Abstract
We report that apoptosis induced by N-hexanoylsphingosine (C6-Cer)in CHP-100 human neuroepithelioma cells associates with accumulation of monohexosylsphingolipids produced not only by short-chain ceramide glycosylation but also through glycosylation of a ceramide pool endogenously produced. By high-performance thin layer chromatography on berate silica gel plates, newly formed monohexosylsphingolipids were identified as glucosylceramides (GluCer); however, accumulation of lactosylceramide or higher-order glycosphingolipids was not observed. GluCer accumulation was fully suppressed by D-threo-1- phenyl-2-decanoylamino-3-morpholino-1-propanol; moreover, while this inhibitor had no effect on cell viability when administered alone, it markedly potentiated the apoptotic effect of C6-Cer. These results provide evidence that activation of GluCer synthesis is an important mechanism through which CHP-100 cells attempt to escape ceramide-induced apoptosis.
Original language | English |
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Pages (from-to) | 785-791 |
Number of pages | 7 |
Journal | Cell Death and Differentiation |
Volume | 5 |
Issue number | 9 |
Publication status | Published - Sep 1998 |
Keywords
- Apoptosis
- Ceramide
- CHP-100
- Glucosylceramide
- Neuroepithelioma cells
ASJC Scopus subject areas
- Cell Biology