The NADPH oxidase of endothelial cells

IUBMB Life

Volumn 50, Issue 4-5, 2000, Pages 267-269

  Babior, B M ^a  

^a SCRIPPS RESEARCH INSTITUTE   (United States)

Author keywords

Superoxide anion

Indexed keywords

REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE;

ENDOTHELIUM CELL; HUMAN; MONOCYTE; NEUTROPHIL; NONHUMAN; OXIDATION; OXIDATIVE STRESS; PHAGOCYTE; REVIEW; SIGNAL TRANSDUCTION;

ANIMALS; ANTICHOLESTEREMIC AGENTS; ENDOTHELIUM, VASCULAR; HUMANS; NADPH OXIDASE; PHAGOCYTES; REACTIVE OXYGEN SPECIES; SUPEROXIDES;

EID: 0034458228     PISSN: 15216543     EISSN: None     Source Type: Journal    
DOI: 10.1080/15216540051080976     Document Type: Review

References (16)

1. Release of hydrogen peroxide in response to hypoxiareoxygenation: Role of an NAD(P)H oxidase-like enzyme in endothelial cell plasma membrane
2. Molecular characterization and localization of the NAD(P)H oxidase component gp91-phox and p22-phox endothelial cells
3. A gp91phox containing NADPH oxidase selectively expressed in endothelial cells is a major source of oxygen radical generation in the arterial wall
4. Expression of functional neutrophil-type NADPH oxidase in cultured rat coronary microvascular endothelial cells
5. Expression of phagocyte NADPH oxidase components in human endothelial cells
6. Identification of a functional leukocyte-type NADPH oxidase in human endothelial cells: A potential atherogenic source of reactive oxygen species
7. The small G-protein Rac mediates depolarization-induced superoxide formation in human endothelial cells
8. +
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10. Simulated ischemia in flow-adapted endothelial cells leads to generation of reactive oxygen species and cell signaling
11. Thrombin stimulated reactive oxygen species production in cultured human endothelial cells
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13. Angiotensin II-induced superoxide anion generation in human vascular endothelial cells: Role of membrane-bound NADH-/NADPH-oxidases
14. Pulsatile stretch stimulates superoxide production in human aortic endothelial cells
15. NADPH Oxidase: An update
16. Improvement of nitric oxide-dependent vasodilatation by HMG-CoA reductase inhibitors through attenuation of endothelial superoxide anion formation