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PPAR Research
Volume 2008, Article ID 720163, 7 pages
http://dx.doi.org/10.1155/2008/720163
Review Article

Prevention of Oxidative Stress-Induced Retinal Pigment Epithelial Cell Death by the PPAR Agonists, 15-Deoxy-Delta 12, 14-Prostaglandin

1Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
2Department of Ophthalmology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
3Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA

Received 30 October 2007; Accepted 15 December 2007

Academic Editor: Suofu Qin

Copyright © 2008 Jason Y. Chang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cellular oxidative stress plays an important role in retinal pigment epithelial (RPE) cell death during aging and the development of age-related macular degeneration. Early reports indicate that during phagocytosis of rod outer segments, there is an increase of RPE oxidative stress and an upregulation of PPAR mRNA in these cells. These studies suggest that activation of PPAR may modulate cellular oxidative stress. This paper presents a brief review of recent studies that investigate RPE oxidative stress under various experimental conditions. This is followed by a detailed review on those reports that examine the protective effect of the natural PPAR ligand, 15d-PG , against RPE oxidative stress. This agent can upregulate glutathione and prevent oxidant-induced intracellular reactive oxygen species accumulation, mitochondrial depolarization, and apoptosis. The cytoprotective effect of this agent, however, is not shared by other PPAR agonists. Nonetheless, this property of 15d-PG may be useful in future development of pharmacological tools against retinal diseases caused by oxidative stress.