NADPH oxidase

Babior, Bernard M.

doi:10.1016/j.coi.2003.12.001

Cited by 973 publications

(979 citation statements)

References 61 publications

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“…The prototypical phagocytic NAD(P)H oxidase comprises five subunits: p47phox ('phox' stands for phagocyte oxidase), p67phox, p40phox, p22phox and the catalytic subunit gp91phox (also termed Nox2). 69,70 In unstimulated cells p47phox, p67phox and p40phox, exist in the cytosol, whereas p22phox and gp91phox are in the membrane, where they occur as a heterodimeric flavoprotein, (cytochrome b558). On stimulation p47phox is phosphorylated and the cytosolic subunits 2 ) and Rho kinase.…”

Section: Vascular Generation Of Rosmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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Increased vascular production of reactive oxygen species (ROS; termed oxidative stress) has been implicated in various chronic diseases, including hypertension. Oxidative stress is both a cause and a consequence of hypertension. Although oxidative injury may not be the sole etiology, it amplifies blood pressure elevation in the presence of other pro-hypertensive factors. Oxidative stress is a multisystem phenomenon in hypertension and involves the heart, kidneys, nervous system, vessels and possibly the immune system. Compelling experimental and clinical evidence indicates the importance of the vasculature in the pathophysiology of hypertension and as such much emphasis has been placed on the (patho)biology of ROS in the vascular system. A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Nox-derived ROS is important in regulating endothelial function and vascular tone. Oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in hypertension. Despite a plethora of data implicating oxidative stress as a causative factor in experimental hypertension, findings in human hypertension are less conclusive. This review highlights the importance of ROS in vascular biology and focuses on the potential role of oxidative stress in human hypertension.

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Section: Vascular Generation Of Rosmentioning

confidence: 99%

Reactive oxygen species and vascular biology: implications in human hypertension

2010

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“…Recently, similar ROS-generating oxidases have been shown to exist also in nonphagocytic cells, including fibroblasts (Babior, 1999). NAD(P)H oxidase affects signal transduction by growth factor receptors (Ammendola et al, 2002) and promotes proliferation in a variety of cell types (Irani and Goldschmidt-Clermont, 1998).…”

Section: Introductionmentioning

confidence: 99%

Regulation of normal cell cycle progression by flavin-containing oxidases

Prakash¹,

Toledo²,

Pandey³

et al. 2007

Oncogene

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Mechanisms underlying the role of reactive oxygen species (ROS) generated by flavin-containing oxidases in regulating cell cycle progression were examined in human and rodent fibroblasts. Incubation of confluent cell cultures with nontoxic/nonclastogenic concentrations of the flavoprotein inhibitor, diphenyleneiodonium (DPI), reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase activity and basal ROS levels, but increased proteolysis of cyclin D1, p21 Waf1 and phospho-p38 MAPK . When these cells were allowed to proliferate by subculture in DPI-free medium, an extensive G 1 delay was observed with concomitant activation of p53/p21 Waf1 signaling and reduced phosphorylation of mitogen-activated kinases. Compensation for decreased oxidant generation by simultaneous exposure to DPI and nontoxic doses of the ROS generators, c-radiation or t-butyl-hydroperoxide, attenuated the G 1 delay. Whereas the DPI-induced G 1 checkpoint was completely dependent on PHOX91, ATM and WAF1, it was only partially dependent on P53. Interestingly, G 1 to S progression was not affected when another flavin-containing enzyme, nitric oxide synthase, was inhibited nor was it associated with changes in mitochondrial membrane potential. Proliferating cells treated with DPI also experienced a significant but attenuated delay in G 2 . We propose that ATM performs a critical function in mediating normal cellular proliferation that is regulated by nonphagocytic NAD(P)H oxidase enzymes activity, which may serve as a novel target for arresting cancer cells in G 1 .

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“…eNOS is a calcium-dependent NADPH oxidase with a C-terminal reductase domain that binds NADPH, FAD, and FMN, and an N-terminal oxygenase domain that binds a heme moiety, tetrahydrobiopterin (BH4), and L-arginine (27)(28)(29). Classically, NADPH oxidase serves a specialized function in host defense against invading microorganisms by catalyzing ROS generation (30,31). Purified recombinant eNOS was shown to catalyze reactive oxygen species (ROS) formation, requiring Ca 2+ /calmodulin and primarily regulated by BH4 (15).…”

Section: Discussionmentioning

confidence: 99%

H. pylori Escape Host Immunoreaction Through Inhibiting ILK Expression by VacA

Yuan

Tao

et al. 2009

Cell Mol Immunol

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Helicobacter pylori (H. pylori) persistently colonizes the gastric mucosa despite a vigorous immune response. Vacuolating cytotoxin secreted by H. pylori has turned out to be a potent immunomodulatory toxin, but the signal transduction pathways involved has not been studied in macrophages. We observed in this study that vacA-deficient H. pylori induced significantly higher expression of integrin-linked kinase (ILK) and endothelial nitric oxygen synthase (eNOS), and significantly more production of reactive oxygen species (

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NADPH oxidase

Cited by 973 publications

References 61 publications

Reactive oxygen species and vascular biology: implications in human hypertension

Reactive oxygen species and vascular biology: implications in human hypertension

Regulation of normal cell cycle progression by flavin-containing oxidases

H. pylori Escape Host Immunoreaction Through Inhibiting ILK Expression by VacA

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