PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18438860-2 2008 PGE2 synthesis under inflammatory conditions is catalyzed by cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), whereas NAD+-dependent 15-hydroxy-PG dehydrogenase (15-PGDH) is the key enzyme implicated in PGE2 catabolism. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 109-116 18438860-8 2008 Visfatin, like IL-1beta, triggered excessive release of PGE2, due to increased mPGES-1 synthesis and decreased 15-PGDH synthesis. Dinoprostone 56-60 prostaglandin E synthase Mus musculus 79-86 18163499-1 2008 OBJECTIVE: Prostaglandin E synthase (PGES) functions as the terminal enzyme in the biosynthesis of prostaglandin E(2) (PGE(2)) and is a potent regulator of bone and cartilage metabolism. Dinoprostone 99-117 prostaglandin E synthase Mus musculus 11-35 18347209-10 2008 CONCLUSIONS: In Ptges(+/+) mice, mPGES-1 in inflammatory cells catalyzes PGE(2) biosynthesis in the LV after MI. Dinoprostone 73-79 prostaglandin E synthase Mus musculus 33-40 18419601-7 2008 Since the latter prostaglandins serve also as mediators of nociception they may compensate the loss of PGE(2) synthesis in mPGES-1-deficient mice. Dinoprostone 103-109 prostaglandin E synthase Mus musculus 123-130 17708577-4 2008 Finally, a selective inhibitor of mPGES-1 strongly suppressed the PAR2-evoked PGE(2) formation. Dinoprostone 78-84 prostaglandin E synthase Mus musculus 34-41 18347209-2 2008 Microsomal prostaglandin (PG) E(2) synthase-1 (mPGES-1), encoded by the Ptges gene, functions downstream from cyclooxygenase-2 in the inducible PGE(2) biosynthetic pathway. Dinoprostone 144-150 prostaglandin E synthase Mus musculus 47-54 18163499-1 2008 OBJECTIVE: Prostaglandin E synthase (PGES) functions as the terminal enzyme in the biosynthesis of prostaglandin E(2) (PGE(2)) and is a potent regulator of bone and cartilage metabolism. Dinoprostone 99-117 prostaglandin E synthase Mus musculus 37-41 17968936-15 2007 CONCLUSION: These results demonstrate that microparticles up-regulate the production of PGE(2) in synovial fibroblasts by inducing COX-2 and mPGES-1. Dinoprostone 88-94 prostaglandin E synthase Mus musculus 141-148 18631945-1 2008 BACKGROUND: The proinflammatory prostaglandin E(2) (PGE(2)) fluctuates over time in the cerebrospinal fluid of patients with Alzheimer"s disease (AD), but the cerebral distribution and expression patterns of microsomal prostaglandin-E synthase (mPGES)-1 have not been compared with those of normal human brains. Dinoprostone 32-50 prostaglandin E synthase Mus musculus 245-253 18631945-1 2008 BACKGROUND: The proinflammatory prostaglandin E(2) (PGE(2)) fluctuates over time in the cerebrospinal fluid of patients with Alzheimer"s disease (AD), but the cerebral distribution and expression patterns of microsomal prostaglandin-E synthase (mPGES)-1 have not been compared with those of normal human brains. Dinoprostone 52-58 prostaglandin E synthase Mus musculus 245-253 17699556-0 2007 Hydrogen peroxide stimulates chloride secretion in primary inner medullary collecting duct cells via mPGES-1-derived PGE2. Dinoprostone 117-121 prostaglandin E synthase Mus musculus 101-108 17699556-8 2007 These data suggest that H2O2 stimulates CFTR Cl(-) channel-mediated Cl(-) secretion through cyclooxygenase- and mPGES-1-dependent release of PGE2 and subsequent activation of PKA. Dinoprostone 141-145 prostaglandin E synthase Mus musculus 112-119 17927823-14 2007 Interestingly, resveratrol dose-dependently reduced the expression (mRNA and protein) of mPGES-1, which is a key enzyme responsible for the synthesis of PGE2 by activated microglia, whereas resveratrol did not affect the expression of COX-2. Dinoprostone 153-157 prostaglandin E synthase Mus musculus 89-96 17604949-7 2007 These results suggest that the mPGES-1 enzyme is strongly needed to provide sufficient PGE(2) production required to stimulate immunosensitive brain regions and they are discussed with regard to the recent works reporting impaired sickness behavior in mPGES-1-/- mice. Dinoprostone 87-93 prostaglandin E synthase Mus musculus 31-38 17604949-7 2007 These results suggest that the mPGES-1 enzyme is strongly needed to provide sufficient PGE(2) production required to stimulate immunosensitive brain regions and they are discussed with regard to the recent works reporting impaired sickness behavior in mPGES-1-/- mice. Dinoprostone 87-93 prostaglandin E synthase Mus musculus 252-259 17437488-7 2007 In papillomas, the increased PGE(2) levels correlate with an increased expression of mPGES-1 and cPGES. Dinoprostone 29-35 prostaglandin E synthase Mus musculus 85-92 18300499-8 2007 CONCLUSION: Luteolin can inhibit significantly the expression of COX-2 and mPGES-1 in PGE2 synthetic pathway. Dinoprostone 86-90 prostaglandin E synthase Mus musculus 75-82 17505022-9 2007 Induction of mPGES-1 and its modulation by cytokines were confirmed at the protein level and correlated with PGE(2) production. Dinoprostone 109-115 prostaglandin E synthase Mus musculus 13-20 17525067-6 2007 Enhanced PGE2 production was most probably due to the enhanced expression of cyclooxygenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1). Dinoprostone 9-13 prostaglandin E synthase Mus musculus 133-140 17707523-2 2007 In this study, we investigated the expression and regulation of the terminal PGE2 synthesizing enzyme prostaglandin E synthases (mPGES-1, mPGES-2 and cPGES) in gingival fibroblasts stimulated with pro-inflammatory cytokines. Dinoprostone 77-81 prostaglandin E synthase Mus musculus 129-136 17707523-4 2007 The cytokines TNFalpha and IL-1beta increased protein expression and activity of mPGES-1, accompanied by increased COX-2 expression and PGE2 production. Dinoprostone 136-140 prostaglandin E synthase Mus musculus 81-88 17707523-11 2007 Moreover, mPGES-1 siRNA did not affect PGE2 levels, whereas PGF(2alpha) increased, suggesting a compensatory pathway of PGE2 synthesis when mPGES-1 is knocked down. Dinoprostone 120-124 prostaglandin E synthase Mus musculus 140-147 17628861-5 2007 The amounts of PGE2 produced by macrophages were significantly reduced in mPGES-1-deficient mice, and these mice displayed enhanced Th1 responses after Propionibacterium acnes treatment compared with wild-type mice. Dinoprostone 15-19 prostaglandin E synthase Mus musculus 74-81 17628861-7 2007 These results indicate that mPGES-1-mediated PGE2 produced by macrophages regulates immune responses, and IL-3 is an important factor for the differentiation of macrophages that produce higher amounts of PGE2 through mPGES-1 activity in BALB/c mice. Dinoprostone 45-49 prostaglandin E synthase Mus musculus 28-35 17628861-7 2007 These results indicate that mPGES-1-mediated PGE2 produced by macrophages regulates immune responses, and IL-3 is an important