Acid sphingomyelinase mediated release of ceramide is essential to trigger the mitochondrial pathway of apoptosis by galectin-1

Gabriela Ion, R. Fajka-Boja, Ferenc Kovács, Gábor Szebeni, I. Gombos, A. Czibula, J. Matkó, E. Monostori

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

The mechanism of apoptosis induced by human galectin-1, a mammalian β-galactoside-binding protein with a remarkable cytotoxic effect on activated peripheral T cells and tumor T cell lines has been extensively investigated in this study. Here we first show that galectin-1 initiate the acid sphingomyelinase mediated release of ceramide and this event is critical in the further steps. Elevation of ceramide level coincides with exposure of phosphatidylserine on the outer cell membrane. The downstream events, decrease of Bcl-2 protein amount, depolarization of the mitochondria and activation of the caspase 9 and caspase 3 depend on production of ceramide. All downstream steps, including production of ceramide, require the generation of membrane rafts and the presence of two tyrosine kinases, p56lck and ZAP70. Based on our findings we suggest a model of the mechanism of galectin-1 triggered cell death.

Original languageEnglish
Pages (from-to)1887-1896
Number of pages10
JournalCellular Signalling
Volume18
Issue number11
DOIs
Publication statusPublished - Nov 2006

Fingerprint

Galectin 1
Sphingomyelin Phosphodiesterase
Ceramides
Apoptosis
Acids
T-Lymphocytes
Galactosides
Caspase 9
Phosphatidylserines
Tumor Cell Line
Caspase 3
Protein-Tyrosine Kinases
Carrier Proteins
Mitochondria
Cell Death
Cell Membrane
Membranes
Proteins

Keywords

  • Acid sphingomyelinase
  • Apoptosis
  • Ceramide
  • Galectin-1
  • p56
  • ZAP70

ASJC Scopus subject areas

  • Cell Biology

Cite this

Acid sphingomyelinase mediated release of ceramide is essential to trigger the mitochondrial pathway of apoptosis by galectin-1. / Ion, Gabriela; Fajka-Boja, R.; Kovács, Ferenc; Szebeni, Gábor; Gombos, I.; Czibula, A.; Matkó, J.; Monostori, E.

In: Cellular Signalling, Vol. 18, No. 11, 11.2006, p. 1887-1896.

Research output: Contribution to journalArticle

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