Exp Mol Med.  2009 Apr;41(4):269-276. 10.3858/emm.2009.41.4.030.

Calcium overload is essential for the acceleration of staurosporine-induced cell death following neuronal differentiation in PC12 cells

Affiliations
  • 1Department of Molecular Bioscience, School of Bioscience and Biotechnology, Kangwon National University, Chuncheon, Korea. suryeonseo@kangwon.ac.kr
  • 2Department of Oral Biology, BK 21 Project, Yonsei University College of Dentistry, Seoul, Korea. suryeonseo@kangwon.ac.kr

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.

Keyword

bcl-X protein; calcium; cell death; cell differentiation; PC12 cells; staurosporine

MeSH Terms

Animals
Calcium/*metabolism
Caspase 3/metabolism
Cell Differentiation/*physiology
DNA Fragmentation
Mitochondria/metabolism
*Neurons/cytology/drug effects/physiology
*PC12 Cells/cytology/drug effects/physiology
Rats
Staurosporine/*pharmacology
bcl-X Protein/metabolism
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