factor for the differentiation of macrophages that produce higher amounts of PGE2 through mPGES-1 activity in BALB/c mice. Dinoprostone 204-208 prostaglandin E synthase Mus musculus 217-224 17403097-12 2007 CONCLUSIONS: mPGES-1 is the main PGES responsible for PGE(2) biosynthesis by VSMC and its induction downregulates VSMC ability to produce PGI(2.) Dinoprostone 54-60 prostaglandin E synthase Mus musculus 13-20 17442791-5 2007 The absence of mPGES1 was associated with a 50% decrease in basal excretion of PGE(2) in urine (P < 0.001). Dinoprostone 79-85 prostaglandin E synthase Mus musculus 15-21 17442791-12 2007 These data suggest that mPGES1 contributes to basal synthesis of PGE(2), but there are other pathways that lead to renal PGE(2) synthesis. Dinoprostone 65-71 prostaglandin E synthase Mus musculus 24-30 17403423-7 2007 CONCLUSION: The vesicles containing mPGES suggest the formation of prostaglandin E2 (PGE2). Dinoprostone 67-83 prostaglandin E synthase Mus musculus 36-41 17403423-7 2007 CONCLUSION: The vesicles containing mPGES suggest the formation of prostaglandin E2 (PGE2). Dinoprostone 85-89 prostaglandin E synthase Mus musculus 36-41 16766159-7 2006 Moreover, the prostaglandin metabolites PGE2 and PGF2alpha induced mPGES-1 expression as well as upregulated the cytokine-induced mPGES-1 expression indicating positive feedback regulation of mPGES-1 by prostaglandin metabolites. Dinoprostone 40-44 prostaglandin E synthase Mus musculus 67-74 17295901-11 2007 CONCLUSION: Our results suggest that expression of mPGES in addition to COX-2 plays a role in increasing PGE(2) production in endometriosis. Dinoprostone 105-111 prostaglandin E synthase Mus musculus 51-56 17012371-4 2007 Herein we tested the hypothesis that L. pneumophila induced COX-2 and mPGES-1-dependent PGE(2) production in pulmonary epithelial cells. Dinoprostone 88-94 prostaglandin E synthase Mus musculus 70-77 17049841-1 2007 Microsomal prostaglandin E synthase (mPGES)-1, which is dramatically induced in macrophages by inflammatory stimuli such as lipopolysaccharide (LPS), catalyzes the conversion of cyclooxygenase-2 (COX-2) reaction product prostaglandin H(2) (PGH(2)) into prostaglandin E(2) (PGE(2)). Dinoprostone 253-271 prostaglandin E synthase Mus musculus 0-45 17049841-8 2007 These results suggest that LXR ligands diminish PGE(2) production by inhibiting the LPS-induced gene expression of the COX-2-mPGES-1 axis in LPS-activated macrophages. Dinoprostone 48-54 prostaglandin E synthase Mus musculus 125-132 17105783-2 2007 Prostaglandin E(2) (PGE(2)) is synthesized by one of three enzymes, cytosolic prostaglandin E synthase (cPGES), microsomal PGES-1 (mPGES-1) and microsomal PGES-2 (mPGES-2). Dinoprostone 0-18 prostaglandin E synthase Mus musculus 131-138 16766159-1 2006 Microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme regulating the synthesis of prostaglandin E2 (PGE2) in inflammatory conditions. Dinoprostone 99-115 prostaglandin E synthase Mus musculus 39-46 16766159-1 2006 Microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme regulating the synthesis of prostaglandin E2 (PGE2) in inflammatory conditions. Dinoprostone 117-121 prostaglandin E synthase Mus musculus 39-46 17258197-9 2007 These results suggest that COX-2-expressing cells may negatively self-regulate their functions by producing PGE2 via mPGES-1: migration into the draining lymph node and their differentiation. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 117-124 17186945-0 2007 Microsomal prostaglandin E synthase-1 deficiency is associated with elevated peroxisome proliferator-activated receptor gamma: regulation by prostaglandin E2 via the phosphatidylinositol 3-kinase and Akt pathway. Dinoprostone 141-157 prostaglandin E synthase Mus musculus 0-37 17012371-3 2007 Cyclooxygenase (COX) and microsomal PGE(2) synthase-1 (mPGES-1)-derived prostaglandins like prostaglandin E(2) (PGE(2)) are considered as important regulators of lung function. Dinoprostone 92-110 prostaglandin E synthase Mus musculus 55-62 17228032-11 2007 DISCUSSION: These data suggest that mPGES-1 is the major form of PGESs contributing to the synthesis of PGE2 in WAT and that its down-regulation might be involved in the alterations of lipolysis and adipogenesis associated with obesity. Dinoprostone 104-108 prostaglandin E synthase Mus musculus 36-43 16766159-7 2006 Moreover, the prostaglandin metabolites PGE2 and PGF2alpha induced mPGES-1 expression as well as upregulated the cytokine-induced mPGES-1 expression indicating positive feedback regulation of mPGES-1 by prostaglandin metabolites. Dinoprostone 40-44 prostaglandin E synthase Mus musculus 130-137 16766159-7 2006 Moreover, the prostaglandin metabolites PGE2 and PGF2alpha induced mPGES-1 expression as well as upregulated the cytokine-induced mPGES-1 expression indicating positive feedback regulation of mPGES-1 by prostaglandin metabolites. Dinoprostone 40-44 prostaglandin E synthase Mus musculus 130-137 17107625-12 2006 CONCLUSION: The increases of COX-1, COX-2, mPGES-1 and EP1-2 in epithelial ovarian cancer, supports the hypothesis that PGE2-synthesis and signalling are of importance for malignant transformation and progression. Dinoprostone 120-124 prostaglandin E synthase Mus musculus 43-50 17095726-9 2006 In primary cultures of CD cells, mPGES-1 expression was significantly increased following exposure to hypertonic NaCl, in parallel with increased prostaglandin E(2) release. Dinoprostone 146-164 prostaglandin E synthase Mus musculus 33-40 17095726-10 2006 These findings have revealed a mPGES-1/prostaglandin E(2)/NO/cGMP pathway that appears to be critically important for salt adaptation. Dinoprostone 39-57 prostaglandin E synthase Mus musculus 31-38 17023389-4 2006 The results show that genetic deletion of mPGES-1 results in a dramatic decrease in PGE2 production in Het and null MEFs under basal conditions and after stimulation with interleukin (IL)-1beta, suggesting that mPGES-1 is critically important for PGE2 production. Dinoprostone 247-251 prostaglandin E synthase Mus musculus 42-49 17023389-1 2006 Microsomal prostaglandin (PG) E synthase (mPGES)-1 is an inducible enzyme that acts downstream of cyclooxygenase (COX) and specifically catalyzes the conversion of prostaglandin (PG)H2 to PGE2, most prominently in inflammatory conditions. Dinoprostone 188-192 prostaglandin E synthase Mus musculus 0-50 17023389-4 2006 The results show that genetic deletion of mPGES-1 results in a dramatic decrease in PGE2 production in Het and null MEFs under basal conditions and after stimulation with interleukin (IL)-1beta, suggesting that mPGES-1 is critically important for PGE2 production. Dinoprostone 247-251 prostaglandin E synthase Mus musculus 211-218 17023389-4 2006 The results show that genetic deletion of mPGES-1 results