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
Dans Anglais
| WPRIM
| ID: wpr-49340
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.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Différenciation cellulaire
/
Calcium
/
Cellules PC12
/
Staurosporine
/
Protéine bcl-X
/
Caspase-3
/
Fragmentation de l'ADN
/
Mitochondries
/
Neurones
Limites du sujet:
Animaux
langue:
Anglais
Texte intégral:
Experimental & Molecular Medicine
Année:
2009
Type:
Article
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