Document Detail


Exercise-induced adaptations of cardiac redox homeostasis and remodeling in heterozygous SOD2-knockout mice.
MedLine Citation:
PMID:  21836049     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
L Richters; N Lange; R Renner; N Treiber; A Ghanem; K Tiemann; K Scharffetter-Kochanek; W Bloch; K Brixius
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Publication Detail:
Type:  Journal Article     Date:  2011-08-11
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  111     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-18     Completed Date:  2012-06-05     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1431-40     Citation Subset:  IM    
Affiliation:
Dept. of Molecular and Cellular Sport Medicine, German Sport Univ. Cologne, Carl-Diem-Weg 6, 50933 Cologne, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / genetics,  physiology*
Animals
Antioxidants / metabolism
Apoptosis / genetics
Cardiomegaly / genetics,  metabolism,  physiopathology
Down-Regulation
Heart / physiology*
Heterozygote
Homeostasis
Male
Mice
Mice, Knockout
Myocytes, Cardiac / metabolism,  physiology
Oxidation-Reduction
Oxidative Stress / genetics,  physiology
Peroxiredoxins / genetics
Physical Conditioning, Animal / physiology*
Protein Isoforms
Reactive Oxygen Species / metabolism
Superoxide Dismutase / deficiency,  genetics*
Up-Regulation
Vascular Endothelial Growth Factor A / metabolism
Ventricular Remodeling / genetics,  physiology*
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Protein Isoforms; 0/Reactive Oxygen Species; 0/Vascular Endothelial Growth Factor A; 0/vascular endothelial growth factor A, mouse; EC 1.11.1.15/Peroxiredoxins; EC 1.15.1.1/Superoxide Dismutase; EC 1.15.1.1/superoxide dismutase 2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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