Expression of NADH/NADPH Oxidase p22
            <sup>phox</sup>
            in Human Coronary Arteries

Azumi, Hiroshi; Inoue, N.; Takeshita, Saori; Rikitake, Yoshiyuki; Kawashima, Seinosuke; Hayashi, Yoshitake; Itoh, Hiroshi; Yokoyama, Mitsuhiro

doi:10.1161/01.cir.100.14.1494

Cited by 244 publications

(195 citation statements)

References 8 publications

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“…In vivo, macrophage-induced expression of phagocytic gp91phox (Nox2) as well as the catalytic subunit p22phox have been characterized within the lesion of atherosclerotic plaques in human coronary arteries as well as an increase in smooth muscle Nox 4 expression within advanced lesions [140]. Sorescu et al observed the increase in p22phox within the medial layer of the vessel wall as well as the plaque, which agree with earlier studies by Azumi and colleagues [6,140]. The novel observation proved to be that gp91phox expression is found in the plaque and adventitial macrophages, particularly the core of the plaque, where Nox 4 expression is complementary to gp91phox located in the medial smooth muscle layer and luminal surface of the plaque smooth muscle cells.…”

Section: Nadph Oxidase Expression and Function In Vascular Injurysupporting

confidence: 78%

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

Ginnan

Guikema

Halligan

et al. 2008

Free Radical Biology and Medicine

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Inflammation plays a critical role in promoting smooth muscle migration and proliferation during vascular diseases such as post-angioplasty restenosis and atherosclerosis. Another common feature of many vascular diseases is the contribution of reactive oxygen (ROS) and nitrogen (RNS) species to vascular injury. Primary sources of ROS and RNS in smooth muscle are several isoforms of NADPH oxidase (Nox) and the cytokine-regulated inducible nitric oxide (NO) synthase (iNOS). One important example of the interaction between NO and ROS is the reaction of NO with superoxide to yield peroxynitrite, which may contribute to the pathogenesis of hypertension. In this review, we discuss the literature that supports an alternate possibility: Nox-derived ROS modulate NO bioavailability by altering the expression of iNOS. We highlight data showing co-expression of iNOS and Nox in vascular smooth muscle and demonstrating the functional consequences of iNOS and Nox during vascular injury. We describe the relevant literature demonstrating that the mitogen activated protein kinases (MAP kinases) are important modulators of pro-inflammatory cytokinedependent expression of iNOS. A central hypothesis discussed is that ROS-dependent regulation of the serine/threonine kinase protein kinase Cδ (PKCδ) is essential to understanding how Nox may regulate signaling pathways leading to iNOS expression. Overall, the integration of non-phagocytic NADPHoxidase with cytokine signaling in general and in vascular smooth muscle in particular is poorly understood and merit further investigation.

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Section: Nadph Oxidase Expression and Function In Vascular Injurysupporting

confidence: 78%

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

Ginnan

Guikema

Halligan

et al. 2008

Free Radical Biology and Medicine

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“…These findings are in line with recent observations that the expression of NAD(P)H oxidase subunits, such as p22phox, is increased in atherosclerotic coronary arteries. 26,29 Increased O 2 ·Ϫ formation by NAD(P)H oxidase may also contribute to impaired endothelium-dependent vasodilation. Guzik et al 30 demonstrated an inverse relationship between NAD(P)H oxidase activity and endothelium-dependent vasodilation in human saphenous veins obtained from patients with coronary artery disease and identified risk factors.…”

