Proteomic analysis of mitochondria reveals a metabolic switch from fatty acid oxidation to glycolysis in the failing heart
| Autor: | Jun Wang, Ping Liu, Chang-cong Cui, Yu Liu, Jing Li, Tingzhong Wang, Youfei Guan, Ke Han, Chaofeng Sun, Fenling Fan, Jin Zhao, Aiqun Ma, Xiaozhen Zhuo, Ling Bai |
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| Rok vydání: | 2009 |
| Předmět: |
Male
Proteome Molecular Sequence Data Oxidative phosphorylation Mitochondrion Biology General Biochemistry Genetics and Molecular Biology Mitochondria Heart Mitochondrial Proteins Rats Sprague-Dawley Animals Humans Glycolysis Beta oxidation Heart metabolism General Environmental Science Heart Failure Myocardium Fatty Acids Organ Size Pyruvate dehydrogenase complex Rats Citric acid cycle Biochemistry Spectrometry Mass Matrix-Assisted Laser Desorption-Ionization General Agricultural and Biological Sciences Energy Metabolism Oxidation-Reduction |
| Zdroj: | Science in China. Series C, Life sciences. 52(11) |
| ISSN: | 1862-2798 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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