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• W2126804985 abstract "Arginase can cause vascular dysfunction by competing with nitric oxide synthase for l-arginine and by increasing cell proliferation and collagen formation, which promote vascular fibrosis/stiffening. We have shown that increased arginase expression/activity contribute to vascular endothelial cell (EC) dysfunction. Here, we examined the roles of the two arginase isoforms, arginase I and II (AI and AII, respectively), in this process. Experiments were performed using streptozotocin-induced diabetic mice: wild-type (WT) mice and knockout mice lacking the AII isoform alone (AI +/+ AII −/− ) or in combination with partial deletion of AI (AI +/− AII −/− ). EC-dependent vasorelaxation of aortic rings and arterial fibrosis and stiffness were assessed in relation to arginase activity and expression. Diabetes reduced mean EC-dependent vasorelaxation markedly in diabetic WT and AI +/+ AII −/− aortas (53% and 44% vs. controls, respectively) compared with a 27% decrease in AI +/− AII −/− vessels. Coronary fibrosis was also increased in diabetic WT and AI +/+ AII −/− mice (1.9- and 1.7-fold vs. controls, respectively) but was not altered in AI +/− AII −/− diabetic mice. Carotid stiffness was increased by 142% in WT diabetic mice compared with 51% in AI +/+ AII −/− mice and 19% in AI +/− AII −/− mice. In diabetic WT and AI +/+ AII −/− mice, aortic arginase activity and AI expression were significantly increased compared with control mice, but neither parameter was altered in AI +/− AII −/− mice. In summary, AI +/− AII −/− mice exhibit better EC-dependent vasodilation and less vascular stiffness and coronary fibrosis compared with diabetic WT and AI +/+ AII −/− mice. These data indicate a major involvement of AI in diabetes-induced vascular dysfunction." @default.
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• W2126804985 date "2012-01-01" @default.
• W2126804985 modified "2023-09-25" @default.
• W2126804985 title "Diabetes-induced vascular dysfunction involves arginase I" @default.
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• W2126804985 doi "https://doi.org/10.1152/ajpheart.00774.2011" @default.
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