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Sphingosine impairs mitochondrial function by opening permeability transition pore.

Sidi Mohamed Hassoun·Steve Lancel·Patrice Petillot·Brigitte Decoster·Raphael Favory·Philippe Marchetti·Remi Neviere
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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.

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AnimalsCalciumCyclosporineCytochromes cEnzyme InhibitorsFemaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaMyocardial ContractionProto-Oncogene Proteins c-bcl-2SphingosineJournal ArticleResearch Support, Non-U.S. Gov't

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Sidi Mohamed Hassoun, Steve Lancel, Patrice Petillot, Brigitte Decoster, Raphael Favory, Philippe Marchetti, Remi Neviere. 2006-05-11. Sphingosine impairs mitochondrial function by opening permeability transition pore.. https://doi.org/10.1016/j.mito.2006.05.001

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