Abstract
Given the hypothesis that inflammation plays a critical role in the progression of cardiovascular diseases, the aim of the present study was to identify new diagnostic and prognostic biomarkers of myocardial proteins involved in early-phase cardiac impairment, using proteomics analysis. Using the two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) combined with MALDI-TOF/TOF tandem mass spectrometry, we compared differences in the expression of proteins in the whole left ventricles between control hamsters, dilated cardiomyopathic hamsters (TO-2), and hypertrophy cardiomyopathic hamsters (Bio14.6) at 6 weeks of age (n = 6, each group). Proteomic analysis identified 10 protein spots with significant alterations, with 7 up-regulated and 3 down-regulated proteins in the left ventricles of both TO-2 and Bio 14.6 hamsters, compared with control hamsters. Of the total alterations, peroxiredoxin 2 (PRDX2) showed significant upregulation in the left ventricles of TO-2 and Bio 14.6 hamsters. Our data suggest that PRDX2, a redox regulating molecule, is involved in early-phase left ventricular impairment in hamsters with cardiomyopathy.
Highlights
Cardiomyopathy leads to serious congestive heart failure (CHF), which is the main cause of mortality and morbidity in children and adults [1]
The body weight of 6-week-old Bio 14.6 hamsters was significantly lower than F1B control hamsters (Fig 1A), but there was no significant difference in body weight between F1B and TO-2 hamsters
The left ventricular (LV) weight of Bio 14.6 hamsters was significantly lower than F1B control hamsters, but there was no significant difference in LV weight/body weight among the three strains (Fig 1B)
Summary
Cardiomyopathy leads to serious congestive heart failure (CHF), which is the main cause of mortality and morbidity in children and adults [1]. Cardiomyopathy is classified mainly into hypertrophic and dilated cardiomyopathies (HCM and DCM, respectively) based on the gross appearance of the heart. The pathology of these cardiomyopathies is overlapping and common genetic mutations exist [2]. The pathogenetic relationship between the causative genes is not well understood. A better understanding of the pathogenetic interplay between each causative gene is crucial to design novel therapeutic strategies for cardiomyopathy. For this purpose, an animal model of hereditary cardiomyopathy is extremely useful [3,4].
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