Adaptation of the rat cardiac proteome in response to intensity-controlled endurance exercise

被引:45
作者
Burniston, Jatin G. [1 ,2 ]
机构
[1] Liverpool John Moores Univ, Res Inst Sport & Exercise Sci, Liverpool L3 2ET, Merseyside, England
[2] Liverpool John Moores Univ, Inst Hlth Res, Liverpool L3 2ET, Merseyside, England
关键词
2-D gel electrophoresis; Animal model; Exercise; Heart; HSP20 heat shock proteins; HEAT-SHOCK-PROTEIN; MYOCARDIAL GENE-EXPRESSION; LIM-ONLY PROTEIN; BINDING-PROTEIN; SKELETAL-MUSCLE; POWER OUTPUT; HSP20; ALPHA; FHL2; CARDIOMYOPATHY;
D O I
10.1002/pmic.200800268
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
Endurance training improves cardiac function and protects against heart disease. The rodent intensity-controlled running model replicates endurance exercise in humans and can be used to investigate molecular adaptations in the heart. Rats (n = 6, 280 +/- 3 g) performed exercise tests to measure their peak oxygen uptake ((V) over dotO(2)peak) and training was prescribed at 70-75% (V) over dotO(2)peak for 30 min, 4 days/wk. Hearts were isolated 4 h after a final (V) over dotO(2)peak test and left ventricle proteomes compared to weight-matched control animals (n = 6, 330 +/- 2 g) using differential analysis of 2-D gels. Proteins were identified by searching MS and MS/MS spectra against Swiss-Prot using MASCOT (www.matrixscience.com). Average (V) over dotO(2)peak increased 23% (p = 0.008) over the 6-week regimen and 23 gel spots differed (p<0.05) between exercised and control hearts. Expression of myofibrillar proteins (e.g. alpha-myosin heavy chain and cardiac alpha-actin) and proteins associated with fatty acid metabolism (e.g. heart fatty acid binding protein, acetyl coenzyme A dehydrogenase and mitochondrial thioesterase-1) increased. in addition, this work discovered a novel increase in phosphorylation of heat shock protein 20 at serine 16. Previously this modification has been associated with improved cardiomyocyte contractility and protection against apoptosis.
引用
收藏
页码:106 / 115
页数:10
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