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NOS2 — PTGS2

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• STRING interaction: NOS2 — PTGS2 (interaction, mapped from dip)
• STRING interaction: PTGS2 — NOS2 (interaction, mapped from dip)

Text-mined interactions from Literome

Pelletier et al., J Rheumatol 1999 (Disease Models, Animal...) : Our study demonstrates for the first time in vivo in an experimental model of OA, that a selective inhibition of iNOS by L-NIL and the subsequent decreased production of NO also results in a marked decrease in production of major catabolic factors such as MMP, IL-1beta and peroxynitrite, as well as a reduction in COX-2 expression
Nagayama et al., J Cereb Blood Flow Metab 1999 (Brain Ischemia) : The authors investigated the role of the prostaglandin synthesizing enzyme cyclooxygenase-2 (COX-2) in the mechanisms of focal cerebral ischemia and its interaction with inducible nitric oxide synthase (iNOS)
Mei et al., FASEB J 2000 : We found that the induction of PGHS-2 and generation of PGE2 in these cells by IFN-gamma and lipopolysaccharide (LPS) were greatly reduced by two selective NOS II inhibitors, L-NIL and SMT. To ascertain the effect of NO on PGHS-2 overexpression, we tested NO-releasing compounds, NOR-1 and SNAP, and found that they caused PGHS-2 expression and PGE2 production
Lomnitski et al., Pharmacol Toxicol 2000 (Liver Diseases) : Effects of apocynin and natural antioxidant from spinach on inducible nitric oxide synthase and cyclooxygenase-2 induction in lipopolysaccharide induced hepatic injury in rat
Okamoto et al., Anesth Analg 2000 (Hyperemia) : To determine the involvement of inducible nitric oxide synthase (iNOS) and cyclooxygenase ( COX-2 ), we tested whether the effect of LPS on halothane induced hyperemia was altered by pretreatment with the selective iNOS inhibitor, aminoguanidine ( 100 mg/kg ), COX-2 inhibitor , NS-398 ( 5 mg/kg ), or enzyme expression inhibitor, dexamethasone ( 4 mg/kg )
Hellio Le Graverand et al., Osteoarthritis Cartilage 2001 (Knee Injuries...) : In the medial meniscus, significant increases in mRNA levels for type II collagen, biglycan as well as iNOS and PAI-1 were detected at both time periods, while mRNA levels for aggrecan, type III collagen and COX-2 were significantly elevated at 3 weeks post-ACL transection and mRNA levels for MMP-1 were significantly elevated at 8 weeks post-ACL transection
Hori et al., Am J Physiol Gastrointest Liver Physiol 2001 : Upregulation of iNOS by COX-2 in muscularis resident macrophage of rat intestine stimulated with LPS
Pelletier et al., J Rheumatol 2001 (Osteoarthritis) : There was evidence of crosstalk between these 2 latter systems ; specific inhibition of COX-2 reduced the iNOS level, and selective inhibition of iNOS reduced COX-2 expression
Rao et al., Cancer Res 2002 (Body Weight...) : iNOS may regulate COX-2 production of proinflammatory prostaglandins, which are known to play a key role in colon tumor development ... The enzymatic activities of COX-2 and iNOS were significantly induced in the AOM treated animals, and administration of the iNOS inhibitors, SC-51 and AG, significantly inhibited the activities of both iNOS and COX-2 in the colonic mucosa
Bolli et al., Cardiovasc Res 2002 (Myocardial Ischemia...) : Since inhibition of iNOS in preconditioned myocardium blocks COX-2 activity whereas inhibition of COX-2 does not affect iNOS activity, COX-2 appears to be downstream of iNOS in the protective pathway of late PC
Li et al., Zhonghua Zhong Liu Za Zhi 2002 (Carcinoma, Squamous Cell...) : Nonsteroidal antiinflammatory drug ( COX-2 inhibitors ) and iNOS inhibitors may possess antitumor activities because of their prevention of bronchial dysplasia, carcinogenesis and metastasis