in a dramatic decrease in PGE2 production in Het and null MEFs under basal conditions and after stimulation with interleukin (IL)-1beta, suggesting that mPGES-1 is critically important for PGE2 production. Dinoprostone 84-88 prostaglandin E synthase Mus musculus 42-49 17023389-5 2006 Furthermore, we show that mPGES-1 gene deletion results in diversion of prostanoid production from PGE2 to 6-keto PGF1alpha (the stable metabolic product of PGI2; prostacyclin) in a gene dose-dependent manner in Het and null MEFs compared with their WT counterparts, suggesting a shunting phenomenon within the arachidonic acid (AA) metabolic pathway. Dinoprostone 99-103 prostaglandin E synthase Mus musculus 26-33 17023389-6 2006 In addition, we show that mPGES-1 gene deletion and subsequent decrease in PGE2 levels results in a differential induction profile of iNOS and nitrite levels (the stable breakdown product of nitric oxide (NO) in mPGES-1 WT MEFs compared with null MEFs. Dinoprostone 75-79 prostaglandin E synthase Mus musculus 26-33 17023389-6 2006 In addition, we show that mPGES-1 gene deletion and subsequent decrease in PGE2 levels results in a differential induction profile of iNOS and nitrite levels (the stable breakdown product of nitric oxide (NO) in mPGES-1 WT MEFs compared with null MEFs. Dinoprostone 75-79 prostaglandin E synthase Mus musculus 212-219 16973753-1 2006 Prostaglandin (PG) E(2) is formed from PGH(2) by a series of PGE synthase (PGES) enzymes. Dinoprostone 0-23 prostaglandin E synthase Mus musculus 75-79 16212965-1 2006 BACKGROUND AND OBJECTIVE: Prostaglandin E2 (PGE(2), a product of the cyclooxygenase 2 (COX-2) and membrane-associated Prostaglandin E Synthase (mPGES-1) pathway, has been implicated in the instability of atherosclerotic plaques. Dinoprostone 26-42 prostaglandin E synthase Mus musculus 144-151 16849500-13 2006 Thus, LPS binds to TLR4 on osteoblasts that directly induce mPGES-1 expression for PGE(2) synthesis, leading to subsequent bone resorption. Dinoprostone 83-89 prostaglandin E synthase Mus musculus 60-67 16598755-16 2006 These findings demonstrate a coordinated induction of COX-2 and mPGES-1 by PDB/TG that proceeds through PKC/ERK and Ca2+ signaling cascades, resulting in increased PGE2 production. Dinoprostone 164-168 prostaglandin E synthase Mus musculus 64-71 16212965-1 2006 BACKGROUND AND OBJECTIVE: Prostaglandin E2 (PGE(2), a product of the cyclooxygenase 2 (COX-2) and membrane-associated Prostaglandin E Synthase (mPGES-1) pathway, has been implicated in the instability of atherosclerotic plaques. Dinoprostone 44-50 prostaglandin E synthase Mus musculus 144-151 16816110-1 2006 Prostaglandin E2 (PGE2) produced by cyclooxygenase-2 (COX-2) and microsomal prostaglandin E2 synthase-1 (mPGES-1) plays an important role in the pathophysiology of inflammation, pain, and fever. Dinoprostone 0-16 prostaglandin E synthase Mus musculus 105-112 16816110-1 2006 Prostaglandin E2 (PGE2) produced by cyclooxygenase-2 (COX-2) and microsomal prostaglandin E2 synthase-1 (mPGES-1) plays an important role in the pathophysiology of inflammation, pain, and fever. Dinoprostone 18-22 prostaglandin E synthase Mus musculus 105-112 16891468-3 2006 We report that constitutive expression of the microsomal prostaglandin E synthase-1 (mPGES-1) is associated with increased prostaglandin E(2) (PGE(2)) production and stimulation of growth in the human astroglioma cell line U87-MG compared with human primary astrocytes. Dinoprostone 123-141 prostaglandin E synthase Mus musculus 85-92 16891468-9 2006 Taken together, these results are consistent with the hypothesis that mPGES-1 plays a critical role in promoting astroglioma cell growth via PGE(2)-dependent activation of type II PKA. Dinoprostone 141-147 prostaglandin E synthase Mus musculus 70-77 16720448-1 2006 CONCLUSION: In laryngeal cancer, arachidonic acid may be metabolized to PGE2 via the cooperative actions of COX-2 and mPGES, which are induced in response to various stimuli. Dinoprostone 72-76 prostaglandin E synthase Mus musculus 118-123 16720448-2 2006 The COX-2-mPGES-PGE2 system may induce differentiation of cancer cells and prevent metastasis, thus improving the survival rate. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 10-15 16855145-3 2006 Early investigations suggested that microsomal PGE synthase-1 (mPGES-1; a terminal PGE2-synthesizing enzyme) plays a pivotal role in bacterial lipopolysaccharide (LPS)-induced systemic inflammation, but overlooked the possibility that the same enzyme could be involved in OA or RA. Dinoprostone 83-87 prostaglandin E synthase Mus musculus 63-70 16864802-2 2006 Here we demonstrate the induction of microsomal PGE synthase 1 (mPGES-1), an inducible terminal enzyme for PGE(2) synthesis, in neurons, microglia, and endothelial cells in the cerebral cortex after transient focal ischemia. Dinoprostone 107-113 prostaglandin E synthase Mus musculus 64-71 16554545-4 2006 The microsomal PGE synthase (mPGES)-1 enzyme is involved in the last step of PGE2 biosynthesis, and its expression is stimulated by proinflammatory agents. Dinoprostone 77-81 prostaglandin E synthase Mus musculus 15-37 16183115-3 2006 mPGES-1 and COX-2 form an inducible pathway for PGE2 production in many cell systems. Dinoprostone 48-52 prostaglandin E synthase Mus musculus 0-7 16183115-4 2006 In this study we investigated whether mPGES-1 is involved in cytokine induced PGE2 biosynthesis in human trophoblast cells. Dinoprostone 78-82 prostaglandin E synthase Mus musculus 38-45 16183115-10 2006 We conclude that mPGES-1 is not involved in the inducible COX-2 mediated pathway for PGE2 biosynthesis at the transcriptional level, however, the treatment with IL-1beta results in a higher degree of co-ordination of the mPGES-1 and COX-2 protein immunolocalization, eliciting PGE2 synthesis. Dinoprostone 277-281 prostaglandin E synthase Mus musculus 221-228 16614384-11 2006 PGE2 biosynthesized through the mPGES-1 pathway may be important for follicular development, ovulation and luteal formation. