Isoform-specific downregulation of peroxiredoxin in human failing myocardium

Brixius, Klara and Schwinger, Robert H. G. and Hoyer, Felix and Napp, Andreas and Renner, Robert and Boelck, Birgit and Kuemin, Angelika and Fischer, Uwe and Mehlhorn, Uwe and Werner, Sabine and Bloch, Wilhelm (2007) Isoform-specific downregulation of peroxiredoxin in human failing myocardium. LIFE SCIENCES, 81 (10). pp. 823-831. ISSN 0024-3205, 1879-0631

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Abstract

Peroxiredoxins (Prx) are a family of antioxidant thioredoxin or glutathione dependent peroxidases. The major functions of Prx comprise modulation of signalling cascades that apply hydrogen peroxide (H2O2) and cellular protection against oxidative stress. Nothing is known about Prx isoforms in human myocardium. We investigated the protein expression of Prx isoforms 1-6 in human non-failing (NF, donor hearts, n =6, male, age: 53.3 +/- 2.1 years) and failing myocardium (DCM, orthotopic heart transplantation, dilated cardiomyopathy, n = 15, male, 57.0 +/- 1.7 years). In addition, we performed immunohistochemical stainings and measured Prx 4 mRNA expression levels (RNAse protection assay). The protein expression of Prx 1-2 was similar in NF and DCM. The protein expression of Prx 3-6 and the mRNA-expression of Prx 4 were decreased in DCM. Immunohistochemical analyses provided evidence that all Prx isoforms are present in cardiomyocytes and endothelial cells. Whereas Prx 1-5 staining was more pronounced in endothelial cells, Prx6 staining was more evident in cardiomyocytes. This study provides evidence that Prx are differentially regulated in DCM. The selective downregulation of peroxiredoxin 3-6 isoforms may point towards a subcellular specific dysregulation of the antioxidative defence during the development of DCM. (c) 2007 Elsevier Inc. All rights reserved.

Item Type: Article
Uncontrolled Keywords: OXIDATIVE STRESS; HEART-FAILURE; MAMMALIAN PEROXIREDOXIN; ANTIOXIDANT DEFENSE; 1-CYS PEROXIREDOXIN; GENE-EXPRESSION; PROTEIN; SYSTEM; OXYGEN; INFARCTION; heart failure; signal transduction; myocardium; peroxiredoxin
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin II
Depositing User: Dr. Gernot Deinzer
Date Deposited: 02 Dec 2020 11:13
Last Modified: 02 Dec 2020 11:13
URI: https://pred.uni-regensburg.de/id/eprint/32384

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