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Proteomic analysis of mitochondria reveals a metabolic switch from fatty acid oxidation to glycolysis in the failing heart

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Science China(Life Sciences) 2009年第11期52卷 1003-1010页

作者： WANG Jun1,2, BAI Ling1,2, LI Jing3, SUN ChaoFeng1,2, ZHAO Jin1, CUI ChangCong1,2, HAN Ke1,2, LIU Yu1,2, ZHUO XiaoZhen1,2, WANG TingZhong1,2, LIU Ping1,2, FAN FenLing1,2, GUAN YouFei3 & ma aiqun1,2 1 Department of Cardiology, First affiliated hospital of medical college of Xi’an Jiaotong University, Xi’an 710061, China 2 Ion Channel Disease Laboratory, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry, Xi’an 710061, China 3 Department of Physiology and Pathophysiology Key Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Peking University Health Science Center, Beijing 100083, China Department of Cardiology First Affiliated Hospital ofMedical College of Xi''an Jiaotong University Xi''an China

This work characterizes the mitochondrial proteomic profile in the failing heart and elucidates the molecular basis of mitochondria in heart failure. Heart failure was induced in rats by myocardial infarction, and mitochondria were isolated from hearts by differential centrifugation. Using two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization-time of flight mass spectrometry, a system biology approach was employed to investigate differences in mitochondrial proteins between normal and failing hearts. mass spectrometry identified 27 proteins differentially expressed that involved in energy metabolism. Among those, the up-regulated proteins included tricarboxylic acid cycle enzymes and pyruvate dehydrogenase complex subunits while the down-regulated proteins were involved in fatty acid oxidation and the OXPHOS complex. These results suggest a substantial metabolic switch from free fatty acid oxidation to glycolysis in heart failure and provide molecular evidence for alterations in the structural and functional parameters of mitochondria that may contribute to cardiac dysfunction during ischemic injury.

关键词： mitochondria heart failure proteome two-dimensional electrophoresis energy metabolism

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