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 32-39 16614756-6 2006 PGE(2) biosynthesis is catalyzed by the coordinate actions of COX enzymes and microsomal PGE synthase-1 (mPGES-1). Dinoprostone 0-6 prostaglandin E synthase Mus musculus 105-112 16621493-0 2006 Elevated prostaglandin E2 level via cPLA2--COX-2--mPGES-1 pathway involved in bladder carcinogenesis induced by terephthalic acid-calculi in Wistar rats. Dinoprostone 9-25 prostaglandin E synthase Mus musculus 50-57 16621493-13 2006 In conclusion, increasing PGE2 level via cPLA2--COX-2--mPGES-1 pathway may play an important role in rat bladder carcinogenesis. Dinoprostone 26-30 prostaglandin E synthase Mus musculus 55-62 16210398-11 2006 CONCLUSION: PGE2 derived from COX-2 and mPGES-1 plays a significant role in the pathogenesis of chronic acid reflux oesophagitis, and possibly in basal hyperplasia and persistent inflammatory cell infiltration. Dinoprostone 12-16 prostaglandin E synthase Mus musculus 40-47 16619662-12 2006 Therefore, the inhibition of PGE2 synthesis, targeting COX-2 and mPGES-1, is an effective treatment for the induction of antiglioma immune responses. Dinoprostone 29-33 prostaglandin E synthase Mus musculus 65-72 16872525-0 2006 Prostaglandin E2 synthesis in cartilage explants under compression: mPGES-1 is a mechanosensitive gene. Dinoprostone 0-16 prostaglandin E synthase Mus musculus 68-75 16299051-9 2006 mPGES induction and, possibly, cPLA2 induction appear to cooperate with COX-2 to determine IL-1beta-mediated PGE2 production in human ASM cells. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 0-5 16353170-5 2006 It is possible that targeting mPGES-1 could decrease PGE(2) production without affecting PGI(2) production. Dinoprostone 53-59 prostaglandin E synthase Mus musculus 30-37 16353170-14 2006 Targeting mPGES-1 might prove to be an alternative therapeutic strategy to inhibit PGE2 production. Dinoprostone 83-87 prostaglandin E synthase Mus musculus 10-17 16912428-4 2006 As the stimulated synthesis of PGE2 originates from the preferential coupling of inducible enzymes, cyclooxygenase-2 (COX-2) and membrane PGE synthase-1 (mPGES-1), we investigated the potency of 15d-PGJ2 to regulate prostaglandins synthesis in rat chondrocytes stimulated with interleukin-1beta (IL-1beta). Dinoprostone 31-35 prostaglandin E synthase Mus musculus 154-161 16424787-1 2006 Prostaglandin E2 (PGE2), the product of cyclooxygenase-2 (COX-2) and prostaglandin E synthase-1 (mPGES-1), acts through its receptors (EPs) and induces matrix metalloproteinase (MMP) expression, which may favor the instability of atherosclerotic plaques. Dinoprostone 0-16 prostaglandin E synthase Mus musculus 97-104 16223862-10 2006 The comparison of endometrial PGFS and mPGES-1 expression on d 10-13 of the estrous cycle and pregnancy suggest a supportive role of these enzymes in determining the increase of uterine PGE2/PGF2alpha ratio during maternal recognition of pregnancy. Dinoprostone 186-190 prostaglandin E synthase Mus musculus 39-46 16424787-1 2006 Prostaglandin E2 (PGE2), the product of cyclooxygenase-2 (COX-2) and prostaglandin E synthase-1 (mPGES-1), acts through its receptors (EPs) and induces matrix metalloproteinase (MMP) expression, which may favor the instability of atherosclerotic plaques. Dinoprostone 18-22 prostaglandin E synthase Mus musculus 97-104 16204198-10 2005 Interestingly, PGE2 levels are similarly reduced in lactating glands of mPGES1-deficient mice, indicating that PGE2 biosynthesis results from the coordinated activity of COX-1 and mPGES1. Dinoprostone 15-19 prostaglandin E synthase Mus musculus 72-78 16204198-0 2005 Coupling of COX-1 to mPGES1 for prostaglandin E2 biosynthesis in the murine mammary gland. Dinoprostone 32-48 prostaglandin E synthase Mus musculus 21-27 16204198-1 2005 The mammary gland, like most tissues, produces measurable amounts of prostaglandin E2 (PGE2), a metabolite of arachidonic acid produced by sequential actions of two cyclooxygenases (COX-1 and COX-2) and three terminal PGE synthases: microsomal prostaglandin E2 synthase-1 (mPGES1), mPGES2, and cytosolic prostaglandin E2 synthase (cPGES). Dinoprostone 69-85 prostaglandin E synthase Mus musculus 273-279 16204198-1 2005 The mammary gland, like most tissues, produces measurable amounts of prostaglandin E2 (PGE2), a metabolite of arachidonic acid produced by sequential actions of two cyclooxygenases (COX-1 and COX-2) and three terminal PGE synthases: microsomal prostaglandin E2 synthase-1 (mPGES1), mPGES2, and cytosolic prostaglandin E2 synthase (cPGES). Dinoprostone 87-91 prostaglandin E synthase Mus musculus 273-279 16204198-10 2005 Interestingly, PGE2 levels are similarly reduced in lactating glands of mPGES1-deficient mice, indicating that PGE2 biosynthesis results from the coordinated activity of COX-1 and mPGES1. Dinoprostone 111-115 prostaglandin E synthase Mus musculus 72-78 16204198-10 2005 Interestingly, PGE2 levels are similarly reduced in lactating glands of mPGES1-deficient mice, indicating that PGE2 biosynthesis results from the coordinated activity of COX-1 and mPGES1. Dinoprostone 111-115 prostaglandin E synthase Mus musculus 180-186 16255020-12 2005 CONCLUSION: These data are the first to demonstrate the effects of antirheumatic treatments on mPGES-1 expression in RA and suggest that the inhibition of PGE(2) biosynthesis, preferably by targeting mPGES-1, might complement anti-TNF treatment for optimal antiinflammatory results in RA. Dinoprostone 155-161 prostaglandin E synthase Mus musculus 95-102 16334960-1 2005 OBJECTIVE: To characterize expression of cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) and regulation of prostaglandin E2 (PGE2) production by equine articular chondrocytes. Dinoprostone 154-158 prostaglandin E synthase Mus musculus 109-116 16334960-10 2005 CONCLUSIONS AND CLINICAL RELEVANCE: Collectively, results indicated that the rhIL-1beta-dependent increase in PGE2 production in equine chondrocytes in monolayer culture was associated with coordinated upregulation of COX-2 and mPGES-1 expression. Dinoprostone 110-114 prostaglandin E synthase Mus musculus 228-235 16000148-6 2005 In microglia-enriched cultures, the induction of mPGES-1, the activity of PGES and the production of PGE2 were preceded by the induction of mPGES-1 mRNA and almost completely inhibited by the synthetic glucocorticoid dexamethasone. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 140-147 15983118-3 2005 We evaluated cooperation between COX-2 and mPGES-1 as a potential mechanism for induced PGE(2) production in WISH cells. Dinoprostone 88-94 prostaglandin E synthase Mus musculus 43-50 15983118-5 2005 Selective pharmacological inhibition of these enzymes demonstrated that induced PGE(2) release occurred through a dominant COX-2/mPGES-1 pathway. Dinoprostone 80-86 prostaglandin E synthase Mus musculus 129-136 15983118-9 2005 We conclude that although mPGES-1 and COX-2 show transcriptional and functional coordination in cytokine-induced PGE(2) synthesis, complementary morphological and biochemical data suggest that a majority of intracellular mPGES-1 and COX-2 are segregated to discrete lipid microdomains in WISH epithelial cells. Dinoprostone 113-119 prostaglandin E synthase Mus musculus 26-33 16120814-9 2005 We conclude that PAR(2)-triggered PGE(2) formation in A549 cells involves a coordinated up-regulation of COX-2 and mPGES-1 involving cPLA(2), increased cytosolic Ca(2+), PKC, Src, MEK-ERK, p38 MAPK, Src-mediated EGF receptor trans-activation, and also metabolic products of both COX-1 and