Apoptosis induced by N-hexanoylsphingosine in CHP-100 cells associates with accumulation of endogenous ceramide and is potentiated by inhibition of glucocerebroside synthesis

Angelo Spinedi, Sabrina Di Bartolomeo, Mauro Piacentini

Research output: Contribution to journalArticle

37 Citations (Scopus)

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 languageEnglish
Pages (from-to)785-791
Number of pages7
JournalCell Death and Differentiation
Volume5
Issue number9
Publication statusPublished - Sep 1998

Fingerprint

Glucosylceramides
Ceramides
Apoptosis
Glycosylation
Glycosphingolipids
Silica Gel
Thin Layer Chromatography
Cell Survival
N-caproylsphingosine

Keywords

  • Apoptosis
  • Ceramide
  • CHP-100
  • Glucosylceramide
  • Neuroepithelioma cells

ASJC Scopus subject areas

  • Cell Biology

Cite this

@article{af505647642844c89ed47b5a0c8a2af6,
title = "Apoptosis induced by N-hexanoylsphingosine in CHP-100 cells associates with accumulation of endogenous ceramide and is potentiated by inhibition of glucocerebroside synthesis",
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.",
keywords = "Apoptosis, Ceramide, CHP-100, Glucosylceramide, Neuroepithelioma cells",
author = "Angelo Spinedi and {Di Bartolomeo}, Sabrina and Mauro Piacentini",
year = "1998",
month = "9",
language = "English",
volume = "5",
pages = "785--791",
journal = "Cell Death and Differentiation",
issn = "1350-9047",
publisher = "Nature Publishing Group",
number = "9",

}

TY - JOUR

T1 - Apoptosis induced by N-hexanoylsphingosine in CHP-100 cells associates with accumulation of endogenous ceramide and is potentiated by inhibition of glucocerebroside synthesis

AU - Spinedi, Angelo

AU - Di Bartolomeo, Sabrina

AU - Piacentini, Mauro

PY - 1998/9

Y1 - 1998/9

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Ceramide

KW - CHP-100

KW - Glucosylceramide

KW - Neuroepithelioma cells

UR - http://www.scopus.com/inward/record.url?scp=0031787361&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031787361&partnerID=8YFLogxK

M3 - Article

C2 - 10200538

AN - SCOPUS:0031787361

VL - 5

SP - 785

EP - 791

JO - Cell Death and Differentiation

JF - Cell Death and Differentiation

SN - 1350-9047

IS - 9

ER -