Abstract
Inflammation enhanced by accumulation of reactive oxygen species plays an essential role in the progression of cardiovascular diseases. Using the 2D-oxyblot analysis and 2D-difference image gel electrophoresis (2D-DIGE), we compared the levels of ROS-induced carbonyl modification of myocardial proteins in the whole left ventricles between 6-week-old hamsters with dilated (TO-2) and hypertrophic cardiomyopathy (Bio14.6) and control hamsters (F1B). Then, 2D electrophoresis combined with MALDI-TOF/TOF tandem mass spectrometry detected 18 proteins with increased carbonyl level in cardiomyopathy hamsters compared with control hamster. Carbonyl modification of proteins related to ATP synthesis, including citric acid cycle and electron transport system, was observed in the hearts of hamsters with both types of cardiomyopathy. Further analysis indicated that left ventricular carbonyl production correlated negatively with succinyl-CoA:3-ketoacid-coenzyme A transferase 1 activity (r2 = 0.60, P = 0.0007) and ATP concentration (r2 = 0.29, P = 0.037), suggesting that protein carbonylation has negative effects on the levels of these biomolecules. Furthermore, carbonyl production significantly correlated with plasma Troponin T level (r2 = 0.33, P = 0.026). Reduction of energy metabolism by oxidative damage may contribute to the development of left ventricular impairment in cardiomyopathy.
Highlights
Cardiomyopathy leads to serious congestive heart failure (CHF) with substantial risk of mortality and morbidity[1]
left ventricular (LV) end-diastolic diameter and LV end-systolic diameter were significantly higher in TO-2 than F1B control hamsters
We performed 2D-oxyblot analysis and identified 9 proteins with increased carbonyl level in cardiomyopathy hamsters compared with control hamsters
Summary
Cardiomyopathy leads to serious congestive heart failure (CHF) with substantial risk of mortality and morbidity[1]. It has been shown that both hypertrophic and dilated cardiomyopathies are caused by mutation of the same gene, delta-sarcoglycan, in these hamsters[6] These findings indicate that the same genetic modifier might be involved in compensatory cardiac hypertrophy or cardiac dysfunction[7]. Current proteomic technology allows us to examine global changes in oxidatively damaged protein levels in the diseased heart and can provide new insights into cellular mechanisms involved in cardiac dysfunction[22, 23]. The aim of the present study was to measure the myocardial levels of carbonylated proteins in cardiomyopathy and to characterize ROS-induced carbonyl modification of myocardial proteins involved in cardiac dysfunction using an animal model of cardiomyopathy
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