Chloride channel protein 2 prevents glutamate-induced apoptosis in retinal ganglion cells

Bi, Miao-Miao and Hong, Sen and Ma, Ling-Jun and Zhou, Hong-Yan and Lu, Jia and Zhao, Jing and Zheng, Ya-Juan (2016) Chloride channel protein 2 prevents glutamate-induced apoptosis in retinal ganglion cells. Iranian Journal of Basic Medical Sciences, 19 (7). pp. 705-711.

IJBMS_Volume 19_Issue 7_Pages 705-711.pdf

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Objective(s): The purpose of this study was to investigate the role of chloride channel protein 2 (ClC-2) in glutamate-induced apoptosis in the retinal ganglion cell line (RGC-5). Materials and Methods: RGC-5 cells were treated with 1 mM glutamate for 24 hr. The expression of ClC-2, Bax, and Bcl-2 was detected by western blot analysis. Cell survival and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Caspase-3 and -9 activities were determined by a colorimetric assay. The roles of ClC-2 in glutamate-induced apoptosis were examined by using ClC-2 complementary deoxyribonucleic acid (cDNA) and small inference ribonucleic acid (RNA) transfection technology. Results: Overexpression of ClC-2 in RGC-5 cells significantly decreased glutamate-induced apoptosis and increased cell viability, whereas silencing of ClC-2 with short hairpin (sh) RNA produced opposite effects. ClC-2 overexpression increased the expression of Bcl-2, decreased the expression of Bax, and decreased caspase-3 and -9 activation in RGC-5 cells treated with glutamate, but silencing of ClC-2 produced opposite effects. Conclusion: Our data suggest that ClC-2 chloride channels might play a protective role in glutamate-induced apoptosis in retinal ganglion cells via the mitochondria-dependent apoptosis pathway.

Item Type: Article
Subjects: QT physiology
Divisions: Journals > Iranian J Basic Medical Sciences
Depositing User: ijbms ijbms
Date Deposited: 28 Sep 2017 14:48
Last Modified: 28 Sep 2017 14:48

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