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Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes

2009Journal article Restricted access
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dc.contributor.authorCosta, Vera Marisa
dc.contributor.authorSilva, Renata
dc.contributor.authorFerreira, Rita
dc.contributor.authorAmado, Francisco
dc.contributor.authorCarvalho, Félix
dc.contributor.authorBastos, Maria de Lourdes
dc.contributor.authorCarvalho, Rui Albuquerque
dc.contributor.authorCarvalho, Márcia
dc.contributor.authorRemião, Fernando
dc.date.accessioned2021-07-02T09:20:49Z
dc.date.available2021-07-02T09:20:49Z
dc.date.issued2009
dc.description.abstractIn several pathologic conditions, like cardiac ischemia/reperfusion, the sustained elevation of plasma and interstitial catecholamine levels, namely adrenaline (ADR), and the generation of reactive oxygen species (ROS) are hallmarks. The present work aimed to investigate in cardiomyocytes which intracellular signalling pathways are altered by ADR redox ability. To mimic pathologic conditions, freshly isolated calcium tolerant cardiomyocytes from adult rat were incubated with ADR alone or in the presence of a system capable of generating ROS [(xanthine with xanthine oxidase) (X/XO)]. ADR elicited a pro-oxidant signal with generation of reactive species, which was largely magnified by the ROS generating system. However, no change in cardiomyocytes viability was observed. The pro-oxidant signal promoted the translocation to the nucleus of the transcription factors, Heat shock factor-1 (HSF-1) and Nuclear factor-kappaB (NF-kappaB). In addition, proteasome activity was compromised in the experimental groups where the generation of reactive species occurred. The decrease in the proteasome activity of the ADR group resulted from its redox sensitivity, since the activity was recovered by adding the ROS scavenger, tiron. Proteasome inhibition seemed to elicit an increase in HSP70 levels. Furthermore, retention of mitochondrial cytochrome c and inhibition of caspase 3 activity were observed by X/XO incubation in presence or absence of ADR. In conclusion, in spite of all the insults inflicted to the cardiomyocytes, they were capable to activate intracellular responses that enabled their survival. These mechanisms, namely the pathways altered by catecholamine proteasome inhibition, should be further characterized, as they could be of relevance in the ischemia preconditioning and the reperfusion injury.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1016/j.tox.2008.12.010pt_PT
dc.identifier.issn0300-483X
dc.identifier.urihttp://hdl.handle.net/10284/10011
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relationThis work received financial support from the Portuguese State through “Fundação para a Ciência e Tecnologia” (FCT) (project PPCDT/SAU-OBS/55849/2004). Vera M. Costa acknowledges FCT for her PhD grant (SFRD/BD/17677/2004).pt_PT
dc.subjectOxidative stresspt_PT
dc.subjectAdrenalinept_PT
dc.subjectNuclear factor-κBpt_PT
dc.subjectHeat shock factor-1pt_PT
dc.subjectHeat shock proteinspt_PT
dc.subjectHeat shock factorspt_PT
dc.subjectCardiomyocytespt_PT
dc.subjectHeartpt_PT
dc.titleAdrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage79pt_PT
oaire.citation.issue1-2pt_PT
oaire.citation.startPage70pt_PT
oaire.citation.titleToxicologypt_PT
oaire.citation.volume257pt_PT
person.familyNameCarvalho
person.givenNameMarcia
person.identifier2017111
person.identifier.ciencia-id8B10-171E-E63E
person.identifier.orcid0000-0001-9884-4751
person.identifier.ridD-5999-2013
person.identifier.scopus-author-id7201413997
rcaap.rightsclosedAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication3837b828-ba57-47f7-a811-cce65e4922c6
relation.isAuthorOfPublication.latestForDiscovery3837b828-ba57-47f7-a811-cce65e4922c6

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