Difference between revisions of "Hassoun 2006 Mitochondrion"
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|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 Neviere R | |mipnetlab=FR Lille Neviere R, FR Lille Lancel Steve | ||
|articletype=Protocol; Manual | |articletype=Protocol; Manual | ||
}} | }} | ||
Latest revision as of 11:50, 22 December 2020
| 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 6:149-54. |
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. • Keywords: Sphingosine, Heart, Mitochondria, Cyclosporine, Bcl-2
• O2k-Network Lab: FR Lille Neviere R, FR Lille Lancel Steve
Labels:
Organism: Mouse
Tissue;cell: Heart
Preparation: Isolated mitochondria
HRR: Oxygraph-2k
