Hassoun 2006 Mitochondrion: Difference between revisions
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{{Publication | {{Publication | ||
|title=Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R (2006) Sphingosine impairs mitochondrial function by opening permeability transition pore. Mitochondrion 6: 149-154. | |title=Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R (2006) Sphingosine impairs mitochondrial function by opening permeability transition pore. Mitochondrion 6: 149-154. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16725383 PMID: 16725383] | |||
|authors=Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R | |authors=Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R | ||
|year=2006 | |year=2006 | ||
|journal=Mitochondrion | |journal=Mitochondrion | ||
|abstract=Growing evidence suggest that, in the heart, sphingosine participates to contractile dysfunction by altering calcium transients and mitochondria function. However, mechanisms underlying sphingosine-induced cardiac mitochondria dysfunction are poorly understood. Here, we studied the effects of sphingosine on isolated cardiac mitochondria of either wild-type or Bcl-2 overexpressing transgenic mice. Sphingosine induced reductions in ADP-coupled respiration, membrane potential, mitochondrial cytochrome c content and ATP production, which were partially prevented by cyclosporine A and mitochondrial Bcl-2 overexpression. These data suggest that sphingosine promotes mitochondrial permeability transition pore opening, which may result in uncoupled respiration and participate in cardiac contractile dysfunction. | |abstract=Growing evidence suggest that, in the heart, sphingosine participates to contractile dysfunction by altering calcium transients and mitochondria function. However, mechanisms underlying sphingosine-induced cardiac mitochondria dysfunction are poorly understood. Here, we studied the effects of sphingosine on isolated cardiac mitochondria of either wild-type or Bcl-2 overexpressing transgenic mice. Sphingosine induced reductions in ADP-coupled respiration, membrane potential, mitochondrial cytochrome c content and ATP production, which were partially prevented by cyclosporine A and mitochondrial Bcl-2 overexpression. These data suggest that sphingosine promotes mitochondrial permeability transition pore opening, which may result in uncoupled respiration and participate in cardiac contractile dysfunction. | ||
|keywords=Sphingosine, Heart, Mitochondria, Cyclosporine, Bcl-2 | |keywords=Sphingosine, Heart, Mitochondria, Cyclosporine, Bcl-2 | ||
| | |mipnetlab=FR_Lille_NeviereR | ||
|articletype=Protocol; Manual | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|instruments=Oxygraph-2k | |||
|organism=Human, Mouse | |organism=Human, Mouse | ||
|tissues=Cardiac Muscle | |tissues=Cardiac Muscle | ||
|preparations=Intact Cell; Cultured; Primary | |preparations=Intact Cell; Cultured; Primary | ||
|kinetics= | |kinetics=Inhibitor; Uncoupler | ||
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential | |topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential | ||
|articletype=Protocol; Manual | |articletype=Protocol; Manual | ||
}} | }} |
Revision as of 15:46, 27 June 2011
Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R (2006) Sphingosine impairs mitochondrial function by opening permeability transition pore. Mitochondrion 6: 149-154. |
Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R (2006) Mitochondrion
Abstract: Growing evidence suggest that, in the heart, sphingosine participates to contractile dysfunction by altering calcium transients and mitochondria function. However, mechanisms underlying sphingosine-induced cardiac mitochondria dysfunction are poorly understood. Here, we studied the effects of sphingosine on isolated cardiac mitochondria of either wild-type or Bcl-2 overexpressing transgenic mice. Sphingosine induced reductions in ADP-coupled respiration, membrane potential, mitochondrial cytochrome c content and ATP production, which were partially prevented by cyclosporine A and mitochondrial Bcl-2 overexpression. These data suggest that sphingosine promotes mitochondrial permeability transition pore opening, which may result in uncoupled respiration and participate in cardiac contractile dysfunction. โข Keywords: Sphingosine, Heart, Mitochondria, Cyclosporine, Bcl-2
โข O2k-Network Lab: FR_Lille_NeviereR
Labels:
Organism: Human, Mouse
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: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" 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., Coupling; Membrane Potential"Coupling; Membrane Potential" 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