A novel role for endogenous thioredoxin 2 in protecting cells against the injurious effect of high ambient glucose

TL;DRAbstract

Our laboratory (Physiol Genomics 17: 271, 2004; 21: 222, 2005) and others have found that cellular thiols may be importantly involved in the development of diabetic complications. However, the specific role of each thiol-related gene in diabetic complications is unclear. We began the present study by systematically determining the expression level of 11 thiol-related genes in several tissues from rats with streptozotocin-induced diabetes with or without the insulin treatment. Several genes were found to exhibit diabetes-associated differential expression, including a suppression of thioredoxin 2, a mitochondrial protein, in the aorta. When thioredoxin 2 expression in human umbilical vein endothelial cells was silenced by small interfering RNA, high ambient glucose elicited substantial injurious effects (n=6–9, P<0.05), including decreases in endothelial nitric oxide synthase expression (by 79 ± 15%), basal accumulation of nitrite/nitrate (by 68 ± 16%), and cellular thiols (by 42 ± 8%),

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