Steer et al., J Immunol 2003 : The selective iPLA ( 2 ) suicide substrate inhibitor bromoenol lactone prevents dsRNA- and EMCV stimulated inducible NO synthase expression ; however, bromoenol lactone does not attenuate dsRNA- or EMCV induced COX-2 expression by macrophages
Kim et al., Cell Signal 2003 : Capsaicin did not affect the COX-2 expression at either the protein or mRNA level, but inhibited the enzyme activity of COX-2 and the expression of the iNOS protein
Xuan et al., J Mol Cell Cardiol 2003 : Targeted disruption of the iNOS gene (iNOS-/-) did not block the increased expression of COX-2 protein 24 h after ischemic PC but completely blocked the increase in COX-2 activity, whereas targeted disruption of the COX-2 gene (COX-2-/-) did not alter ischemic PC-induced iNOS induction ... We conclude that ( i ) the upregulation of COX-2 protein expression after ischemic PC is mediated by a JAK1/2-STAT1/3 signaling cascade ; ( ii ) COX-2 activity requires upregulated iNOS and iNOS derived NO; and (iii) COX-2 forms complexes with iNOS, supporting a direct interaction between these two proteins
Chen et al., Br J Pharmacol 2003 : Signal transduction for inhibition of inducible nitric oxide synthase and cyclooxygenase-2 induction by capsaicin and related analogs in macrophages
Blume et al., Eur J Pharmacol 2004 : iNOS and cyclooxygenase-2 protein expression increased threefold ( iNOS : 2.77+/-0.53/cyclooxygenase-2 : 3.49+/-1.25 )
Ishimura et al., Am J Physiol Gastrointest Liver Physiol 2004 : Inducible nitric oxide synthase upregulates cyclooxygenase-2 in mouse cholangiocytes promoting cell growth ... Because iNOS activity has been associated with diverse gene expression, the aim of this study was to determine whether iNOS induces COX-2 ... In conclusion, iNOS induces COX-2 expression in cholangiocytes, which promotes cell growth
Rigas et al., Trends Mol Med 2004 (Neoplasms) : Mechanistically, NO-aspirin, the best studied NO-NSAID, has pleiotropic effects on cell signaling ( it inhibits Wnt signaling, induces nitric oxide synthase and NF-kappaB activation and induces cyclooxygenase-2 expression ), and this mechanistic redundancy might be central to its mode of action against cancer
Ejima et al., Antioxid Redox Signal 2004 (Endotoxemia) : The present article reviews our recent studies involving the role of cyclooxygenase (COX)-2 in host responses to bacterial endotoxemia and its role in the regulation of nitric oxide synthase (NOS)2 and heme oxygenase (HO)-1
Beltrán et al., Eur J Pharmacol 2004 : Vimang ( 0.5-0.1 mg/ml ) and mangiferin ( 0.025 mg/ml ) inhibited the interleukin-1beta ( 1 ng/ml ) -induced iNOS expression more in SHR than in WKY, and cyclooxygenase-2 expression more in WKY than in SHR. Vimang ( 0.25-1 mg/ml ) reduced noradrenaline ( 0.1-30 microM ) - and U46619 ( 1 nM-30 microM ) - but not KCl ( 15-70 mM ) -induced contractions
Clark et al., Biochem J 2005 (Inflammation) : PGHS-2 ( prostaglandin H synthase-2 ) is induced in mammalian cells by pro-inflammatory cytokines in tandem with iNOS [ high-output ( ` inducible ' ) nitric oxide synthase ], and is co-localized with iNOS and nitrotyrosine in human atheroma macrophages
Sheu et al., Cell Signal 2005 (Inflammation) : LPS/IFN-gamma induced COX-2 expression in mesangial cells could be inhibited by iNOS inhibitor, aminoguanidine
Rodriguez et al., Am J Physiol Heart Circ Physiol 2006 : In addition, we conclude that the activation of mitogen activated protein kinases p42/p44, protein kinase C, and nitric oxide synthase is necessary for the increase in COX-2 levels induced by BK because either of the specific inhibitors for these enzymes blocked the effect of BK. Using a similar approach, we further demonstrated that reactive oxygen species and cAMP were not mediators on this pathway
Datta et al., Nephrol Dial Transplant 2006 (Disease Models, Animal...) : Regulatory effects of inducible nitric oxide synthase on cyclooxygenase-2 and heme oxygenase-1 expression in experimental glomerulonephritis
