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Difference between revisions of "Hassoun 2006 Mitochondrion"

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{{Publication
{{Publication
|title=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. Β 
|title=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.
|authors=Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R Β 
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16725383 PMID: 16725383]
|authors=Hassoun SM, Lancel S, Petillot P, Decoster B, Favory R, Marchetti P, Neviere R
|year=2006
|year=2006
|mipnetlab=FR_Lille_NeviereR
|journal=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.
|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
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16725383 PMID: 16725383]
|mipnetlab=FR Lille Neviere R, FR Lille Lancel Steve
|articletype=Protocol; Manual
}}
}}
{{Labeling
{{Labeling
|organism=Human, Mouse
|organism=Mouse
|tissues=Cardiac Muscle
|tissues=Heart
|preparations=Intact Cell; Cultured; Primary
|preparations=Isolated mitochondria
|kinetics=Oxygen, Inhibitor; Uncoupler
|instruments=Oxygraph-2k
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential
|instruments=Oxygraph-2k, Chemicals; Media
|articletype=Protocol; Manual
|articletype=Protocol; Manual
}}
}}

Latest revision as of 11:50, 22 December 2020

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