Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes
Autor(a) principal: | |
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Data de Publicação: | 2009 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10284/10011 |
Resumo: | In 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. |
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Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytesOxidative stressAdrenalineNuclear factor-κBHeat shock factor-1Heat shock proteinsHeat shock factorsCardiomyocytesHeartIn 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.ElsevierRepositório Institucional da Universidade Fernando PessoaCosta, Vera MarisaSilva, RenataFerreira, RitaAmado, FranciscoCarvalho, FélixBastos, Maria de LourdesCarvalho, Rui AlbuquerqueCarvalho, MárciaRemião, Fernando2021-07-02T09:20:49Z2009-01-01T00:00:00Z2009-01-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10284/10011eng0300-483X10.1016/j.tox.2008.12.010metadata only accessinfo:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2022-09-06T02:09:18Zoai:bdigital.ufp.pt:10284/10011Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T15:46:47.160740Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes |
title |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes |
spellingShingle |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes Costa, Vera Marisa Oxidative stress Adrenaline Nuclear factor-κB Heat shock factor-1 Heat shock proteins Heat shock factors Cardiomyocytes Heart |
title_short |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes |
title_full |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes |
title_fullStr |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes |
title_full_unstemmed |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes |
title_sort |
Adrenaline in pro-oxidant conditions elicits intracellular survival pathways in isolated rat cardiomyocytes |
author |
Costa, Vera Marisa |
author_facet |
Costa, Vera Marisa Silva, Renata Ferreira, Rita Amado, Francisco Carvalho, Félix Bastos, Maria de Lourdes Carvalho, Rui Albuquerque Carvalho, Márcia Remião, Fernando |
author_role |
author |
author2 |
Silva, Renata Ferreira, Rita Amado, Francisco Carvalho, Félix Bastos, Maria de Lourdes Carvalho, Rui Albuquerque Carvalho, Márcia Remião, Fernando |
author2_role |
author author author author author author author author |
dc.contributor.none.fl_str_mv |
Repositório Institucional da Universidade Fernando Pessoa |
dc.contributor.author.fl_str_mv |
Costa, Vera Marisa Silva, Renata Ferreira, Rita Amado, Francisco Carvalho, Félix Bastos, Maria de Lourdes Carvalho, Rui Albuquerque Carvalho, Márcia Remião, Fernando |
dc.subject.por.fl_str_mv |
Oxidative stress Adrenaline Nuclear factor-κB Heat shock factor-1 Heat shock proteins Heat shock factors Cardiomyocytes Heart |
topic |
Oxidative stress Adrenaline Nuclear factor-κB Heat shock factor-1 Heat shock proteins Heat shock factors Cardiomyocytes Heart |
description |
In 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. |
publishDate |
2009 |
dc.date.none.fl_str_mv |
2009-01-01T00:00:00Z 2009-01-01T00:00:00Z 2021-07-02T09:20:49Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10284/10011 |
url |
http://hdl.handle.net/10284/10011 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
0300-483X 10.1016/j.tox.2008.12.010 |
dc.rights.driver.fl_str_mv |
metadata only access info:eu-repo/semantics/openAccess |
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metadata only access |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Elsevier |
publisher.none.fl_str_mv |
Elsevier |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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RCAAP |
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RCAAP |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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