Calcium overload is essential for the acceleration of staurosporine-induced cell death following neuronal differentiation in PC12 cells
Experimental & Molecular Medicine
; : 269-276, 2009.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-49340
Responsible library:
WPRO
ABSTRACT
Differentiation of neuronal cells has been shown to accelerate stress-induced cell death, but the underlying mechanisms are not completely understood. Here, we find that early and sustained increase in cytosolic ([Ca2+]c) and mitochondrial Ca2+ levels ([Ca2+]m) is essential for the increased sensitivity to staurosporine-induced cell death following neuronal differentiation in PC12 cells. Consistently, pretreatment of differentiated PC12 cells with the intracellular Ca2+-chelator EGTA-AM diminished staurosporine-induced PARP cleavage and cell death. Furthermore, Ca2+ overload and enhanced vulnerability to staurosporine in differentiated cells were prevented by Bcl-XL overexpression. Our data reveal a new regulatory role for differentiation-dependent alteration of Ca2+ signaling in cell death in response to staurosporine.
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Cell Differentiation
/
Calcium
/
PC12 Cells
/
Staurosporine
/
Bcl-X Protein
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Caspase 3
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DNA Fragmentation
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Mitochondria
/
Neurons
Limits:
Animals
Language:
English
Journal:
Experimental & Molecular Medicine
Year:
2009
Document type:
Article