Difference between revisions of "Ter Veld 2005 FEBS J"
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|authors=ter Veld F, Jeneson JA, Nicolay K | |authors=ter Veld F, Jeneson JA, Nicolay K | ||
|year=2005 | |year=2005 | ||
|journal= | |journal=FEBS J. | ||
|abstract=Adaptations of the kinetic properties of mitochondria in striated muscle lacking cytosolic (M) and/or mitochondrial (Mi) creatine kinase (CK) isoforms in comparison to wild-type (WT) were investigated in vitro. Intact mitochondria were isolated from heart and gastrocnemius muscle of WT and single- and double CK-knock-out mice strains (cytosolic (M-CK<sup>–/–</sup>), mitochondrial (Mi-CK<sup>–/–</sup>) and double knock-out (MiM-CK<sup>–/–</sup>), respectively). Maximal ADP-stimulated oxygen consumption flux (State3 Vmax; nmol O2·mg mitochondrial protein<sup>–1</sup>·min<sup>–1</sup>) and ADP affinity (inline image; µm) were determined by respirometry. State 3 Vmax and inline image of M-CK<sup>–/–</sup> and MiM-CK<sup>–/–</sup> gastrocnemius mitochondria were twofold higher than those of WT, but were unchanged for Mi-CK<sup>–/–</sup>. For mutant cardiac mitochondria, only the inline image of mitochondria isolated from the MiM-CK<sup>–/–</sup> phenotype was different (i.e. twofold higher) than that of WT. The implications of these adaptations for striated muscle function were explored by constructing force-flow relations of skeletal muscle respiration. It was found that the identified shift in affinity towards higher ADP concentrations in MiM-CK<sup>–/–</sup> muscle genotypes may contribute to linear mitochondrial control of the reduced cytosolic ATP free energy potentials in these phenotypes. | |abstract=Adaptations of the kinetic properties of mitochondria in striated muscle lacking cytosolic (M) and/or mitochondrial (Mi) creatine kinase (CK) isoforms in comparison to wild-type (WT) were investigated in vitro. Intact mitochondria were isolated from heart and gastrocnemius muscle of WT and single- and double CK-knock-out mice strains (cytosolic (M-CK<sup>–/–</sup>), mitochondrial (Mi-CK<sup>–/–</sup>) and double knock-out (MiM-CK<sup>–/–</sup>), respectively). Maximal ADP-stimulated oxygen consumption flux (State3 Vmax; nmol O2·mg mitochondrial protein<sup>–1</sup>·min<sup>–1</sup>) and ADP affinity (inline image; µm) were determined by respirometry. State 3 Vmax and inline image of M-CK<sup>–/–</sup> and MiM-CK<sup>–/–</sup> gastrocnemius mitochondria were twofold higher than those of WT, but were unchanged for Mi-CK<sup>–/–</sup>. For mutant cardiac mitochondria, only the inline image of mitochondria isolated from the MiM-CK<sup>–/–</sup> phenotype was different (i.e. twofold higher) than that of WT. The implications of these adaptations for striated muscle function were explored by constructing force-flow relations of skeletal muscle respiration. It was found that the identified shift in affinity towards higher ADP concentrations in MiM-CK<sup>–/–</sup> muscle genotypes may contribute to linear mitochondrial control of the reduced cytosolic ATP free energy potentials in these phenotypes. | ||
|keywords=Heart, Metabolic control, Mitochondrial respiration, Skeletal muscle, Transgenic mice | |keywords=Heart, Metabolic control, Mitochondrial respiration, Skeletal muscle, Transgenic mice | ||
Revision as of 11:57, 20 October 2010
| ter Veld F, Jeneson JA, Nicolay K (2005) Mitochondrial affinity for ADP is twofold lower in creatine kinase knock-out muscles. Possible role in rescuing cellular energy homeostasis. FEBS J. 272:956-965. |
ter Veld F, Jeneson JA, Nicolay K (2005) FEBS J.
Abstract: Adaptations of the kinetic properties of mitochondria in striated muscle lacking cytosolic (M) and/or mitochondrial (Mi) creatine kinase (CK) isoforms in comparison to wild-type (WT) were investigated in vitro. Intact mitochondria were isolated from heart and gastrocnemius muscle of WT and single- and double CK-knock-out mice strains (cytosolic (M-CK–/–), mitochondrial (Mi-CK–/–) and double knock-out (MiM-CK–/–), respectively). Maximal ADP-stimulated oxygen consumption flux (State3 Vmax; nmol O2·mg mitochondrial protein–1·min–1) and ADP affinity (inline image; µm) were determined by respirometry. State 3 Vmax and inline image of M-CK–/– and MiM-CK–/– gastrocnemius mitochondria were twofold higher than those of WT, but were unchanged for Mi-CK–/–. For mutant cardiac mitochondria, only the inline image of mitochondria isolated from the MiM-CK–/– phenotype was different (i.e. twofold higher) than that of WT. The implications of these adaptations for striated muscle function were explored by constructing force-flow relations of skeletal muscle respiration. It was found that the identified shift in affinity towards higher ADP concentrations in MiM-CK–/– muscle genotypes may contribute to linear mitochondrial control of the reduced cytosolic ATP free energy potentials in these phenotypes. • Keywords: Heart, Metabolic control, Mitochondrial respiration, Skeletal muscle, Transgenic mice
Labels:
Organism: Rat
Tissue;cell: Cardiac Muscle"Cardiac Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
