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
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- 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
- KMID: 1088602
- DOI: http://doi.org/10.3858/emm.2009.41.4.030
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.
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