Articles

  • the Korean Society for Brain and Neural Sciences

Article

Original Article

Exp Neurobiol 2014; 23(2): 173-177

Published online June 30, 2014

https://doi.org/10.5607/en.2014.23.2.173

© The Korean Society for Brain and Neural Sciences

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

Won-Seok Choi1,2* and Young J. Oh2*

1School of Biological Sciences and Technology, College of Natural Sciences, College of Medicine, Chonnam National University, Gwangju 500-757, 2Department of Biology, Yonsei University College of Life Science and Biotechnology, Seoul 120-749, Korea

Correspondence to: *To whom correspondence should be addressed.
Won-Seok Choi
TEL: 82-62-530-1912, FAX: 82-62-530-2199
e-mail: choiw@chonnam.ac.kr
Young J. Oh
TEL: 82-2-2123-2662, FAX: 82-2-312-5657
e-mail: yjoh@yonsei.ac.kr

Received: March 3, 2014; Revised: March 20, 2014; Accepted: March 21, 2014

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.

Keywords: calbindin-D28k, calcium, calpain, neuronal cell death