Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2069545 | Mitochondrion | 2006 | 6 Pages |
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.
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Authors
Sidi Mohamed Hassoun, Steve Lancel, Patrice Petillot, Brigitte Decoster, Raphael Favory, Philippe Marchetti, Remi Neviere,