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. Author manuscript; available in PMC: 2019 Mar 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2018 Jan 4;38(3):529–541. doi: 10.1161/ATVBAHA.117.309819

Figure 2. Decreased ATP7A expression in T2DM vessels contributes to reduced SOD3 activity, resulting in impaired endothelium-dependent relaxation.

Figure 2

A, Activities of SOD3 and SOD1 in T2DM or control mice aorta were measured by inhibition of cytochrome c reduction by xanthine/xanthine oxidase. Con A-Sepharose chromatography was used to isolate SOD3 from tissue homogenates. Protein levels of SOD1, SOD3 and actin (bottom). Specific activity of SOD1 and SOD3 were determined by the ratio of activity to relative amount of protein (n=4). B, Aortic superoxide production in T2DM and control mice was measured by a lucigenin-enhanced chemiluminescence (5 µmol/L) (n=6). C, Decreased SOD3 activity in T2DM mice aorta is restored in T2DM ATP7A overexpressing mice. Activity and specific activity of SOD3 and SOD1 were assayed, as described (n=4). D, E, F, G, and H, Isometric tension of mesenteric resistance arteries from T2DM with SOD mimetic or SOD3 gene transfer (D and H), transgenic mice overexpressing ATP7A with T2DM (E and F), SOD3KO with T2DM (G), or control mice was measured using a wire myograph. Vasodilation was evoked by ACh and SNP after preconstriction with phenylephrine (1–5 µmol/L) in the presence and absence of cell-permeable SOD mimetic tempol (1 mmol/L) (D), or after injection of adeno-SOD3 or adeno-null (control) (H) (n=5–8). Results are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001, NS, not significant.