COX-2. Dinoprostone 34-40 prostaglandin E synthase Mus musculus 115-122 16103419-1 2005 Prostaglandin E2 synthase (mPGES-1), the enzyme which catalyzes the synthesis of PGE2, is induced during the inflammatory response. Dinoprostone 81-85 prostaglandin E synthase Mus musculus 27-34 16000148-7 2005 The induction of mPGES-1 and production of PGE2 were also either attenuated or absent in microglia treated with mPGES-1 antisense oligonucleotide or microglia from mPGES-1 knockout (KO) mice, respectively, suggesting the necessity of mPGES-1 for microglial PGE2 production. Dinoprostone 257-261 prostaglandin E synthase Mus musculus 17-24 16000148-8 2005 These results suggest that the activation of microglia contributes to PGE2 production through the concerted de novo synthesis of mPGES-1 and COX-2 at sites of inflammation of the brain parenchyma. Dinoprostone 70-74 prostaglandin E synthase Mus musculus 129-136 15910650-5 2005 Recent studies using adjuvant induced arthritis model have shown the increase of mPGES-1 expression resulted in the increase of PGE2 production at the sites of inflammation. Dinoprostone 128-132 prostaglandin E synthase Mus musculus 81-88 15644490-4 2005 We hypothesize that the expression of the major PGE2 synthesis enzymes cyclooxygenases 1 and 2 (COX-1, COX-2) and membrane-associated PGE2 synthase (mPGES) is altered in the kidneys of rats with NDI and CDI. Dinoprostone 48-52 prostaglandin E synthase Mus musculus 149-154 15774546-10 2005 CONCLUSIONS: These data indicate that mPGES-1 is a gonadotropin-regulated PG synthesis enzyme expressed by granulosa cells of primate periovulatory follicles and suggest that mPGES-1 may be the primary PGES responsible for the increased follicular PGE2 levels necessary for primate ovulation. Dinoprostone 248-252 prostaglandin E synthase Mus musculus 38-45 15774546-10 2005 CONCLUSIONS: These data indicate that mPGES-1 is a gonadotropin-regulated PG synthesis enzyme expressed by granulosa cells of primate periovulatory follicles and suggest that mPGES-1 may be the primary PGES responsible for the increased follicular PGE2 levels necessary for primate ovulation. Dinoprostone 248-252 prostaglandin E synthase Mus musculus 175-182 15677520-2 2005 In the present work, using genetically modified mice, we examined the role of the inducible terminal PGE2-synthesizing enzyme microsomal prostaglandin E synthase-1 (mPGES-1) for the generation of immune-elicited fever. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 126-163 15677520-2 2005 In the present work, using genetically modified mice, we examined the role of the inducible terminal PGE2-synthesizing enzyme microsomal prostaglandin E synthase-1 (mPGES-1) for the generation of immune-elicited fever. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 165-172 15722356-5 2005 In contrast, we detected in mPGES-1-/- macrophages a >95% reduction in PGE2 production resulting in the following altered prostaglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha>PGE2, despite the comparable release of total prostaglandins. Dinoprostone 190-194 prostaglandin E synthase Mus musculus 28-35 15677520-7 2005 Taken together with previous observations on mPGES-1 induction in the brain vasculature during various inflammatory conditions and its role in endotoxin-induced pyresis, the present findings indicate that central PGE2 synthesis by mPGES-1 is a general and critical mechanism for fever during infectious and inflammatory conditions that is distinct from the mechanism(s) underlying the circadian temperature regulation and stress-induced hyperthermia, as well as the inflammation-induced activity depression. Dinoprostone 213-217 prostaglandin E synthase Mus musculus 45-52 15677520-7 2005 Taken together with previous observations on mPGES-1 induction in the brain vasculature during various inflammatory conditions and its role in endotoxin-induced pyresis, the present findings indicate that central PGE2 synthesis by mPGES-1 is a general and critical mechanism for fever during infectious and inflammatory conditions that is distinct from the mechanism(s) underlying the circadian temperature regulation and stress-induced hyperthermia, as well as the inflammation-induced activity depression. Dinoprostone 213-217 prostaglandin E synthase Mus musculus 231-238 15868626-14 2005 These data suggest that mPGES-1 may prove to be an interesting therapeutic target for controlling PGE2 synthesis. Dinoprostone 98-102 prostaglandin E synthase Mus musculus 24-31 16128405-3 2005 Prostaglandin E synthase (PGES) is a terminal prostanoid synthase and can catalyse the isomerization of the COX product PGH2 to PGE2, including microsomal PGES-1 (mPGES-1), cytosolic PGES (cPGES) and mPGES-2. Dinoprostone 128-132 prostaglandin E synthase Mus musculus 0-24 16128405-3 2005 Prostaglandin E synthase (PGES) is a terminal prostanoid synthase and can catalyse the isomerization of the COX product PGH2 to PGE2, including microsomal PGES-1 (mPGES-1), cytosolic PGES (cPGES) and mPGES-2. Dinoprostone 128-132 prostaglandin E synthase Mus musculus 26-30 16128405-3 2005 Prostaglandin E synthase (PGES) is a terminal prostanoid synthase and can catalyse the isomerization of the COX product PGH2 to PGE2, including microsomal PGES-1 (mPGES-1), cytosolic PGES (cPGES) and mPGES-2. Dinoprostone 128-132 prostaglandin E synthase Mus musculus 155-161 16128405-3 2005 Prostaglandin E synthase (PGES) is a terminal prostanoid synthase and can catalyse the isomerization of the COX product PGH2 to PGE2, including microsomal PGES-1 (mPGES-1), cytosolic PGES (cPGES) and mPGES-2. Dinoprostone 128-132 prostaglandin E synthase Mus musculus 155-159 15722356-5 2005 In contrast, we detected in mPGES-1-/- macrophages a >95% reduction in PGE2 production resulting in the following altered prostaglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha>PGE2, despite the comparable release of total prostaglandins. Dinoprostone 74-78 prostaglandin E synthase Mus musculus 28-35 15722356-9 2005 The dramatic reduction in [3H]PGE2 formation from mPGES-1-/- macrophages compared with controls resulted in TxB2 and 6-keto PGF1alpha becoming the two most abundant prostaglandins in these samples. Dinoprostone 30-34 prostaglandin E synthase Mus musculus 50-57 15722356-11 2005 Our data support the hypothesis that mPGES-1 induction in response to an inflammatory stimulus is essential for PGE2 synthesis. Dinoprostone 112-116 prostaglandin E synthase Mus musculus 37-44 15458923-8 2005 N-(2-cyclohexyloxy-4-nitrophenyl)-methanesulfonamide (NS-398), a selective COX-2 inhibitor, totally inhibited PGE2 production at both the 8-h and 24-h time points, suggesting that COX-2-dependent PGE2 generation does not depend on mPGES-1 activity at the early stage. Dinoprostone 110-114 prostaglandin E synthase Mus musculus 231-238 