Functional Expression of NAD(P)H Oxidase p47 in Lung Microvascular Endothelial Cells

Murphy, Hedwig S.; Yu, Chuliang; Quddus, Jawaid

doi:10.1006/bbrc.2000.3848

Cited by 12 publications

(14 citation statements)

References 37 publications

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“…Precise mechanisms underlying agonist-induced nonphagocyte NADPH oxidase activation are not yet understood, but it is clear that both acute protein modification and chronic changes in expression levels may be involved. Several studies have shown a crucial role of the p47 phox subunit in agonist-induced (angiotensin II [Ang II], PMA, TNF-␣, growth factors, and thrombin) vascular cell NADPH oxidase activation (18,(21)(22)(23) and in the development of atherosclerotic lesions in ApoEϪ/Ϫ mice (24). We also found that coronary microvascular endothelial cells isolated from wild-type mice respond to PMA and TNF-␣ with a significant increase in O 2 Ϫ generation.…”

Section: Agonist-induced Nadph Oxidase Activationsupporting

confidence: 60%

ROS Generation by Nonphagocytic NADPH Oxidase

Shah

2003

Journal of the American Society of Nephrology

269

192

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Abstract. Oxidative stress has emerged as an important pathogenic factor in the development of long-term complications, such as atherosclerosis and nephropathy, in patients with diabetes. Whereas multiple enzymes and processes can contribute to oxidative stress, recent studies indicate that a multicomponent phagocyte-type NADPH oxidase is a major source of reactive oxygen species (ROS) production in many nonphagocytic cells, including fibroblasts, vascular smooth muscle cells, endothelial cells, renal mesangial cells, and tubular cells. Under physiologic conditions, nonphagocytic NADPH oxidases have very low-level constitutive activity. However, enzyme activity can be upregulated both acutely and chronically in response to stimuli such as growth factors, cytokines, high glucose, and hyperlipidemia. ROS production by the oxidase may serve a signaling role or may lead to oxidative damage. This article reviews current knowledge of the nonphagocyte-NADPH oxidases at both structural and biochemical levels and discusses the possible role of these enzymes in the pathophysiology of diabetic nephropathy.

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Section: Agonist-induced Nadph Oxidase Activationsupporting

confidence: 60%

ROS Generation by Nonphagocytic NADPH Oxidase

Shah

2003

Journal of the American Society of Nephrology

269

192

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“…A recent study has demonstrated that NADPH oxidase is responsible for the generation of superoxide in mouse lung microvascular endothelial cells stimulated with PMA, and that the superoxide release is inhibited by DPI. 34) These results indicate that NADPH oxidases, originating from lung microvascular endothelial cells as well as from neutrophils, participate in superoxide generation.…”

Section: Discussionmentioning

confidence: 85%

“…The doses of DPI, a NADPH oxidase inhibitor, 32) and allopurinol, a xanthine oxidase inhibitor, 33) to inhibit superoxide generation were chosen as follows. Some in vitro studies have reported that DPI at concentrations ranging from 10 to 100 mM exerted an inhibitory effect on superoxide generation from pulmonary microvascular endothelial cells stimulated with paraquat or phorbol ester (PMA), 4,34) and the inhibition of NADPH oxidase activity in neutrophils was complete at DPI concentrations above 10 mM. 33) A dose of 600 mg/kg DPI (i.v.)…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress in Early Stage of Acute Lung Injury Induced with Oleic Acid in Guinea Pigs.

Chen

Moriuchi

Takase

et al. 2003

Biological & Pharmaceutical Bulletin

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Changes in several biomarkers in bronchoalveolar lavage fluid (BALF) during an early stage of lung injury induced with oleic acid were examined in guinea pigs. In addition, a possible contribution of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase to the oxidative changes in the lung injury was investigated. An intravenous injection of oleic acid increased the levels of lipid peroxidation products, lactate dehydrogenase, and total proteins, decreased the ratio of glutathione to glutathione disulfide in the BALF, and also affected the levels of other oxidative biomarkers such as superoxide dismutase and catalase in the BALF in a dose-dependent manner. Diphenyleneiodonium chloride, a NADPH oxidase inhibitor, inhibited the oxidative changes in the BALF and the decrease in partial pressure of oxygen in artery induced with oleic acid, while allopurinol, a xanthine oxidase inhibitor, had no inhibitory effects. The results demonstrate that oxidative stress would be an important mechanism of oleic acid-induced lung injury, and indicate that the NADPH oxidase-dependent pathway contributes significantly to the generation of reactive oxygen species in oleic acid-induced lung injury.Key words oleic acid; acute lung injury; oxidative stress; nicotinamide adenine dinucleotide phosphate (NADPH) oxidase; diphenyleneiodonium chloride; bronchoalveolar lavage fluid 424

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“…generation may play a critical role. 3,5 Two potential inducible intracellular sources of reactive oxygen species (ROS) are nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a flavin-containing enzyme present in polymorphonuclear cells and in the systemic and pulmonary vasculature, 6,7 and xanthine oxidase, a modified form of the ubiquitous enzyme xanthine dehydrogenase. 8 In resting cells, NADPH oxidase has a low level of activity, and its protein components are segregated into cytoplasmic and plasma membrane compartments.…”

mentioning

confidence: 99%

Stable Compounds of Cigarette Smoke Induce Endothelial Superoxide Anion Production via NADPH Oxidase Activation

Jaimes

DeMaster

Tian

et al. 2004

ATVB

229

155

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Objective-Endothelial dysfunction is an early manifestation of cigarette smoke (CS) toxicity. We have previously demonstrated that CS impairs nitric oxide (NO)-mediated endothelial function via increased generation of superoxide anion (O 2 . ). In these studies, we investigated whether stable compounds present in CS activate specific pathways responsible for the increased endothelial O 2 . production.Methods and Results-Short exposure of bovine pulmonary artery endothelial cells (BPAECs), human pulmonary artery endothelial cells, and rat pulmonary arteries to CS extracts (CSEs) resulted in a large increase in O 2 . production (20-fold, 3-fold, and 2-fold increase, respectively; PϽ0.05 versus control), which was inhibited by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors diphenyleneiodinium, apocynin, and gp91 docking sequence-tat peptide but not by oxypurinol, the NO synthase inhibitor N G -nitro-L-arginine methyl ester, or the mitochondrial respiration inhibitor rotenone. Exposure of BPAECs to acrolein, a stable thiol-reactive agent found in CS, increased O 2. production 5-fold, which was prevented by prior inhibition of NADPH oxidase. Conclusions-These

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Functional Expression of NAD(P)H Oxidase p47 in Lung Microvascular Endothelial Cells

Cited by 12 publications

References 37 publications

ROS Generation by Nonphagocytic NADPH Oxidase

ROS Generation by Nonphagocytic NADPH Oxidase

Oxidative Stress in Early Stage of Acute Lung Injury Induced with Oleic Acid in Guinea Pigs.

Stable Compounds of Cigarette Smoke Induce Endothelial Superoxide Anion Production via NADPH Oxidase Activation

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