Rosca 2008 Cardiovasc Res: Difference between revisions
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{{Publication | {{Publication | ||
|title=Rosca MG, Vazquez EJ, Kerner J, Parland W, Chandler MP, Stanley W, Sabbah HN, Hoppel CL (2008) Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation. Cardiovasc Res 80:30-39. | |title=Rosca MG, Vazquez EJ, Kerner J, Parland W, Chandler MP, Stanley W, Sabbah HN, Hoppel CL (2008) Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation. Cardiovasc Res 80:30-39. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/18710878 PMID:18710878] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/18710878 PMID:18710878] | ||
|authors=Rosca MG, Vazquez EJ, Kerner J, Parland W, Chandler MP, Stanley W, Sabbah HN, Hoppel CL | |authors=Rosca MG, Vazquez EJ, Kerner J, Parland W, Chandler MP, Stanley W, Sabbah HN, Hoppel CL | ||
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|organism=Dog | |organism=Dog | ||
|tissues=Heart | |tissues=Heart | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|enzymes=Marker | |enzymes=Marker enzyme | ||
|couplingstates=LEAK, OXPHOS, | |couplingstates=LEAK, OXPHOS, ET | ||
| | |pathways=N, S, CIV, NS | ||
}} | }} | ||
Latest revision as of 15:51, 13 November 2017
| Rosca MG, Vazquez EJ, Kerner J, Parland W, Chandler MP, Stanley W, Sabbah HN, Hoppel CL (2008) Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation. Cardiovasc Res 80:30-39. |
Rosca MG, Vazquez EJ, Kerner J, Parland W, Chandler MP, Stanley W, Sabbah HN, Hoppel CL (2008) Cardiovasc Res
Abstract: AIMS:
Mitochondrial dysfunction is a major factor in heart failure (HF). A pronounced variability of mitochondrial electron transport chain (ETC) defects is reported to occur in severe acquired cardiomyopathies without a consistent trend for depressed activity or expression. The aim of this study was to define the defect in the integrative function of cardiac mitochondria in coronary microembolization-induced HF.
METHODS AND RESULTS:
Studies were performed in the canine coronary microembolization-induced HF model of moderate severity. Oxidative phosphorylation was assessed as the integrative function of mitochondria, using a comprehensive variety of substrates in order to investigate mitochondrial membrane transport, dehydrogenase activity and electron-transport coupled to ATP synthesis. The supramolecular organization of the mitochondrial ETC also was investigated by native gel electrophoresis. We found a dramatic decrease in ADP-stimulated respiration that was not relieved by an uncoupler. Moreover, the ADP/O ratio was normal, indicating no defect in the phosphorylation apparatus. The data point to a defect in oxidative phosphorylation within the ETC. However, the individual activities of ETC complexes were normal. The amount of the supercomplex consisting of complex I/complex III dimer/complex IV, the major form of respirasome considered essential for oxidative phosphorylation, was decreased.
CONCLUSIONS:
We propose that the mitochondrial defect lies in the supermolecular assembly rather than in the individual components of the ETC.
• O2k-Network Lab: US OH Cleveland Hoppel CL
Labels: MiParea: Respiration, mt-Medicine
Organism: Dog
Tissue;cell: Heart
Preparation: Isolated mitochondria
Enzyme: Marker enzyme
Coupling state: LEAK, OXPHOS, ET Pathway: N, S, CIV, NS
