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NOS2 — NOX5

Text-mined interactions from Literome

Wakita et al., Brain Res 2001 (Encephalitis...) : These results suggest that the increased NOx ( - ) after the treatment with mixed cytokines were dependent on iNOS activity
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
Chou et al., Toxicol Appl Pharmacol 2002 : These data suggested that JNK and p38 signaling kinases are activated partly by endogenous NO that are generated from NOx activated iNOS in MRC-5 cells
Shin et al., Arch Pharm Res 2002 (Brain Ischemia) : In brain, NOx was increased by about 40 % vs. normal and it was significantly inhibited by aminoguanidine, selective iNOS inhibitor
Tatsumi et al., J Appl Physiol 2004 (Ventricular Dysfunction, Left) : Aminoguanidine, an inhibitor of iNOS , significantly attenuated the LPS induced NOx production and contractile dysfunction
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
Min et al., Glia 2004 (Encephalitis) : Expression of IL-1beta, TNF-alpha, and iNOS in ganglioside treated cells was significantly reduced in the presence of inhibitors of PKC ( GF109203X, Go6976, Ro31-8220, and rottlerin ) and NADPH oxidase ( diphenyleneiodonium chloride [ DPI ] )
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
Lanone et al., FASEB J 2005 (Jaundice...) : This effect was secondary to inhibition of NAD ( P ) H oxidase since 1 ) inhibition of NAD ( P ) H oxidase attenuated NOS2 induction by LPS, 2 ) bilirubin decreased NAD ( P ) H oxidase activity in vivo and in vitro, and 3 ) down-regulation of NOS2 by bilirubin was reversed by addition of NAD ( P ) H
Bai et al., Exp Mol Med 2005 : The inhibition of NADPH oxidase also inhibited NO production, iNOS expression, and iNOS promoter activity
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
Li et al., Am J Physiol Heart Circ Physiol 2007 (Heart Injuries) : These oxidative/nitrative stresses and the resultant cardiomyocyte caspase-3 activation can be blocked by neutralization of TNF-alpha ( anti-TNF-alpha antibody ), inhibition of iNOS ( 1400W ), or NADPH oxidase ( apocynin ) and scavenging of peroxynitrite ( FP15 ) ( P < 0.01 )
Deng et al., Zhonghua Xin Xue Guan Bing Za Zhi 2007 : NOx production by 10 ( -7 ) mol/L and 10 ( -6 ) mol/L ALD increased by 50.0 % and 58.7 % respectively ( P < 0.01 ) and iNOS activity was also significantly increased ( P < 0.01 ) in ALD + RU486 group than that in ALD group. ( 2 ) LPS significantly increased the NOx production and iNOS activity ( P < 0.01 ) and these effects were not augmented by adding ALD to LPS ( P > 0.05 ) and SP significantly blocked and RU486 significantly enhanced the effects by LSP and ALD on NOx production and iNOS activity ( P < 0.05 )
Kim et al., J Ethnopharmacol 2007 : The suppression of NADPH oxidase also inhibited NO production and iNOS protein expression
Wu et al., J Cell Physiol 2008 (Sepsis) : iNOS expression was prevented by the antioxidant ascorbate and by NADPH oxidase inhibition ( apocynin, DPI and p47phox deficiency ), but not by inhibition of mitochondrial respiration ( rotenone ) and xanthine oxidase ( allopurinol )
Xiong et al., Atherosclerosis 2009 (Aortic Aneurysm, Abdominal...) : In conclusion, both iNOS deficiency and NADPH oxidase inhibition suppressed aneurysm formation in association with decreased NO ( x ) levels
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
Zhao et al., Biosci Rep 2010 : Inhibition of PKCzeta by its myristoylated pseudosubstrate significantly decreased the PMA stimulated phosphorylation of the p47phox in LPS pretreated cells, suggesting that PKCzeta is involved in the iNOS dependent assembly and activation of NOX
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
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 ] )
Qian et al., Free Radic Biol Med 2012 : Nox5 activity was reduced by NO donors, iNOS , and eNOS and in endothelial cells and LPS stimulated smooth muscle cells in a manner dependent on NO concentration
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
Katsuyama et al., Endocrinology 1998 (Translocation, Genetic) : Therefore, the present study was designed to examine whether SMase induces iNOS gene expression via the NF-kappaB activation pathway similar to that of IL-1beta and TNF alpha in cultured rat VSMCs. Neutral SMase, although less potently than IL-1beta and TNF alpha, stimulated nitrite/nitrate ( NOx ) production, and iNOS messenger RNA and protein expression, as assessed by Northern and Western blot analyses, respectively