Proteomics analysis identified peroxiredoxin 2 involved in early-phase left ventricular impairment in hamsters with cardiomyopathy

• Published in: PloS one Vol. 13; no. 2; p. e0192624
• Main Authors: Kuzuya, Kentaro, Ichihara, Sahoko, Suzuki, Yuka, Inoue, Chisa, Ichihara, Gaku, Kurimoto, Syota, Oikawa, Shinji
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 13.02.2018; Public Library of Science (PLoS)
• Subjects: Alterations; Biological markers; Biology and Life Sciences; Biomarkers; Cardiomyopathy; Cardiovascular diseases; Diagnosis; Diagnostic systems; Fluorescence; Gel electrophoresis; Genes; Genetic aspects; Genomics; Hamsters; Heart; Heart diseases; Hypertrophy; Impairment; Kinases; Laboratory animals; Life sciences; Mass spectrometry; Mass spectroscopy; Medicine and Health Sciences; Mutation; Myocardial diseases; Oxidative stress; Peroxiredoxin; Physiology; Preventive medicine; Prognosis; Proteins; Proteomics; Research and Analysis Methods; Rodents; Two dimensional analysis; Ventricle; Japan
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0192624

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.