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• W4253431212 endingPage "1070" @default.
• W4253431212 startingPage "1068" @default.
• W4253431212 abstract "Cell survival reflects a balance between death and protective pathways. Because sphingolipids have emerged as putative death signals and because transcription factor-kappa B (NF-κB) activates a survival pathway, we analyzed the role of C2-ceramide (C2) and GD3 ganglioside (GD3) on the generation of reactive oxygen species (ROS), NF-ΚB activation, and survival of rat hepatocytes or HepG2 cells. Although both C2 and GD3 generated similar dose-dependent levels of ROS derived from mitochondria, hepatocytes displayed a selective sensitivity to GD3 treatment. Consistent with this finding, C2 and GD3 differed in the activation of NF-ΚB as C2, unlike GD3, and enhanced the DNA binding of NF-ΚB despite the fact that both sphingolipids signaled the degradation of IΚB-Α. Glucosylceramide (GluCer), lactosylceramide (LactCer), and ganglioside GM1 (GM1) mimicked the repressing effect of GD3 on NF-ΚB activation, which suggests the presence of common structural features among these glycosphingolipids. Competent DNA binding NF-ΚB complexes were observed predominantly in the cytosol of GD3-stimulated cells, which paralleled the absence of NF-ΚB p65 in the nuclei and indicated that GD3 blocks the nuclear translocation of NF-ΚB complexes. Pretreatment of hepatocytes with a sublethal dose of GD3 blocked the activation of NF-ΚB and subsequent ΚB-dependent gene expression induced by tumor necrosis factor α (TNF-α), which sensitized hepatocytes to TNF-α-induced apoptosis. Thus, gangliosides are efficient death effectors by a dual mechanism that involves mitochondrial recruitment and suppression of the NF-κB-dependent survival pathway, which may be of potential therapeutic use in conditions aimed to control apoptosis resistance." @default.
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• W4253431212 date "2001-02-05" @default.
• W4253431212 modified "2023-10-18" @default.
• W4253431212 title "Ganglioside GD3 enhances apoptosis by suppressing the nuclear factor‐κB‐dependent survival pathway" @default.
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• W4253431212 doi "https://doi.org/10.1096/fsb2fj000574fje" @default.
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