Document Detail


Redox-sensitive prosurvival and proapoptotic protein expression in the myocardial remodeling post-infarction in rats.
MedLine Citation:
PMID:  20352476     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In this study, we investigated the oxidative stress influence in some prosurvival and proapoptotic proteins after myocardial infarction (MI). Male Wistar rats were divided in two groups: Sham-operated (control) and MI. MI was induced by left coronary artery occlusion. 28-days after surgery, echocardiographic, morphometric, and hemodynamic parameters were evaluated. Redox status (reduced to oxidized glutathione ratio, GSH/GSSG) and hydrogen peroxide levels (H(2)O(2)) were measured in heart tissue. The p-ERK/ERK, p-Akt/Akt, p-mTOR/mTOR and p-GSK-3beta/GSK-3beta ratios, as well as apoptosis-inducing factor (AIF) myocardial protein expression were quantified by Western blot. MI group showed an increase in cardiac hypertrophy (23%) associated with a decrease in ejection fraction (38%) and increase in left ventricular end-diastolic pressure (82%) when compared to control, characterizing ventricular dysfunction. Redox status imbalance was seen in MI animals, as evidenced by the decrease in the GSH/GSSG ratio (30%) and increased levels of H(2)O(2) (45%). This group also showed an increase in the ERK phosphorylation and a reduction of Akt and mTOR phosphorylation when compared to control. Moreover, we showed a reduction in the GSK-3beta phosphorylation and an increase in AIF protein expression in MI group. Taken together, our results show increased H(2)O(2) levels and cellular redox imbalance associated to a higher p-ERK and AIF immunocontent, which would contribute to a maladaptive hypertrophy phenotype.
Authors:
Paulo Cavalheiro Schenkel; Angela Maria Vicente Tavares; Rafael Oliveira Fernandes; Gabriela Placoná Diniz; Mariane Bertagnolli; Alex Sander da Rosa Araujo; Maria Luiza Barreto-Chaves; Maria Flavia Marques Ribeiro; Nadine Clausell; Adriane Belló-Klein
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-30
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  341     ISSN:  1573-4919     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-26     Completed Date:  2010-12-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1-8     Citation Subset:  IM    
Affiliation:
Physiology Department, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 Porto Alegre, RS CEP 90050-170, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Apoptosis Inducing Factor / analysis*
Apoptosis Regulatory Proteins / analysis*
Cardiomegaly / etiology,  metabolism
Cell Survival
Extracellular Signal-Regulated MAP Kinases / metabolism
Glutathione / blood
Hydrogen Peroxide / blood
Male
Myocardial Infarction / pathology*
Myocardium / metabolism*
Oxidation-Reduction
Oxidative Stress / physiology*
Phosphorylation
Rats
Rats, Wistar
Ventricular Remodeling / physiology*
Chemical
Reg. No./Substance:
0/Apoptosis Inducing Factor; 0/Apoptosis Regulatory Proteins; 70-18-8/Glutathione; 7722-84-1/Hydrogen Peroxide; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases

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