Section: Discussionmentioning

confidence: 99%

Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease

et al. 2003

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Background-Increased inactivation of nitric oxide by superoxide (O 2 ·Ϫ ) contributes to endothelial dysfunction in patients with coronary disease (CAD). We therefore characterized the vascular activities of xanthine oxidase and NAD(P)H oxidase, 2 major O 2 ·Ϫ -producing enzyme systems, and their relationship with flow-dependent, endothelium-mediated vasodilation (FDD) in patients with CAD. Methods and Results-Xanthine-and NAD(P)H-mediated O 2 ·Ϫ formation was determined in coronary arteries from 10 patients with CAD and 10 controls by using electron spin resonance spectroscopy. Furthermore, activity of endothelium-bound xanthine oxidase in vivo and FDD of the radial artery were determined in 21 patients with CAD and 10 controls. FDD was measured before and after infusion of the antioxidant vitamin C (25 mg/min i.a.) to determine the portion of FDD inhibited by radicals. In coronary arteries from patients with CAD, xanthine-and NAD (P) 05).Conclusions-The present study represents the first electron spin resonance measurements of xanthine and NAD(P)H oxidase activity in human coronary arteries and supports the concept that increased activities of both enzymes contribute to increased vascular oxidant stress in patients with CAD. Furthermore, the present study suggests that increased xanthine oxidase activity contributes to endothelial dysfunction in patients with CAD and may thereby promote the atherosclerotic process.

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“…One of its components, the p22phox is required for oxidase activity. 1 This enzyme complex plays a major role in superoxide ion production in blood vessels. [1][2][3][4] Superoxide ions are known to avidly interact with nitric oxide (NO), reducing its bioactivity by generating peroxynitrite.…”

Section: Introductionmentioning

confidence: 99%

“…1 This enzyme complex plays a major role in superoxide ion production in blood vessels. [1][2][3][4] Superoxide ions are known to avidly interact with nitric oxide (NO), reducing its bioactivity by generating peroxynitrite. [2][3][4] Increased activity of the NAD(P)H oxidase system is expected to be associated with reduced NO levels, vascular dysfunction, hypertension and salt sensitivity.…”

Section: Introductionmentioning

confidence: 99%

NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

et al. 2006

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Mutations in the NAD(P)H oxidase gene may be associated with abnormal superoxide generation, nitric oxide (NO) availability and cardiovascular diseases. We investigated the prevalence of the NAD(P)H oxidase p22phox gene C242T polymorphism, and its possible association with blood pressure, NO production, salt sensitivity and cardiovascular risk factors in Hispanics. Genotype frequencies were as follows: CC, 52.9%; CT, 40.3%; and TT, 6.8%. There were no significant differences in systolic blood pressure, diastolic blood pressure, age, weight, fasting and post-load glucose levels, LDL and HDL cholesterol, triglyceride and urinary albumin levels in subjects with CC, CT or the TT genotypes. Presence of the T allele was associated with increased salt sensitivity in women, but not in men.NO metabolite excretion was markedly decreased both in women and men with the TT genotype (CC: 868779 lmol/day; CT: 839775 lmol/day; TT: 5347 78 lmol/day; Po0.05). In conclusion, the prevalence of the NAD(P)H oxidase p22phox gene C242T polymorphism in Venezuelans was comparable to that of Caucasians, but different from that of Chinese and Japanese. Although the T allele was not associated with cardiovascular risk factors, hyperinsulinaemia or hypertension, in women, it appeared to be a genetic susceptibility factor for salt sensitivity. Both in women and men, the p22phox gene may play a role in the genetic control of NO levels.

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Expression of NADH/NADPH Oxidase p22 ^phox in Human Coronary Arteries

Abstract: As atherosclerosis progressed, the expression of p22phox increased through the vessel wall. p22phox might participate in the pathogenesis and pathophysiology of atherosclerotic coronary disease.

Cited by 244 publications

References 8 publications

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease

NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

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Expression of NADH/NADPH Oxidase p22 phox in Human Coronary Arteries

Abstract: As atherosclerosis progressed, the expression of p22phox increased through the vessel wall. p22phox might participate in the pathogenesis and pathophysiology of atherosclerotic coronary disease.

Cited by 244 publications

References 8 publications

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases

Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease

NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

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Product

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About

Expression of NADH/NADPH Oxidase p22 ^phox in Human Coronary Arteries