Exp Neurobiol.  2014 Jun;23(2):173-177. 10.5607/en.2014.23.2.173.

Calbindin-D28K Prevents Staurosporin-induced Bax Cleavage and Membrane Permeabilization

Affiliations
  • 1School of Biological Sciences and Technology, College of Natural Sciences, College of Medicine, Chonnam National University, Gwangju 500-757, Korea. choiw@chonnam.ac.kr
  • 2Department of Biology, Yonsei University College of Life Science and Biotechnology, Seoul 120-749, Korea. yjoh@yonsei.ac.kr

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.

Keyword

calbindin-D28k; calcium; calpain; neuronal cell death

MeSH Terms

Apoptosis
Calbindin 1*
Calcium
Calpain
Cell Death
Cell Line
Cell Membrane
Membranes*
Necrosis
Neurons
Staurosporine
Calcium
Calpain
Staurosporine
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