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Journals Molecular and Cellular Biochemistry Volume 341 Issue 1

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 +552151-33083621 +552151-33083656 belklein@ufrgs.br pcschenkel@yahoo.com.br Physiology Department Federal University of Rio Grande do Sul Rua Sarmento Leite, 500 Porto Alegre RS CEP 90050-170 Brazil Cardiovascular Research Laboratory Clinical Hospital of Rio Grande do Sul Porto Alegre Brazil Laboratory of Cellular Biology and Functional Anatomy University of São Paulo São Paulo Brazil Abstract 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-3β/GSK-3β 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-3β 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.

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Redox-sensitive prosurvival and proapoptotic protein expression in the myocardial remodeling post-infarction in rats

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  • Publisher Springer US
  • Copyright Copyright © 2010 by Springer Science+Business Media, LLC.
  • Subject Life Sciences; Cardiology; Oncology ; Medical Biochemistry; Biochemistry, general
  • ISSN 0300-8177
  • eISSN 1573-4919
  • D.O.I. 10.1007/s11010-010-0431-8
  • Publisher site Get PDF  

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