Format

Send to

Choose Destination
BMC Ophthalmol. 2003 Mar 21;3:5.

Oxidative stress causes ERK phosphorylation and cell death in cultured retinal pigment epithelium: prevention of cell death by AG126 and 15-deoxy-delta 12, 14-PGJ2.

Author information

1
Departments of Anatomy & Neurobiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. gargtarunk@uams.edu

Abstract

BACKGROUND:

The retina, which is exposed to both sunlight and very high levels of oxygen, is exceptionally rich in polyunsaturated fatty acids, which makes it a favorable environment for the generation of reactive oxygen species. The cytotoxic effects of hydrogen peroxide (H2O2) induced oxidative stress on retinal pigment epithelium were characterized in this study.

METHODS:

The MTT cell viability assay, Texas-Red phalloidin staining, immunohistochemistry and Western blot analysis were used to assess the effects of oxidative stress on primary human retinal pigment epithelial cell cultures and the ARPE-19 cell line.

RESULTS:

The treatment of retinal pigment epithelial cells with H2O2 caused a dose-dependent decrease of cellular viability, which was preceded by a significant cytoskeletal rearrangement, activation of the Extracellular signal-Regulated Kinase, lipid peroxidation and nuclear condensation. This cell death was prevented partially by the prostaglandin derivative, 15d-PGJ2 and by the protein kinase inhibitor, AG126.

CONCLUSION:

15d-PGJ2 and AG126 may be useful pharmacological tools in the future capable of preventing oxidative stress induced RPE cell death in human ocular diseases.

PMID:
12659653
PMCID:
PMC153521
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center