Calbindin-D28K Prevents Staurosporin-induced Bax Cleavage and Membrane Permeabilization
Experimental Neurobiology 2014³â 23±Ç 2È£ p.173 ~ p.177
ÃÖ¿ø¼®(Choi Won-Seok) - Chonnam National University College of Medicine
(Oh Young-J) - Yonsei University College of Life Science and Biotechnology Department of Biology
Abstract
Calbindin-D28K has been implicated in the regulation of neuronal cell death. Previously, we demonstrated that calbindin-D28K prevents staurosporine (STS)-induced caspase activation and subsequent apoptosis in a neuronal cell line. However, the role of calbindin-D28K in STS-induced activation of calpain and necrotic cell death was not identified. Staurosporine induced the elevation of intracellular calcium after 1 hr of treatment. Overexpression of calbindin-D28K and presence of a calcium chelator, BAPTA, prevented the increase of calcium in STS-treated cells. Cleavage of Bax by calpain was prevented by the overexpressed calbindin-D28K. Permeabilization of the plasma membrane, a factor in necrosis, as well as apoptotic change of the nucleolus induced by STS, was prevented by calbindin-D28K. Thus, our study suggests that calbindin-D28K may exert its protective functions by preventing calpain activation in necrotic cell death, in addition to its effect on the caspase-apoptosis pathway.
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calbindin-D28k, calcium, calpain, neuronal cell death
KMID :
0892920140230020173
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