Differential bradykinin B-1 and B-2 receptor regulation in cell death induced by hepatic ischaemia/reperfusion injury

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dc.contributor.author Paio, Mayra de Almeida [UNIFESP]
dc.contributor.author Kouyoumdjian, Maria [UNIFESP]
dc.contributor.author Borges, Durval R. [UNIFESP]
dc.contributor.author Nagaoka, Marcia Regina [UNIFESP]
dc.date.accessioned 2016-01-24T14:37:50Z
dc.date.available 2016-01-24T14:37:50Z
dc.date.issued 2014-09-01
dc.identifier http://dx.doi.org/10.1042/CS20130313
dc.identifier.citation Clinical Science. London: Portland Press Ltd, v. 127, n. 5-6, p. 405-413, 2014.
dc.identifier.issn 0143-5221
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/38182
dc.description.abstract The biological and pharmacological effects of BK (bradykinin) are mediated by two receptors: the constitutive B2R (B-2 receptor) and the inducible B1R (B-1 receptor). BK plays a role in the hepatic microcirculation by inducing the PHR (portal hypertensive response) via B2R, whereas DABK (des-Arg(9)-BK), a B1R agonist, does not elicit the response. During IRI (ischaemia/reperfusion injury), important changes occur in the microcirculation, and cell death by necrosis and apoptosis is involved in poor graft function. the aim of the present study was to analyse the role of B1R and B2R in liver cell death induced by IRI. Livers from Wistar rats were submitted to ischaemia (4 degrees C) for 4 or 24 h. After this period, livers were reperfused ex vivo with Krebs Henseleit solution (37 degrees C). BK or DABK was then injected as a bolus during reperfusion in the absence or presence of HOE-140 (a B2R antagonist) or DALBK (des-Arg(9)-Leu(9)-BK) (a B1R antagonist) respectively. Liver viability was analysed by glucose release and bile secretion. the PHR to kinins did not change. Cell death was higher in the DABK group and its antagonist significantly decreased cell death. Interestingly, the B1R antagonist did not alter the number of necrotic cells, but it decreased the number of apoptotic cells. On the other hand, the B2R antagonist decreased the number of necrotic cells, but did not alter the number of apoptotic cells. Therefore B1R may participate in apoptotic cell death signalling, and B2R may be involved in necrotic cell death. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 405-413
dc.language.iso eng
dc.publisher Portland Press Ltd
dc.relation.ispartof Clinical Science
dc.rights Acesso restrito
dc.subject apoptosis en
dc.subject bradykinin en
dc.subject ischaemia/reperfusion injury en
dc.subject kinin en
dc.subject liver en
dc.subject necrosis en
dc.title Differential bradykinin B-1 and B-2 receptor regulation in cell death induced by hepatic ischaemia/reperfusion injury en
dc.type Artigo
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo UNIFESP, Dept Med, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo UNIFESP, Dept Biochem, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo UNIFESP, Dept Biosci, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo UNIFESP, Dept Med, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo UNIFESP, Dept Biochem, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo UNIFESP, Dept Biosci, São Paulo, Brazil
dc.description.sponsorshipID FAPESP: MRN 08/55928-0
dc.description.sponsorshipID FAPESP: MAP 08/08916-6
dc.description.sponsorshipID CNPq: 477869/2008-4
dc.description.sponsorshipID CNPq: 300045/2010-7
dc.identifier.doi 10.1042/CS20130313
dc.description.source Web of Science
dc.identifier.wos WOS:000339859900012



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