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Updated: Aug 30, 2026
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Chemokine-induced cell death in CCR5-expressing neuroblastoma cells
Laetitia Cartier1, Michel Dubois-Dauphin, Oliver Hartley
1Biology of Ageing Laboratory, Department of Geriatrics, Geneva University Hospitals, 1225 Chêne-Bourg, Switzerland.
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.
Insights
Chemokine receptor CCR5 acts as a death receptor in neuronal cells, triggering apoptosis and enhancing microglial-mediated killing. This suggests CCR5
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- The role of C-C chemokine receptor type 5 (CCR5) in neurons is largely unknown.
- CCR5 is a receptor implicated in immune cell trafficking and inflammatory responses.
Purpose of the Study:
- To investigate the function of CCR5 in neuronal cells.
- To determine if CCR5 mediates cell death in neuronal lineage cells.
Main Methods:
- Generation of SH-SY5Y neuroblastoma cells engineered to express CCR5.
- Treatment of CCR5-expressing and control cells with CCR5 ligands.
- Assessment of apoptosis via caspase-3 activation and inhibition.
- Evaluation of microglial-mediated cell killing.
Main Results:
- CCR5 ligands induced apoptosis specifically in CCR5-expressing neuroblastoma cells, not in control cells or fibroblasts.
- Caspase-3 activation confirmed an apoptotic pathway, preventable by a caspase-3 inhibitor.
- Activated microglia exhibited more rapid and extensive killing of CCR5-expressing neuroblastoma cells.
Conclusions:
- CCR5 may function as a death receptor in cells of neuronal origin.
- CCR5's role in neuronal apoptosis suggests involvement in inflammatory neurodegeneration.
