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NOS3 — NOX1
Text-mined interactions from Literome
Yang et al., J Cardiovasc Pharmacol 2000
:
We conclude that estrogen increases
NOx release in HCAECs, which is independent of cytosolic Ca2+ mobilization and is
mediated by the upregulation of
eNOS
Kobayashi et al., J Physiol Pharmacol 2001
(Stomach Ulcer) :
In addition the expression of cyclooxygenase-2 and inducible
nitric oxide synthase proteins increased PGE2 generation and
NOx secretion in the ulcerated stomach were
suppressed by FR167653
Endres et al., Stroke 2004
(Substance Withdrawal Syndrome) :
Rho negatively
regulates endothelial
nitric oxide synthase and Rac contributes to
NAD ( P ) H-oxidase activation and superoxide production
Rask-Madsen et al., Arterioscler Thromb Vasc Biol 2005
(Arteriosclerosis...) :
Furthermore, the review summarizes studies that implicate PKC in promoting proatherogenic mechanisms or inhibiting antiatherogenic mechanisms, including studies of endothelial dysfunction ; gene induction and
activation of vascular
NAD ( P ) H oxidase ; endothelial
nitric oxide synthase expression and function ; endothelin-1 expression ; growth, migration, and apoptosis of vascular smooth muscle cells ; induction of adhesion molecules ; and oxidized low-density lipoprotein uptake by monocyte derived macrophages
Polytarchou et al., Eur J Pharmacol 2005
:
Superoxide dismutase ( SOD ), tempol ( membrane permeable SOD mimetic ) and the
NADPH oxidase inhibitors, 4- ( 2-aminoethyl ) -benzenesulfonyl fluoride and apocynin, but not allopurinol,
inhibited HUVEC proliferation and migration, as well as activity of
endothelial NOS (eNOS)
Basu et al., Crit Rev Microbiol 2005
:
Perturbation of macrophage surface with different bacterial pathogens leads to activate general signal transduction pathways of macrophages, including
activation of
NADPH oxidase ,
nitric oxide synthase , and so on
Hu et al., Am J Hypertens 2006
(Hypertension) :
In male SD rats, apocynin but not l-arginine prevented and reversed Dex-hypertension, suggesting that
NAD ( P ) H oxidase mediated superoxide production but not endothelial
nitric oxide synthase uncoupling is important in Dex-hypertension
Oak et al., Diabetes 2007
(Diabetes Mellitus, Experimental...) :
Attenuation of angiotensin II signaling recouples
eNOS and
inhibits nonendothelial
NOX activity in diabetic mice
Zhang et al., Arterioscler Thromb Vasc Biol 2008
:
Paradoxical
activation of endothelial
nitric oxide synthase by
NADPH oxidase
Besler et al., Expert Rev Cardiovasc Ther 2008
(Atherosclerosis...) :
The underlying mechanisms remain largely to be defined ; however, they likely include activation of the PI3-kinase/Akt pathway and endothelial
nitric oxide synthase , as well as
inhibition of
NAD ( P ) H oxidase activity of progenitor cells
Signorello et al., Biochim Biophys Acta 2009
:
Thus NO, cGMP and superoxide anion level, the phosphorylation status of
nitric oxide synthase , the protein kinase C ( PKC ), and
NADPH oxidase activation were measured
McCarty et al., Med Hypotheses 2010
(Atrial Fibrillation...) :
Nox2- and Nox4 dependent NADPH oxidase activity appears to be a major source of this oxidative stress, and oxidants can
induce conformational changes in xanthine dehydrogenase,
nitric oxide synthase , and the mitochondrial respiratory chain which increase their capacity to generate superoxide as well
Ikeda et al., Free Radic Biol Med 2010
:
This increase was significantly inhibited by N ( ? ) -nitro-l-arginine (
nitric oxide synthase inhibitor ) and diphenyleneiodonium chloride (
NADPH oxidase inhibitor )
Zanette et al., Toxicol In Vitro 2011
(Necrosis) :
Apocynin,
NADPH-oxidase inhibitor, or N ( G ) -monomethyl-L-argynine,
nitric oxide synthase inhibitor , did not prevent NPs induced reduction of cell viability
Jarajapu et al., Invest Ophthalmol Vis Sci 2011
(Diabetic Retinopathy...) :
The authors tested the hypothesis that either increasing
eNOS expression or
inhibiting NADPH oxidase would restore the reparative function in diabetic EPCs
Schuhmacher et al., Diabetes 2011
(Diabetes Mellitus, Experimental...) :
Diabetes is associated with vascular oxidative stress,
activation of
NADPH oxidase , and uncoupling of
nitric oxide ( NO ) synthase ( endothelial NO synthase [eNOS ] )
Shuttleworth et al., J Auton Nerv Syst 1995
:
NOx release was
inhibited by an inhibitor of
nitric oxide synthase activity ( N ( G ) -monomethyl-L-arginine ) or by reduction in extracellular Ca2+ concentration