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W. Lee, M.A. Marchetti, T.M. Wells, E. Karlin, C. DeLeo, M. Kantorow; Peroxiredoxins Are Induced by H2O2 in Human Lens Cells and Mitochondria–Specific PRX3 Protects Against Oxidative Stress Damage . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3518.
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© ARVO (1962-2015); The Authors (2016-present)
Peroxiredoxins (PRXs) are thioredoxin–dependent peroxidases induced by oxidative stress that can protect multiple cells against oxidative stress damage. Of the six known PRXs, PRX3 is specific for the mitochondria. In the present study we tested the hypothesis that human lens cells respond to oxidative stress through the induction of mitochondrial PRX3 and that PRX3 could defend lens cells against oxidative stress damage.
The transcript levels of PRXs 1–6 were evaluated in microdissected human lens epithelium and fiber cells. The induction of these genes upon H2O2–oxidative stress exposure was monitored in human lens epithelial cells by semi–quantitative RT–PCR and the corresponding protein level of PRX3 was evaluated by western blotting. The ability of PRX 3 to protect lens cells against oxidative stress damage was evaluated by examining lens cell viability upon siRNA targeted silencing of the PRX3 gene in the presence of H2O2.
Prxs 1–6 are expressed in human lens epithelium and fiber cells. PRXs 2–6 were induced in human lens epithelia cells by H2O2. The mitochondrial–specific PRX3 gene was induced at levels 10–20 times higher than endogenous levels in the presence of 2–50µM H2O2. Targeted gene silencing of PRX 3 resulted in a 50% loss of lens cell viability upon exposure to 50µM H2O2.
The induction of PRXs in human lens cells provides evidence that PRX expression is a key lens defense response to oxidative stress. Protection of lens cells against oxidative stress by PRX3 suggests that maintenance of mitochondrial function is important for the survival of lens cells under oxidative conditions. Collectively, the present data implicates PRX3 and other PRXs as key lens defense enzymes that could play major roles in the formation of cataract if their normal functions are lost.
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