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Y. Chen, N. Ha, G.E. McClellan, P. Sternberg, J. Cai; Hyperglycemia–Induced Oxidation of Mitochondrial Thioredoxin in the RPE . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5534.
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To determine whether mitochondrial thioredoxin (mtTrx) is a target of oxidative injury induced by hyperglycemia in cultured human RPE cells.
Human RPE cells were isolated from donor eyes and cultured in vitro. Cells were treated with either 1 or 4.5 g/L glucose for up to 4 days. Time–dependent changes in the redox status of mtTrx was measured by a modified Western blot approach. Intracellular glutathione was measured by HPLC. The mRNA levels of VEGF and PEDF expression were measured by real–time RT–PCR analyses.
High glucose caused oxidation of mtTrx, in a time course that was comparable to the oxidation of the glutathione pool. High glucose also caused upregulation of VEGF and downregulation of PEDF. Overexpression of mtTrx in the RPE cells inhibited the hyperglycemia–induced decrease in the ratio between PEDF and VEGF.
Oxidative stress is known to contribute to the chronic complications of diabetes mellitus. Oxidative damage to mtTrx is likely to be a key event in hyperglycemia–induced retinal damage and increased mtTrx may protect against diabetic retinopathy.
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