15584915-7 2004 Also, the PGE2 biosynthetic pathway downstream from COX-2 was affected in the COX-2(-/-) mice, as decreased expression of microsomal prostaglandin E synthase-2 (mPGES-2), but not mPGES-1 or cytosolic PGES, was observed. Dinoprostone 10-14 prostaglandin E synthase Mus musculus 179-186 15899061-1 2005 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme that catalyzes the conversion of prostaglandin (PG)H2 to PGE2. Dinoprostone 128-132 prostaglandin E synthase Mus musculus 39-46 15899061-3 2005 mPGES-1 knockout studies and animal models of inflammatory arthritis also provide a strong basis for the contribution of mPGES-1 in the increased local production of PGE2 observed in inflammatory arthritis. Dinoprostone 166-170 prostaglandin E synthase Mus musculus 0-7 15899061-3 2005 mPGES-1 knockout studies and animal models of inflammatory arthritis also provide a strong basis for the contribution of mPGES-1 in the increased local production of PGE2 observed in inflammatory arthritis. Dinoprostone 166-170 prostaglandin E synthase Mus musculus 121-128 15642051-7 2005 Treatment of gingival fibroblasts with triclosan (1 microg/ml) significantly reduced the stimulatory effect of TNFalpha (10 ng/ml) on the expression of mPGES-1 at both the mRNA and the protein level by an average of 21% and 43%, respectively, and subsequently the production of PGE2 (p<0.01). Dinoprostone 278-282 prostaglandin E synthase Mus musculus 152-159 15642051-9 2005 CONCLUSION: The results show that triclosan reduces the augmented biosynthesis of PGE2 by inhibiting the mRNA and the protein expression of mPGES-1 in gingival fibroblasts. Dinoprostone 82-86 prostaglandin E synthase Mus musculus 140-147 16218485-2 2005 MMP biosynthesis is mediated by prostaglandin (PG)E2, the product of cyclooxygenase (COX)-2/inducible PGE synthase (mPGES) activity. Dinoprostone 32-52 prostaglandin E synthase Mus musculus 116-121 16277686-2 2005 We investigated the kinetics of inducible cyclo-oxygenase (COX)-2 and mPGES-1 expression with respect to the production of 6-keto-PGF1alpha and PGE2 in rat chondrocytes stimulated with 10 ng/ml IL-1beta, and compared their modulation by peroxisome-proliferator-activated receptor (PPAR)gamma agonists. Dinoprostone 144-148 prostaglandin E synthase Mus musculus 70-77 16277686-10 2005 These data demonstrate the following in IL-1-stimulated rat chondrocytes: first, mPGES-1 is rate limiting for PGE2 synthesis; second, activation of the prostaglandin cascade requires NF-kappaB activation; third, 15d-PGJ2 strongly inhibits the synthesis of prostaglandins, in contrast with rosiglitazone; fourth, inhibition by 15d-PGJ2 occurs independently of PPARgamma through inhibition of the NF-kappaB pathway; fifth, mPGES-1 is the main target of 15d-PGJ2. Dinoprostone 110-114 prostaglandin E synthase Mus musculus 81-88 15584915-7 2004 Also, the PGE2 biosynthetic pathway downstream from COX-2 was affected in the COX-2(-/-) mice, as decreased expression of microsomal prostaglandin E synthase-2 (mPGES-2), but not mPGES-1 or cytosolic PGES, was observed. Dinoprostone 10-14 prostaglandin E synthase Mus musculus 162-166 15314505-8 2004 Studies from mPGES-1-deficient mice and animal models of inflammatory arthritis strongly suggest a role of mPGES-1 in the production of PGE2 and the pathogenesis of arthritis. Dinoprostone 136-140 prostaglandin E synthase Mus musculus 13-20 15284079-7 2004 In contrast, in nuclei of brain parenchymal and endothelial cells, mPGES-1 and cPGES colocalized exclusively with COX-2 (determined by immunoblotting and immunohistochemistry); these PGESs contributed to conversion of PGH2 into PGE2. Dinoprostone 228-232 prostaglandin E synthase Mus musculus 67-74 15457451-1 2004 OBJECTIVE: Microsomal prostaglandin E synthase 1 (mPGES-1) is the final enzyme of the cascade that produces prostaglandin E(2) (PGE(2)), a key actor in arthritis. Dinoprostone 108-126 prostaglandin E synthase Mus musculus 50-57 15314505-9 2004 SUMMARY: This article reviews the regulation of mPGES-1 expression and provides evidence for a role of mPGES-1 in inducible PGE2 production and arthritis. Dinoprostone 124-128 prostaglandin E synthase Mus musculus 103-110 15194860-3 2004 PGE2 is produced from arachidonic acid via PGH2 by at least three PGE synthases (PGES), cytosolic PGES (cPGES), and membrane-associated PGES (mPGES)-1 and -2. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 116-157 15254968-5 2004 This higher production of PGE2 in mesenchymal stem cells was due to higher expression of membrane-associated PGE synthase (mPGES) regulated by early growth response factor-1 (Egr-1). Dinoprostone 26-30 prostaglandin E synthase Mus musculus 123-128 15140897-1 2004 We examined the in vivo role of membrane-bound prostaglandin E synthase (mPGES)-1, a terminal enzyme in the PGE2-biosynthetic pathway, using mPGES-1 knockout (KO) mice. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 32-81 15140897-3 2004 LPS-stimulated production of PGE2, but not other PGs, was impaired markedly in mPGES-1-null macrophages, although a low level of cyclooxygenase-2-dependent PGE2 production still remained. Dinoprostone 29-33 prostaglandin E synthase Mus musculus 79-86 15140897-8 2004 Collectively, our present results provide unequivocal evidence that mPGES-1 contributes to the formation of PGE2 involved in pain hypersensitivity and inflammation. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 68-75 15194860-6 2004 These results demonstrate that PGE2 produced by mPGES-1 is involved in neuropathic pain. Dinoprostone 31-35 prostaglandin E synthase Mus musculus 48-55 15379214-3 2004 In present study the involvement of microsomal prostaglandin E synthase-1 (mPGES-1) in relation to PGE2 production was investigated. Dinoprostone 99-103 prostaglandin E synthase Mus musculus 75-82 15188353-2 2004 Microsomal PGES-1 is induced by proinflammatory cytokines and is strongly linked to conditions that result in high PGE(2) biosynthesis. Dinoprostone 115-121 prostaglandin E synthase Mus musculus 11-17 15188353-15 2004 Microsomal PGES-1 might be a potential new target for treatment strategies to control PGE(2) synthesis in patients with RA, without the systemic side effects associated with cyclooxygenase inhibitors. Dinoprostone 86-92 prostaglandin E synthase Mus musculus 11-17 15016822-1 2004 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible protein recently shown to be an important source of inflammatory PGE2. Dinoprostone 129-133 prostaglandin E synthase Mus musculus 0-37 15016822-1 2004 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible protein recently shown to be an important source of inflammatory PGE2. Dinoprostone 129-133 prostaglandin E synthase Mus musculus 39-46 15016822-2 2004 Here we have used mPGES-1 wild type, heterozygote, and null