Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3035866 | Autonomic Neuroscience | 2006 | 7 Pages |
Abstract
Superoxide anion (O2
- â) is increased throughout the arterial wall in atherosclerosis. The oxidative stress contributes to lesion formation and vascular dysfunction. In the present study, we tested the hypothesis that NAD(P)H oxidase-derived O2
- â is increased in nodose sensory ganglia and sympathetic ganglia of apolipoprotein E deficient (apoEâ/â) mice, an established animal model of atherosclerosis. O2
- â measured ex vivo by L-012-enhanced chemiluminescence was increased by 79 ± 17% in whole sympathetic ganglia from apoEâ/â mice (n = 5) compared with sympathetic ganglia from control mice (n = 5) (P < 0.05). In contrast, O2
- â was not elevated in nodose ganglia from apoEâ/â mice. Dihydroethidium staining confirmed the selective increase in O2
- â in sympathetic ganglia of apoEâ/â mice, and revealed the contribution of both neurons and non-neuronal cells to the O2
- â generation. We investigated the enzymatic source of increased O2
- â in sympathetic ganglia of apoEâ/â mice. The mRNA expression of gp91phox, p22phox, p67phox, and p47phox subunits of NAD(P)H oxidase measured by real time RT-PCR was increased â¼Â 3-4 fold in sympathetic ganglia of apoEâ/â mice (n = 5) compared with control ganglia (n = 5). NADPH oxidase activity measured by lucigenin chemiluminescence was increased by 68 ± 12% in homogenates of sympathetic ganglia from apoEâ/â mice (n = 7) compared with control ganglia (n = 7) (P < 0.05). The results identify sympathetic ganglia as a novel site of oxidative stress in atherosclerosis, and suggest that upregulation of NAD(P)H oxidase is the source of increased O2
- â generation. We speculate that oxidative stress in sympathetic ganglia may contribute to impaired baroreflex control of sympathetic nerve activity.
- â) is increased throughout the arterial wall in atherosclerosis. The oxidative stress contributes to lesion formation and vascular dysfunction. In the present study, we tested the hypothesis that NAD(P)H oxidase-derived O2
- â is increased in nodose sensory ganglia and sympathetic ganglia of apolipoprotein E deficient (apoEâ/â) mice, an established animal model of atherosclerosis. O2
- â measured ex vivo by L-012-enhanced chemiluminescence was increased by 79 ± 17% in whole sympathetic ganglia from apoEâ/â mice (n = 5) compared with sympathetic ganglia from control mice (n = 5) (P < 0.05). In contrast, O2
- â was not elevated in nodose ganglia from apoEâ/â mice. Dihydroethidium staining confirmed the selective increase in O2
- â in sympathetic ganglia of apoEâ/â mice, and revealed the contribution of both neurons and non-neuronal cells to the O2
- â generation. We investigated the enzymatic source of increased O2
- â in sympathetic ganglia of apoEâ/â mice. The mRNA expression of gp91phox, p22phox, p67phox, and p47phox subunits of NAD(P)H oxidase measured by real time RT-PCR was increased â¼Â 3-4 fold in sympathetic ganglia of apoEâ/â mice (n = 5) compared with control ganglia (n = 5). NADPH oxidase activity measured by lucigenin chemiluminescence was increased by 68 ± 12% in homogenates of sympathetic ganglia from apoEâ/â mice (n = 7) compared with control ganglia (n = 7) (P < 0.05). The results identify sympathetic ganglia as a novel site of oxidative stress in atherosclerosis, and suggest that upregulation of NAD(P)H oxidase is the source of increased O2
- â generation. We speculate that oxidative stress in sympathetic ganglia may contribute to impaired baroreflex control of sympathetic nerve activity.
Keywords
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Authors
Xiuying Ma, Hannah J. Zhang, Carol A. Whiteis, Xin Tian, Robin L. Davisson, Kevin C. Kregel, Francois M. Abboud, Mark W. Chapleau,