Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Hassoun 2006 Mitochondrion

From Bioblast
Revision as of 10:50, 22 December 2020 by Beno Marija (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision β†’ (diff)
Publications in the MiPMap
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.

Β» 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. β€’ Keywords: Sphingosine, Heart, Mitochondria, Cyclosporine, Bcl-2

β€’ O2k-Network Lab: FR Lille Neviere R, FR Lille Lancel Steve


Labels:


Organism: Mouse  Tissue;cell: Heart  Preparation: Isolated mitochondria 



HRR: Oxygraph-2k