Effect of Heat Shock Protein 72 Expression on Etoposide-induced Cell Death of Rat Retinal Ganglion Cells.
- Author:
Seongsoo SOHN
1
;
Ji Eun IM
;
Tae Eun KIM
;
Changwon KEE
Author Information
- Publication Type:Original Article ; Comparative Study ; Research Support, Non-U.S. Gov't
- Keywords: Adenoviral vector; Apoptosis; Glaucoma; Hsp72 heat-shock proteins; Retinal ganglion cells
- MeSH: Animals; Blotting, Western; Cell Death/*genetics; Cell Survival; Cells, Cultured; DNA/*genetics; Disease Models, Animal; Etoposide/toxicity; *Gene Expression Regulation; HSP72 Heat-Shock Proteins/biosynthesis/*genetics; Immunohistochemistry; Rats; Retinal Degeneration/*genetics/metabolism/pathology; Retinal Ganglion Cells/drug effects/*metabolism/pathology
- From:Korean Journal of Ophthalmology 2013;27(1):48-51
- CountryRepublic of Korea
- Language:English
- Abstract: PURPOSE: To assess whether the expression of heat shock protein 72 (Hsp72) protects rat retinal ganglion cells (RGC-5) from apoptotic cell death. METHODS: Hsp72 expression in RGC-5 cells transduced with replication-deficient recombinant adenovirus was analyzed by Western blot analysis and immunofluorescence. The effect of Hsp72 expression on etoposide-induced apoptotic cell death was examined by microscopic analysis and confirmed by cell proliferation assay. RESULTS: Western blot analysis and immunofluorescence clearly showed adenovirus-mediated Hsp72 expression in RGC-5 cells. Treatment with etoposide resulted in the death of a proportion of the cells by apoptosis. However, this apoptotic cell death was significantly reduced in cells expressing Hsp72, with the reduction in cell death correlating to the level of Hsp72 expression. CONCLUSIONS: Over-expression of Hsp72 alone is sufficient to rescue neuronal cells from apoptotic cell death, suggesting that fine-tuning its expression may be an effective neuroprotective approach in retinal degenerative disease.
