Loss of cardiolipin in palmitate-treated GL15 glioblastoma cells favors cytochrome c release from mitochondria leading to apoptosis

Journal of Neurochemistry
Morena BurattaLanfranco Corazzi

Abstract

Unlike oleate and linoleate, palmitate induced mitochondrial apoptosis in GL15 glioblastoma cells. Decrease in membrane potential in a subpopulation of mitochondria of palmitate-treated cells was revealed using the 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide probe. The diminished ability to reduce a tetrazolium salt indicated an impairment of mitochondrial function. Up to 50% cytochrome c (cyt c) was detached from the inner mitochondrial membrane and released outside mitochondria in palmitate-treated cells, whereas no release was detected after oleate and linoleate treatments. Cyt c release into the cytosol was followed by caspase 3 activation. Released cyt c and caspase 3 activity were not affected by neutral and acid sphingomyelinase inhibitors and by the inhibitor of serine palmitoyltransferase cycloserine, indicating that apoptosis was independent of the ceramide pathway, nor the mitochondrial pro-apoptotic AIF or Bcl-2/Bax factors appeared to be involved in the effect. Utilization of palmitate by GL15 cells altered phospholipid composition. Cardiolipin (CL), the lipid involved in cyt c interaction with the inner mitochondrial membrane, was decreased and highly saturated. This produced an imb...Continue Reading

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Citations

Aug 13, 2011·Journal of Bioenergetics and Biomembranes·Lara MacchioniEmilia Castigli
Feb 10, 2012·Journal of Bioenergetics and Biomembranes·Magdalena DavidescuLanfranco Corazzi
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May 5, 2021·Neurochemistry International·Peter Schönfeld, Georg Reiser
Feb 28, 2020·Biochimica Et Biophysica Acta. Molecular Basis of Disease·Mohammed El-HafidiCecilia Zazueta

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