The Effect of Induced Heat Shock Protein 33 in Human Corneal Epithelial Cell.
- Author:
Jung Soon HAN
1
;
Sun Mi KO
;
Hee Gu LEE
;
Jae Chan KIM
Author Information
1. Department of Ophthalmology, Chung-Ang University, College of Medicine, Korea. jck50eye@kornet.net
- Publication Type:Original Article
- Keywords:
Apoptosis;
Heat shock protein 33 (HSP 33);
Human corneal cell (HCE)
- MeSH:
Apoptosis;
Blotting, Western;
Cell Count;
Epithelial Cells*;
Etoposide;
Heat-Shock Proteins*;
Hot Temperature*;
Humans*;
Hydrogen Peroxide;
Oxidative Stress;
Shock;
Transfection
- From:Journal of the Korean Ophthalmological Society
2003;44(10):2353-2357
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The purposes of study was to assess the expression patterns of heat shock protein 33 (HSP33) after gene transfection and to evaluate the protective effects of heat shock protein 33 from apoptosis and oxidative stress in transfected human corneal epithelial cell. METHODS: The cultured human corneal epithelial cells were divided control and experimental group. Experimental group was transfected with HSP 33. After transfection, the experimental group was treated with etoposide (induced apoptosis) and hydrogen peroxide (induced oxidative stress). The expression patterns of HSP 33 was0 examined by western blot. The viability (cell protection rate of heat shock protein) and protective effect against apoptosis after etoposide and hydrogen peroxide treatment were measured using 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay. RESULTS: Expression of Heat shock protein 33 was increased in the transfection group compared with non-transfection group. The increased cell number (viability=anti-apoptotic effect of heat shock protein) of transfection group with induced HSP 33 etoposide and hydrogen peroxide treatment show that Hsp 33 appeared to have protective effect in Human corneal epithelial cell from apoptosis and oxidative stress. CONCLUSIONS: These data suggest that experimentally induced heat shock protein 33 could protect etoposide-generated apoptosis and hydreogen peroxide generated oxidative stress in human corneal epithelial cell.
