Isoform-specific downregulation of peroxiredoxin in human failing myocardium

Klara Brixius, Robert H G Schwinger, Felix Hoyer, Andreas Napp, Robert Renner, Birgit Bölck, Angelika Kümin, Uwe Fischer, Uwe Mehlhorn, Sabine Werner, Wilhelm Bloch

Publikation: Beitrag in FachzeitschriftZeitschriftenaufsätzeForschungBegutachtung

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 (H(2)O(2)) 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.

OriginalspracheEnglisch
ZeitschriftLife sciences
Jahrgang81
Ausgabenummer10
Seiten (von - bis)823-831
Seitenumfang9
ISSN0024-3205
DOIs
PublikationsstatusVeröffentlicht - 16.08.2007

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