Chang et al., Cell Signal 2006 (MAP Kinase Signaling System) : This study was carried out to further investigate the roles of COX-2 and prostaglandin E2 ( PGE2 ) in LTA induced iNOS expression and NO release in RAW 264.7 macrophages ... LTA induced iNOS expression and NO release were inhibited by a non-selective COX inhibitor ( indomethacin ), a selective COX-2 inhibitor ( NS-398 ), an adenylyl cyclase ( AC ) inhibitor ( dideoxyadenosine, DDA ), and a protein kinase A (PKA) inhibitor ( KT-5720 )
Jiang et al., Life Sci 2006 (Disease Models, Animal...) : Therefore, we investigated the role of COX-2 in morphine induced cardioprotection and the effect of iNOS on COX-2 ... The iNOS-selective inhibitor SMT and iNOS gene-knockout mice were used to investigate the effect of iNOS on COX-2
Yoshida et al., J Invest Dermatol 2006 (Inflammation) : Thus, the gamma-TDMG derived gamma-Toc acts as an antioxidant, suppresses iNOS expression and directly inhibits COX-2 activity, all of which likely play a role in mediating its suppressive effects on photo-inflammation
Tang et al., Life Sci 2006 : We found that preconditioning with H ( 2 ) O ( 2 ) at 10 microM significantly protected PC12 cells against apoptosis induced by lethal H ( 2 ) O ( 2 ) ( 50 microM ) and increased the expression of iNOS and COX-2 and that selective iNOS inhibitor, aminoguanidine ( AG ) and COX-2 inhibitor, NS-398 obviously blocked the protective effects induced by preconditioning with 10 microM H ( 2 ) O ( 2 )
Chen et al., Eur J Pharmacol 2006 : We show that dipyridamole inhibited interleukin-6 and monocyte chemoattractant protein-1 secretion, inducible nitric oxide synthase protein expression, nitrite accumulation, and cyclooxygenase-2 (COX-2) induction in lipopolysaccharide (LPS) activated RAW 264.7 macrophages
Ozveren et al., Pharmacol Res 2006 : Incubation with endotoxin ( 100 microg ml(-1) ) for 4h caused vascular hyporeactivity to norepinephrine which was completely abolished by phenylene-1,3-bis [ ethane-2-isothiourea ] dihydrobromide ( 1,3-PBIT ), a selective iNOS inhibitor, methyl arachidonyl fluorophosphonate ( MAFP ), a selective 85kDa cPLA ( 2alpha ) inhibitor, DFU, a selective COX-2 inhibitor , and KN-93, a selective CaMKII inhibitor
Jang et al., BJU Int 2006 (Urinary Incontinence) : To examine the effects of intravesical cyclooxygenase-2 (COX-2) inhibitors on the expression of inducible nitric oxide synthase (iNOS) and nerve growth factor (NGF) in cyclophosphamide ( CYP ) -induced overactive bladder ( OAB )
Ramana et al., Circulation 2006 (Cardiomyopathies...) : These changes were associated with decreased myocardial nuclear factor-kappaB and activating protein-1 activity, prostaglandin E2 production, induction of cyclooxygenase 2 , and inducible nitric oxide synthase
Kim et al., Vascul Pharmacol 2007 : Furthermore, N-nitro-L-arginine ( NLA ) and N-nitro-L-arginine methyl ester ( L-NAME ) pretreatment enhanced LPS induced iNOS protein expression, which was inhibited by these PCWE and two agents, although LPS induced COX-2 protein expression was not affected by NLA and L-NAME
Pindado et al., J Immunol 2007 : Moreover, COX-2 derived PGE2 production appears to participate in iNOS expression, because siRNA inhibition of COX-2 also leads to inhibition of iNOS , the latter of which is restored by exogenous addition of PGE2 ... Finally, cellular depletion of TLR3 by siRNA inhibits COX-2 expression, PGE2 generation, and iNOS induction by poly-IC
Chen et al., Food Chem Toxicol 2008 (Pain) : On the other hand, expression of iNOS was inhibited by alpha- and gamma-mangostins in LPS stimulated RAW 264.7 cells, but not by COX-2
Kim et al., J Neurosci Res 2008 (Inflammation) : Interestingly, all-trans retinoic acid ( ATRA ) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence
