Modulation of Fas-induced apoptosis by p75 neurotrophin receptor in a human neuroblastoma cell line

Fas and p75 neurotrophin receptors (p75(NTR)) are death receptors that alone induce apoptosis of SH-SY5Y neuroblastoma cell line respectively by Fas ligand or brain-derived neurotrophic factor (BDNF, a p75(NTR) ligand). We report on the modulation of Fas-mediated apoptosis by concomitant p75(NTR) ac...

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Bibliographic Details
Published in:Apoptosis (London) 2005-12, Vol.10 (6), p.1271-1283
Main Authors: Giraud, S, Lautrette, C, Bessette, B, Decourt, C, Mathonnet, M, Jauberteau, M-O
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis - drug effects
Brain-derived neurotrophic factor
Brain-Derived Neurotrophic Factor - pharmacology
Caspase Inhibitors
Cell Line, Tumor
Cells
Enzyme Inhibitors - pharmacology
Fas Ligand Protein - pharmacology
fas Receptor - genetics
fas Receptor - metabolism
Gene Expression Regulation, Neoplastic - drug effects
Humans
Models, Biological
Neuroblastoma - enzymology
Neuroblastoma - genetics
Neuroblastoma - metabolism
Neuroblastoma - pathology
Protein Transport - drug effects
Receptor, Nerve Growth Factor - genetics
Receptor, Nerve Growth Factor - metabolism
Receptor, trkB - metabolism
RNA, Messenger - genetics
RNA, Messenger - metabolism
Sphingomyelin Phosphodiesterase - antagonists & inhibitors
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Summary:Fas and p75 neurotrophin receptors (p75(NTR)) are death receptors that alone induce apoptosis of SH-SY5Y neuroblastoma cell line respectively by Fas ligand or brain-derived neurotrophic factor (BDNF, a p75(NTR) ligand). We report on the modulation of Fas-mediated apoptosis by concomitant p75(NTR) activation. The exposure to both ligands suppressed the apoptotic effect. A co-localisation of Fas and p75(NTR) receptors was evidenced by co-capping and immunoprecipitation assays. Moreover, a caspase-8 inhibitor suppressed the protective effect of the concomitant BDNF and Fas ligand stimulation, suggesting that p75(NTR) and Fas receptors could share common signalling pathways.
ISSN:1360-8185
1573-675X
DOI:10.1007/s10495-005-2649-6