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Chemokine-induced cell death in CCR5-expressing neuroblastoma cells

Cartier, Laetitia
Irminger-Finger, Irmgard
Published in Journal of Neuroimmunology. 2003, vol. 145, no. 1-2, p. 27-39
Abstract CCR5 is expressed in neurons but its function in this cellular context is hitherto poorly understood. We have generated CCR5-expressing SH-SY5Y neuroblastoma cells. CCR5 ligands induced cell death in these cells, but not in control neuroblastoma cells or in CCR5-expressing fibroblasts. CCR5-dependent killing of neuroblastoma cells occurred through apoptosis, since it was accompanied by caspase-3 activation and could be prevented by a caspase-3 inhibitor. Finally, cell killing by activated microglia was more rapid and extensive in CCR5-expressing neuroblastoma cells than in control cells. In summary, CCR5 may act as a death receptor in cells of neuronal lineage and therefore be involved in inflammatory neurodegeneration.
Keywords AnimalsApoptosis/ immunologyCaspase 3Caspases/metabolismCell Culture Techniques/methodsCell Death/immunologyCell Line, TumorChemokines, CC/metabolism/ physiology/ toxicityCoculture TechniquesEnzyme Activation/immunologyGenetic VectorsHumansLigandsMiceMicroglia/immunology/metabolismNIH 3T3 CellsNeuroblastoma/enzymology/ immunology/ pathologyNeurons/enzymology/immunology/pathologyPhagocytosis/immunologyReceptors, CCR5/ biosynthesis/genetics/physiologyTransfection
Stable URL http://archive-ouverte.unige.ch/unige:11178
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PMID: 14644028
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