Dudar et al., Am J Physiol Gastrointest Liver Physiol 2008 (Stomach Ulcer) : The enhancement of ulcer healing by the VEGF mimetic occurred independently of cyclooxygenase-2 (COX-2) activity but was blocked by inhibitors of inducible nitric oxide synthase (iNOS)
Isakovic et al., Eur J Pharmacol 2008 (Glioma) : However, blockade of TNF-alpha action and COX-2 activity with anti-TNF-alpha antibodies and indomethacin, respectively, revealed that modulation of TNF-alpha and COX-2 was not involved in adenosine mediated iNOS suppression
Tsoyi et al., Cell Signal 2008 : However, AG490, a specific JAK-2/STAT-1 inhibitor, efficiently prevented LPS mediated iNOS induction but not the induction of COX-2 , and CKD712 completely blocked STAT-1 phosphorylation by LPS, suggesting that the NF-kappaB and JAK-2/STAT-1 pathways but not the JNK pathway are important for CKD712 action ... When examined plasma NO and PGE ( 2 ) levels and iNOS and COX-2 protein levels in lung tissues of mice injected with LPS ( 10 mg/kg ), pretreatment with CKD712 greatly prevented NO and iNOS induction in a dose dependent manner and slightly affected PGE ( 2 ) and COX-2 production as expected
Lee et al., J Ethnopharmacol 2009 : BV suppressed the LPS induced NO generation and iNOS expression, and it also inhibited the expressions of LPS induced pro-inflammatory molecules including Cox-2 and IL-1 beta in rat C6 glioma cells
Franco et al., Med Princ Pract 2009 (Gastritis...) : The 11 patients with H. pylori infection showed a marked expression of COX-2 and iNOS proteins and high levels of PGE ( 2 ) and NO, as a consequence of iNOS and COX-2 activation, while proteins were absent and the level of nitrite and PGE ( 2 ) was low in the 9 noninfected patients
Prandota et al., Int J Neurosci 2010 (Foramen Ovale, Patent...) : Hypoxia is associated with an increase in the generation of several proinflammatory cytokines and other inflammation mediators, such as TNF-alpha, IL-1-beta, IL-6, IL-8, chemokines ( monocyte chemoattractant protein-1, CC-chemokine receptor 2, macrophage inflammatory protein-1alpha, intercellular adhesion molecule-1 ), acute-phase protein gene expressions, COX-2 gene transcription, induction of iNOS , and reactive oxygen species
Ohtsu et al., Oncol Rep 2010 (Carcinoma, Squamous Cell) : Antitumor effects of inhibitors of nitric oxide synthase or cyclooxygenase-2 on human KB carcinoma cells overexpressing COX-2
Resta-Lenert et al., Am J Physiol Gastrointest Liver Physiol 2011 : Reduction of endogenous MUC17 is associated with increased permeability, inducible nitric oxide synthase and cyclooxygenase 2 induction , and enhanced bacterial invasion in response to EIEC exposure
Zhu et al., Exp Cell Res 2012 : Interestingly, activation of COX-2 signaling by LPS was not involved in activation of iNOS signaling, while activation of iNOS signaling by LPS contributed in part to activation of COX-2 signaling
Wu et al., Journal of neuroinflammation 2012 (Disease Models, Animal...) : Neuroinflammation in RVLM was also associated with a COX-2 dependent downregulation of endothelial nitric oxide synthase and an upregulation of intercellular adhesion molecule-1
Obermajer et al., Transplantation research 2012 : We observed that PGE2 induces endogenous cyclooxygenase (COX)2 expression in cultured monocytes, blocking their differentiation into CD1a+ dendritic cells (DCs) and inducing the expression of indoleamine 2,3-dioxygenase 1, IL-4Ra, nitric oxide synthase 2 and IL-10 - typical MDSC associated suppressive factors
Pang et al., Eur J Pharmacol 1996 : Induction of cyclooxygenase and nitric oxide synthase in endotoxin activated J774 macrophages is differentially regulated by indomethacin : enhanced cyclooxygenase-2 protein expression but reduction of inducible nitric oxide synthase
Liu et al., Brain Res Mol Brain Res 1998 (Glioma) : These results suggest that Tau-Cl inhibits the transcriptional expression of the iNOS gene but inhibits expression of COX-2 protein by post-transcriptional mechanisms