mice to assess the impact of reduction or absence mPGES-1 protein on the production of PGE2 and other prostaglandins in lipopolysaccharide (LPS)-treated macrophages and mice. Dinoprostone 147-151 prostaglandin E synthase Mus musculus 110-117 15016822-4 2004 Resident mPGES-1(-/-) peritoneal macrophages exhibited severely impaired PGE2-releasing activity but retained some LPS-inducible PGE2 production capacity. Dinoprostone 73-77 prostaglandin E synthase Mus musculus 9-16 15016822-4 2004 Resident mPGES-1(-/-) peritoneal macrophages exhibited severely impaired PGE2-releasing activity but retained some LPS-inducible PGE2 production capacity. Dinoprostone 129-133 prostaglandin E synthase Mus musculus 9-16 15016822-6 2004 In vivo, mPGES-1 deletion abolished the LPS-stimulated production of PGE2 in spleen, kidney, and brain. Dinoprostone 69-73 prostaglandin E synthase Mus musculus 9-16 15016822-7 2004 Surprisingly, lack of mPGES-1 activity resulted in an 80-90% decrease in basal, cyclooxygenase-1 (COX-1)-dependent PGE2 production in stomach and spleen, and a 50% reduction in brain and kidney. Dinoprostone 115-119 prostaglandin E synthase Mus musculus 22-29 15016822-10 2004 These data demonstrate for the first time a dual role for mPGES-1 in both inflammatory and COX-1-mediated PGE2 production and suggest an interdependence of prostanoid production with tissue-specific alterations of prostaglandin levels in the absence of mPGES-1. Dinoprostone 106-110 prostaglandin E synthase Mus musculus 58-65 15379214-7 2004 The results demonstrate that mPGES-1 regulates PGE2 production in gingival fibroblasts stimulated by inflammatory mediators IL-1beta and TNFa. Dinoprostone 47-51 prostaglandin E synthase Mus musculus 29-36 15044444-10 2004 The data also indicate that the up-regulation of mPGES-1 contributes to COX-2-mediated PGE(2) production in the CNS during peripheral inflammation. Dinoprostone 87-93 prostaglandin E synthase Mus musculus 49-56 15014433-9 2004 Furthermore, Helicobacter infection upregulated epithelial PGE2 production, suggesting that the COX-2/mPGES-1 pathway contributes to the Helicobacter-associated gastric tumorigenesis. Dinoprostone 59-63 prostaglandin E synthase Mus musculus 102-109 14871981-2 2004 Cyclooxygenase (COX) catalyzes the synthesis of PGH2, which is converted, in turn, by microsomal prostaglandin E synthase (mPGES-1) to PGE2. Dinoprostone 135-139 prostaglandin E synthase Mus musculus 123-130 15086459-12 2004 CONCLUSION: Together, these studies suggest mPGES-1 colocalizes with both COX-1 and COX-2 to mediate the biosynthesis of PGE2 in the kidney. Dinoprostone 121-125 prostaglandin E synthase Mus musculus 44-51 14975584-3 2004 Elevated mRNA and protein expression of the PGE2-synthetic-related enzymes cyclooxygenase (COX)-2 and membrane-associated PGE synthase (PGES) accompanied local PGE2 production. Dinoprostone 44-48 prostaglandin E synthase Mus musculus 122-134 14975584-3 2004 Elevated mRNA and protein expression of the PGE2-synthetic-related enzymes cyclooxygenase (COX)-2 and membrane-associated PGE synthase (PGES) accompanied local PGE2 production. Dinoprostone 44-48 prostaglandin E synthase Mus musculus 136-140 14975584-3 2004 Elevated mRNA and protein expression of the PGE2-synthetic-related enzymes cyclooxygenase (COX)-2 and membrane-associated PGE synthase (PGES) accompanied local PGE2 production. Dinoprostone 160-164 prostaglandin E synthase Mus musculus 122-134 14975584-3 2004 Elevated mRNA and protein expression of the PGE2-synthetic-related enzymes cyclooxygenase (COX)-2 and membrane-associated PGE synthase (PGES) accompanied local PGE2 production. Dinoprostone 160-164 prostaglandin E synthase Mus musculus 136-140 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 0-4 prostaglandin E synthase Mus musculus 15-19 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 0-4 prostaglandin E synthase Mus musculus 161-165 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 0-4 prostaglandin E synthase Mus musculus 167-172 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 0-4 prostaglandin E synthase Mus musculus 161-165 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 120-124 prostaglandin E synthase Mus musculus 15-19 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 120-124 prostaglandin E synthase Mus musculus 161-165 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 120-124 prostaglandin E synthase Mus musculus 167-172 15047937-2 2004 PGE2 synthase (PGES) is a terminal prostanoid synthase and can enzymatically convert the cyclooxygenase product PGH2 to PGE2, including two isoforms: microsomal PGES (mPGES) and cytosolic PGES (cPGES). Dinoprostone 120-124 prostaglandin E synthase Mus musculus 161-165 15047937-4 2004 mPGES is preferentially coupled with the inducible COX-2 to promote delayed PGE2 generation. Dinoprostone 76-80 prostaglandin E synthase Mus musculus 0-5 14991895-3 2004 Thus, the expression of COX-2 and the downstream enzyme involved in PGE2 biosynthesis, microsomal PGE-synthase1 (mPGES1), was correlated with P-gp, the product of MDR-1, and the anti-apoptotic protein, Bcl-xL, in gastric biopsies from patients with H pylori infection and in patients with gastric cancer. Dinoprostone 68-72 prostaglandin E synthase Mus musculus 113-119 14630996-3 2004 To determine the intrarenal source of PGE(2) synthesis, we analyzed the expression of microsomal PGE(2) synthase (mPGES; EC: 5.3.99.3), whose product PGE(2) has been shown to stimulate renin secretion in vitro. Dinoprostone 38-44 prostaglandin E synthase Mus musculus 114-119 14630996-3 2004 To determine the intrarenal source of PGE(2) synthesis, we analyzed the expression of microsomal PGE(2) synthase (mPGES; EC: 5.3.99.3), whose product PGE(2) has been shown to stimulate renin secretion in vitro. Dinoprostone 97-103 prostaglandin E synthase Mus musculus 114-119 12835414-10 2003 We also show that mPGES1 is responsible for the production of PGE2 that mediates acute pain during an inflammatory response. Dinoprostone 62-66 prostaglandin E synthase Mus musculus 18-24 15225371-13 2004 Conversion of PGH2 to PGE2 (PGES activity) was significantly increased in the lysate from IL-1beta-stimulated chondrocytes and it was inhibited by MK-886, which has an inhibitory effect on mPGES-1 activity. Dinoprostone 22-26 prostaglandin E synthase Mus musculus 189-196 14555660-3 2003 The inducible prostaglandin E2 (PGE2) biosynthetic enzymes cyclooxygenase-2 (COX-2) and mPGES-1 are up-regulated in many cancers. Dinoprostone 14-30 prostaglandin E synthase Mus musculus 88-95 14555660-3 2003 The inducible prostaglandin E2 (PGE2) biosynthetic enzymes cyclooxygenase-2 (COX-2) and mPGES-1 are up-regulated in many cancers. Dinoprostone 32-36 prostaglandin E synthase Mus musculus 88-95 12746259-3 2003 However, much less is known