Hassoun 2006 Mitochondrion

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.

» PMID: 16725383

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

Labels:

Organism: Mouse  Tissue;cell: Heart  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. 

HRR: Oxygraph-2k