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  • Title: Endothelial MnSOD overexpression prevents retinal VEGF expression in diabetic mice.
    Author: Goto H, Nishikawa T, Sonoda K, Kondo T, Kukidome D, Fujisawa K, Yamashiro T, Motoshima H, Matsumura T, Tsuruzoe K, Araki E.
    Journal: Biochem Biophys Res Commun; 2008 Feb 15; 366(3):814-20. PubMed ID: 18083119.
    Abstract:
    We previously proposed that hyperglycemia-induced mitochondrial ROS overproduction is a key event in the development of diabetic complications. In this study, we established a novel transgenic mouse (eMnSOD-Tg), which specifically expressed MnSOD in endothelial cells, by employing a Tie2 promoter/enhancer, and investigated the impact of mitochondrial ROS production on diabetic retinopathy in vivo. Using immunohistochemistry, overexpression of MnSOD in endothelial cells was confirmed in eMnSOD-Tg mice. By introduction of diabetes by streptozotocin, levels of urinary 8-hydroxydeoxyguanosine, a marker of mitochondrial oxidative stress, and expression of VEGF mRNA and protein and fibronectin mRNA in retinas were increased in wild-type littermates. However, these observations were ameliorated in eMnSOD-Tg mice, although control and eMnSOD-Tg mice showed a comparable level of hyperglycemia. In the present study, we newly developed a line of transgenic mice, which specifically express MnSOD in endothelium. In addition, overexpression of mitochondrial-specific SOD in endothelium could prevent diabetic retinopathy in vivo.
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