Universität zu Köln

Richters, L., Lange, N., Renner, R., Treiber, N., Ghanem, A., Tiemann, K., Scharffetter-Kochanek, K., Bloch, W. and Brixius, K. (2011). Exercise-induced adaptations of cardiac redox homeostasis and remodeling in heterozygous SOD2-knockout mice. J. Appl. Physiol., 111 (5). S. 1431 - 1441. BETHESDA: AMER PHYSIOLOGICAL SOC. ISSN 8750-7587

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Abstract

Richters L, Lange N, Renner R, Treiber N, Ghanem A, Tiemann K, Scharffetter-Kochanek K, Bloch W, Brixius K. Exercise-induced adaptations of cardiac redox homeostasis and remodeling in heterozygous SOD2-knockout mice. J Appl Physiol 111: 1431-1440, 2011. First published August 11, 2011; doi: 10.1152/japplphysiol.01392.2010.-A reduced expression of the manganese-dependent superoxide dismutase (SOD2) is characterized by increased cardiac oxidative stress. Oxidative stress has also been described in situations of physical exercise. We investigated the influence of physical exercise (EX; treadmill 1 h/day at 15 m/min, 5 days/wk, at an angle of 5 for a duration of 8 wk) on cardiac function [heart frequency (HF), echocardiography, morphometry], oxidative stress [reactive oxygen species (ROS)], and antioxidative defence capacity (peroxiredoxin 1-6) in male SOD2-knockout (SOD2_EX) and wild-type mice (WT_EX) compared with untrained age-matched animals (WT_CON; SOD2_CON). In SOD2_CON, heart weight, cardiomyocyte diameter, and cardiac ROS were significantly larger and peroxiredoxin isoforms 4-6 lower than in WT_CON. The vessel-to-cardiomyocyte ratio, cardiac VEGF-concentration, and cardiac function were similar in SOD2_CON and WT_CON. Both groups tolerated the exercise protocol well. In WT, exercise significantly increased vessel-to-cardiomyocyte ratio and ROS-generation and downregulated peroxiredoxin isoforms 4-6 and VEGF generation. The vessel-to-cardiomyocyte ratio, cardiac VEGF concentration, and cardiac ROS were not altered in SOD2_EX compared with SOD2_CON, but a significant upregulation of cardiac peroxiredoxin 1 and 4 was observed. Similar to the result observed in WT_EX, peroxiredoxin 3 was upregulated in SOD2_EX. Chronic exercise shifted the (mal) adaptive hypertrophic into a compensated dilated cardiac phenotype in SOD2_EX. In conclusion, downregulation of SOD2 induces a maladaptive cardiac hypertrophy. In this situation, physical exercise results in a further deterioration of cardiac remodeling despite an upregulation of the antioxidative defense system.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Richters, L. UNSPECIFIED UNSPECIFIED UNSPECIFIED Lange, N. UNSPECIFIED UNSPECIFIED UNSPECIFIED Renner, R. UNSPECIFIED UNSPECIFIED UNSPECIFIED Treiber, N. UNSPECIFIED UNSPECIFIED UNSPECIFIED Ghanem, A. UNSPECIFIED UNSPECIFIED UNSPECIFIED Tiemann, K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Scharffetter-Kochanek, K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Bloch, W. UNSPECIFIED UNSPECIFIED UNSPECIFIED Brixius, K. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-485901
DOI:	10.1152/japplphysiol.01392.2010
Journal or Publication Title:	J. Appl. Physiol.
Volume:	111
Number:	5
Page Range:	S. 1431 - 1441
Date:	2011
Publisher:	AMER PHYSIOLOGICAL SOC
Place of Publication:	BETHESDA
ISSN:	8750-7587
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language MANGANESE-SUPEROXIDE-DISMUTASE; ACTIVATED PROTEIN-KINASE; HUMAN FAILING MYOCARDIUM; HEART-FAILURE; OXIDATIVE STRESS; SKELETAL-MUSCLE; REACTIVE OXYGEN; DILATED CARDIOMYOPATHY; PROTEOMIC ANALYSIS; PEROXIREDOXIN-III Multiple languages Physiology; Sport Sciences Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/48590