◀ Back to PTGS2

MRXS5 — PTGS2

Text-mined interactions from Literome

Wang et al., Zhonghua Jie He He Hu Xi Za Zhi 1999 (Respiratory Distress Syndrome, Adult) : Selective COX-2 inhibitor Meloxicam alleviated histopathologic damage in the lung, inhibited production of PGs and attenuated PaO2 decline
FitzGerald et al., Am J Cardiol 2002 (Arthritis...) : However, later research has demonstrated a role of COX-2 in production of PGs that have functions under normal physiologic conditions
Yokota et al., J Clin Invest 2002 : They also link adiponectin to the COX-2 dependent PGs that are critical in this process
Okada et al., J UOEH 2003 (Bone Resorption) : Stimulated production of PGs by osteoblasts requires both the induction of COX-2 expression and the availability of arachidonic acid substrate
Kuo et al., Cancer Lett 2004 (Mouth Neoplasms) : Because cyclooxygenase-2 (COX-2) plays a key role in prostaglandins (PGs) synthesis, which is elevated in inflammation, we examined whether the anti-inflammatory mechanism of berberine is mediated through COX-2 regulation
Brune et al., Rheumatology (Oxford) 2004 (Disease Progression...) : Cyclooxygenase (COX)-1 and COX-2 are responsible for the production of PGs
Hinz et al., FASEB J 2005 (MAP Kinase Signaling System) : A contribution of cyclooxygenase-2 (COX-2) dependent PGs to this process was emphasized by a recent study showing an impaired COX-2 expression in the nonpigmented ciliary epithelium ( NPE ) of patients with primary open-angle glaucoma
Rösch et al., J Pharmacol Exp Ther 2006 : Our results further imply an involvement of COX-2 dependent PGs in MMP-9 and TIMP-1 expression
Neild et al., J Immunol 2005 (Legionellosis) : Cyclooxygenase-2 dependent production of PGs by IFN-gamma treated BMphi infected with Legionella was required for inhibition of effector T cell responses
Ho et al., J Clin Periodontol 2008 (Chronic Disease...) : COX-2 , which is induced in an inflammatory response, is responsible for PGs synthesis at sites of inflammation
Mayoral et al., Biochem J 2008 : These results show, in a genetic model, that tissue-specific COX-2 dependent PGs exert an efficient protection against acute liver injury by an antiapoptotic/antinecrotic effect and by accelerated early hepatocyte proliferation
Twarock et al., Br J Pharmacol 2009 (Carcinoma, Squamous Cell...) : Furthermore, COX2 dependent synthesis of prostaglandins (PGs) stimulates HA synthase-1 (HAS1) and HAS2 mRNA expression, together with HA synthesis via the cAMP/protein kinase A pathway in vascular smooth muscle cells
Cella et al., Br J Pharmacol 2010 (Disease Models, Animal...) : Co-administration of meloxicam, a cyclooxygenase-2 inhibitor, or aminoguanidine, an inducible NOS inhibitor, prevented LPS induced preterm delivery and blocked the increase in PGs and NO
Llorente Izquierdo et al., Am J Pathol 2011 (Body Weight...) : The effect of COX-2 dependent PGs in chronic liver disease, hepatitis, fibrosis, and chemical hepatocarcinogenesis, has been investigated in transgenic ( Tg ) mice that express human COX-2 in hepatocytes and in Tg hepatic human cell lines ... The contribution of COX-2 dependent PGs to the development of DEN induced hepatocarcinogenesis was evaluated in Tg mice, Tg hepatocyte-like cells, and nude mice and the analysis revealed that COX-2 expression favors the development of preneoplastic foci without affecting malignant transformation
Ramer et al., Mol Cancer Ther 2013 (Lung Neoplasms) : Together, our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-? and a subsequent nuclear translocation of PPAR-? by COX-2 dependent PGs
Xu et al., Endocrinology 2013 : Collectively, these data indicate that NF?B/COX-2 induced PGs regulate leukocyte influx, leading to endometrial breakdown
Charpigny et al., Endocrinology 1997 : Collectively these results suggest that the developing ability of the uterus to synthesize PGs is due to the induction of cox-2
Kusuhara et al., Brain Res Mol Brain Res 1997 : Time-course studies on the mRNA expression for c-fos in the hind brain and cyclooxygenase (COX) isoforms in the peritoneal cells, as well as on the peritoneal 6-keto-PGF1alpha accumulation, after stimulation indicated that COX-1 but not COX-2 was responsible for the peritoneal synthesis of PGs which were suggested to evoke c-fos expression in the hind brain
Terao et al., Neuroreport 1998 : These results indicate that COX-2 mediated hyperproduction of PGs is critically involved in the enhancement of SWS, fever, and anorexia but not in the suppression of PS, caused by TNFalpha infused into the PGD2-sensitive zone