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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titlePotent Cardioprotective Effect of the 4-Anilinoquinazoline Derivative PD153035: Involvement of Mitochondrial K-ATP Channel Activationpt_BR
dc.contributor.authorCavalheiro, RApt_BR
dc.contributor.authorMarin, RMpt_BR
dc.contributor.authorRocco, SApt_BR
dc.contributor.authorCerqueira, FMpt_BR
dc.contributor.authorda Silva, CCCpt_BR
dc.contributor.authorRittner, Rpt_BR
dc.contributor.authorKowaltowski, AJpt_BR
dc.contributor.authorVercesi, AEpt_BR
dc.contributor.authorFranchini, KGpt_BR
dc.contributor.authorCastilho, RFpt_BR
unicamp.authorCavalheiro, Renata A. Vercesi, Anibal E. Castilho, Roger F. Univ Estadual Campinas, Fac Ciencias Med, Dept Patol Clin, Campinas, SP, Brazilpt_BR
unicamp.authorMarin, Rodrigo M. Rocco, Silvana A. Franchini, Kleber G. Univ Estadual Campinas, Fac Ciencias Med, Dept Clin Med, Campinas, SP, Brazilpt_BR
unicamp.authorCerqueira, Fernanda M. Caldeira da Silva, Camille C. Kowaltowski, Alicia J. Univ Sao Paulo, Inst Quim, Dept Bioquim, BR-01498 Sao Paulo, Brazilpt_BR
unicamp.authorRittner, Roberto Univ Estadual Campinas, Inst Quim, Dept Quim Organ, Campinas, SP, Brazilpt_BR
dc.subject.wosReceptor Tyrosine Kinasept_BR
dc.subject.wosPermeability Transitionpt_BR
dc.subject.wosReperfusion Injurypt_BR
dc.subject.wosPossible Mechanismpt_BR
dc.subject.wosOxidative Stresspt_BR
dc.subject.wosEgf Receptorpt_BR
dc.description.abstractBackground: The aim of the present study was to evaluate the protective effects of the 4-anilinoquinazoline derivative PD153035 on cardiac ischemia/reperfusion and mitochondrial function. Methodology/Principal Findings: Perfused rat hearts and cardiac HL-1 cells were used to determine cardioprotective effects of PD153035. Isolated rat heart mitochondria were studied to uncover mechanisms of cardioprotection. Nanomolar doses of PD153035 strongly protect against heart and cardiomyocyte damage induced by ischemia/reperfusion and cyanide/aglycemia. PD153035 did not alter oxidative phosphorylation, nor directly prevent Ca2+ induced mitochondrial membrane permeability transition. The protective effect of PD153035 on HL-1 cells was also independent of AKT phosphorylation state. Interestingly, PD153035 activated K+ transport in isolated mitochondria, in a manner prevented by ATP and 5-hydroxydecanoate, inhibitors of mitochondrial ATP-sensitive K+ channels (mitoK(ATP)). 5-Hydroxydecanoate also inhibited the cardioprotective effect of PD153035 in cardiac HL-1 cells, demonstrating that this protection is dependent on mitoK(ATP) activation. Conclusions/Significance: We conclude that PD153035 is a potent cardioprotective compound and acts in a mechanism involving mitoK(ATP)
dc.relation.ispartofPlos Onept_BR
dc.relation.ispartofabbreviationPLoS Onept_BR
dc.publisher.citySan Franciscopt_BR
dc.publisherPublic Library Sciencept_BR 17pt_BR
dc.identifier.citationPlos One. Public Library Science, v. 5, n. 5, 2010.pt_BR
dc.sourceWeb of Sciencept_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorship1Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
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