Miao-Miao Bi - Department of Ophthalmology, The Second Hospital of Jilin University, Jilin University, Changchun, Jilin, ۱۳۰۰۴۱, P.R. China
Sen Hong - Department of Colon and Anal Surgery, the First hospital of Jilin University, Jilin University, Changchun, Jilin, ۱۳۰۰۲۱, P.R. China
Ling-Jun Ma - Department of Ophthalmology, The China-Japan Union Hospitial of Jilin University, Jilin University, Changchun, Jilin, ۱۳۰۰۳۳, Xiantai Street No. ۱۲۶, Jilin Province, China
Hong-Yan Zhou - Department of Ophthalmology, The China-Japan Union Hospitial of Jilin University, Jilin University, Changchun, Jilin, ۱۳۰۰۳۳, Xiantai Street No. ۱۲۶, Jilin Province, China
Jia Lu - Department of Ophthalmology, The China-Japan Union Hospitial of Jilin University, Jilin University, Changchun, Jilin, ۱۳۰۰۳۳, Xiantai Street No. ۱۲۶, Jilin Province, China
Jing Zhao - Department of Ophthalmology, The China-Japan Union Hospitial of Jilin University, Jilin University, Changchun, Jilin, ۱۳۰۰۳۳, Xiantai Street No. ۱۲۶, Jilin Province, China
Ya-Juan Zheng - Department of Ophthalmology, The Second Hospital of Jilin University, Jilin University, Changchun, Jilin, ۱۳۰۰۴۱, P.R. China

Objective(s): The purpose of this study was to investigate the role of chloride channel protein ۲ (ClC-۲) in glutamate-induced apoptosis in the retinal ganglion cell line (RGC-۵). Materials and Methods: RGC-۵ cells were treated with ۱ mM glutamate for ۲۴ hr. The expression of ClC-۲, Bax, and Bcl-۲ was detected by western blot analysis. Cell survival and apoptosis were measured by ۳-(۴,۵-dimethylthiazol-۲-yl)-۲,۵-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Caspase-۳ and -۹ activities were determined by a colorimetric assay. The roles of ClC-۲ in glutamate-induced apoptosis were examined by using ClC-۲ complementary deoxyribonucleic acid (cDNA) and small inference ribonucleic acid (RNA) transfection technology. Results: Overexpression of ClC-۲ in RGC-۵ cells significantly decreased glutamate-induced apoptosis and increased cell viability, whereas silencing of ClC-۲ with short hairpin (sh) RNA produced opposite effects. ClC-۲ overexpression increased the expression of Bcl-۲, decreased the expression of Bax, and decreased caspase-۳ and -۹ activation in RGC-۵ cells treated with glutamate, but silencing of ClC-۲ produced opposite effects. Conclusion: Our data suggest that ClC-۲ chloride channels might play a protective role in glutamate-induced apoptosis in retinal ganglion cells via the mitochondria-dependent apoptosis pathway.

Apoptosis, Chloride channels, Chloride channel protein ۲ Neuroprotection, Retinal ganglion cells