2 may be downstream PKA and PKC-epsilon. Significance These findings show that TRPA1 is essential to the in vivo nociceptive effects induced by one of the most important mediators of inflammatory pain, PGE2. This is one of the crucial findings necessary to support TRPA1 as a promising target for the development of future drugs to pain treatment and control.pt_BR
dc.relation.ispartofLife sciencespt_BR
dc.relation.ispartofabbreviationLife scipt_BR
dc.publisher.cityPhiladelphia, PApt_BR
dc.publisher.countryReino Unidopt_BR
dc.publisherElsevierpt_BR
dc.date.issued2014-
dc.date.monthofcirculationJunept_BR
dc.language.isoengpt_BR
dc.description.volume105pt_BR
dc.description.issuenumber1-2pt_BR
dc.description.firstpage7pt_BR
dc.description.lastpage13pt_BR
dc.rightsFechadopt_BR
dc.sourceSCOPUSpt_BR
dc.identifier.issn0024-3205pt_BR
dc.identifier.eissn1879-0631pt_BR
dc.identifier.doi10.1016/j.lfs.2014.02.031pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0024320514002884pt_BR
dc.description.sponsorshipCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQpt_BR
dc.description.sponsorshipCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESpt_BR
dc.date.available2020-12-10T16:38:37Z-
dc.date.accessioned2020-12-10T16:38:37Z-
dc.description.provenanceSubmitted by Sanches Olivia (olivias@unicamp.br) on 2020-12-10T16:38:37Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-02-25T19:55:33Z : No. of bitstreams: 1 2-s2.0-84901617412.pdf: 5046717 bytes, checksum: dbae27b3e227ed49459ef315fef6c211 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-12-10T16:38:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2014en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/353074-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.subject.keywordInflammatory painpt_BR
dc.subject.keywordNociceptor sensitizationpt_BR
dc.subject.keywordTRPA1pt_BR
dc.subject.keywordProstaglandin E2pt_BR
dc.subject.keywordProtein kinase Apt_BR
dc.subject.keywordProtein kinase C-epsilonpt_BR
dc.identifier.source2-s2.0-84901617412pt_BR
dc.creator.orcid0000-0002-6008-3237pt_BR
dc.creator.orcid0000-0001-5566-710Xpt_BR
dc.type.formArtigopt_BR
dc.description.otherSponsorshipsem informaçãopt_BR
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