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Journal of Ophthalmology
Volume 2013, Article ID 185825, 7 pages
http://dx.doi.org/10.1155/2013/185825
Research Article

Essential Role of Thioredoxin 2 in Mitigating Oxidative Stress in Retinal Epithelial Cells

1Department of Chemistry and Bioengineering, Faculty of Engineering, Graduate School of Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan
2School of Medicine, Tohoku University, 2-1 Seiryou-machi, Sendai 980-8574, Japan
3Graduate School of Medicine, Tohoku University, 2-1 Seiryou-machi, Sendai 980-8574, Japan
4Clinical Research, Innovation and Education Center, Tohoku University Hospital, 2-1 Seiryou-machi, Sendai 980-8574, Japan
5Laboratory of Visual Neuroscience, Department of Chemistry and Bioengineering, Faculty of Engineering, Graduate School of Engineering, Iwate University, 4-3-5 Ueda, Morioka, Iwate 020-8551, Japan

Received 7 June 2013; Revised 6 August 2013; Accepted 19 September 2013

Academic Editor: Yoshihiko Usui

Copyright © 2013 Eriko Sugano 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

The retina is constantly subjected to oxidative stress, which is countered by potent antioxidative systems present in retinal pigment epithelial (RPE) cells. Disruption of these systems leads to the development of age-related macular degeneration. Thioredoxin 2 (Trx2) is a potent antioxidant, which acts directly on mitochondria. In the present study, oxidative stress was induced in the human RPE cell line (ARPE-19) using 4-hydroxynonenal (4-HNE) or C2-ceramide. The protective effect of Trx2 against oxidative stress was investigated by assessing cell viability, the kinetics of cell death, mitochondrial metabolic activity, and expression of heat shock proteins (Hsps) in Trx2-overexpressing cell lines generated by transfecting ARPE cells with an adeno-associated virus vector encoding Trx2. We show that overexpression of Trx2 reduced cell death induced by both agents when they were present in low concentrations. Moreover, early after the induction of oxidative stress Trx2 played a key role in the maintenance of the cell viability through upregulation of mitochondrial metabolic activity and inhibition of Hsp70 expression.