about the recently cloned microsomal PGE2 synthase (mPGES), the terminal enzyme of PGE2 synthesis, which converts COX-derived PGH2 to the biologically important PGE2. Dinoprostone 65-69 prostaglandin E synthase Mus musculus 80-85 12746259-3 2003 However, much less is known about the recently cloned microsomal PGE2 synthase (mPGES), the terminal enzyme of PGE2 synthesis, which converts COX-derived PGH2 to the biologically important PGE2. Dinoprostone 111-115 prostaglandin E synthase Mus musculus 80-85 12890577-2 2003 This unstable intermediate can be enzymatically metabolized to PGE2 by the actions of a microsomal 17 kDa PGE synthase (mPGES1). Dinoprostone 63-67 prostaglandin E synthase Mus musculus 120-126 12890577-4 2003 To understand the relationship between expression of mPGES1 and PGE2 formation, IL-1beta treated cells were incubated with increasing concentrations of antisense oligonucleotides (ASO) and their effects compared to cells treated with reverse sense oligonucleotides (RSO) designed against the ATG translation initiation codon of mPGES1. Dinoprostone 64-68 prostaglandin E synthase Mus musculus 53-59 12890577-9 2003 These results demonstrate the direct association between mPGES1 expression, its enzymatic activity, and total PGE2 production following an inflammatory stimulus. Dinoprostone 110-114 prostaglandin E synthase Mus musculus 57-63 14566964-2 2003 For the PGE(2) biosynthesis two isoforms of the terminal and specific enzymes, membrane-associated PGE(2) synthase (mPGES) and cytosolic PGES (cPGES) have recently been identified. Dinoprostone 8-14 prostaglandin E synthase Mus musculus 116-121 14566964-6 2003 An antisense oligonucleotide blocking mPGES expression inhibited not only PGE(2) production, but also osteoclastogenesis and bone resorption stimulated by the cytokines, which was reversed by addition of exogenous PGE(2). Dinoprostone 74-80 prostaglandin E synthase Mus musculus 38-43 14566340-3 2003 Our findings identify mPGES-1 as the central switch during immune-induced pyresis and as a target for the treatment of fever and other PGE2-dependent acute phase reactions elicited by the brain. Dinoprostone 135-139 prostaglandin E synthase Mus musculus 22-29 14558087-16 2003 It also seems that cyclooxygenase 2 (COX-2) inhibitors decrease PGE(2) production not only by direct inhibition of COX-2, but also by reducing mPGES expression in activated RASFs. Dinoprostone 64-70 prostaglandin E synthase Mus musculus 143-148 12528468-8 2002 COX-2 and mPGES-1 are essential components for delayed PGE2 synthesis, which may be linked to inflammation, fever, osteogenesis, and even cancer. Dinoprostone 55-59 prostaglandin E synthase Mus musculus 10-17 12657565-3 2003 We have performed a comprehensive histochemical analysis by comparing rat and mouse kidneys for cellular and subcellular localization of COX-1 and -2 and microsomal-type PGE synthase (PGES), the rate-limiting biosynthetic enzyme in PGE2 synthesis. Dinoprostone 232-236 prostaglandin E synthase Mus musculus 170-182 12657565-3 2003 We have performed a comprehensive histochemical analysis by comparing rat and mouse kidneys for cellular and subcellular localization of COX-1 and -2 and microsomal-type PGE synthase (PGES), the rate-limiting biosynthetic enzyme in PGE2 synthesis. Dinoprostone 232-236 prostaglandin E synthase Mus musculus 184-188 12626523-1 2003 Microsomal prostaglandin E2 synthase-1 (mPGES-1) is a stimulus-inducible enzyme that functions downstream of cyclooxygenase (COX)-2 in the PGE2-biosynthetic pathway. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 12626523-1 2003 Microsomal prostaglandin E2 synthase-1 (mPGES-1) is a stimulus-inducible enzyme that functions downstream of cyclooxygenase (COX)-2 in the PGE2-biosynthetic pathway. Dinoprostone 139-143 prostaglandin E synthase Mus musculus 40-47 12657620-8 2003 RESULTS: Vitreous treatment of RPE cells resulted in increased expression of two critical enzymes in the synthesis of prostaglandin E(2): membrane-associated prostaglandin E-synthase (mPGES) and cyclooxygenase (COX)-2. Dinoprostone 118-136 prostaglandin E synthase Mus musculus 184-189 12657620-10 2003 The increase in the expression of mPGES was associated with an increase in the production of prostaglandin E(2) that was observed at 12 and 24 hours of treatment but not at 48 hours. Dinoprostone 93-111 prostaglandin E synthase Mus musculus 34-39 12626523-5 2003 Treatment of HCA-7 cells with an mPGES-1 inhibitor or antisense oligonucleotide attenuated, whereas overexpression of mPGES-1 accelerated, PGE2 production and cell proliferation. Dinoprostone 139-143 prostaglandin E synthase Mus musculus 118-125 12743173-5 2003 Osteoblastic bone marrow stromal cells induced the expression of cyclooxygenase (COX)-2 and membrane-bound PGE2 synthase (mPGES) in response to IL-1 and lipopolysaccharide (LPS) to produce PGE2. Dinoprostone 107-111 prostaglandin E synthase Mus musculus 122-127 12802720-4 2003 These findings suggest that the inhibitory effect of furanocoumarins on the LPS-induced PGE2 production is due to the inhibition of the expression of COX-2 and mPGES. Dinoprostone 88-92 prostaglandin E synthase Mus musculus 160-165 11564815-8 2001 The LPS-induced increase in PGE(2) concentration was mediated by NOS2-derived NO-dependent activation of COX-1 pathway and by induction of mPGES. Dinoprostone 28-34 prostaglandin E synthase Mus musculus 139-144 12233875-9 2002 Conversion of PGH2 to PGE2 increased by IL-1beta and was correlated with mPGES expression. Dinoprostone 22-26 prostaglandin E synthase Mus musculus 73-78 12233875-10 2002 Increased conversion of arachidonic acid to PGE2 was maintained when mPGES and COX-2 were coexpressed. Dinoprostone 44-48 prostaglandin E synthase Mus musculus 69-74 12233875-13 2002 CONCLUSION: The results suggest that abundant PGE2 production at inflammation sites such as rheumatoid synovia is caused by the coordinated upregulation of mPGES and COX-2. Dinoprostone 46-50 prostaglandin E synthase Mus musculus 156-161 12233875-14 2002 Thus mPGES might be a potential new target for therapeutic strategies to control PGE2 synthesis specifically in patients with RA and other inflammatory diseases. Dinoprostone 81-85 prostaglandin E synthase Mus musculus 5-10 12021206-7 2002 These results show that mPGES-1 is expressed coordinately with COX-1 and COX-2 and is involved in PGE(2) production in male genital organs. Dinoprostone 98-104 prostaglandin E synthase Mus musculus 24-31 11847219-11 2002 These results indicate that the induction of PGHS-2 and mPGES by IL-1beta underlies robust PGE(2) production in orbital fibroblasts. Dinoprostone 91-97 prostaglandin E synthase Mus musculus 56-61 11795891-2 2002 The membrane fraction containing recombinant mPGES-1 catalyzed the isomerization of PGH2 to PGE2 in the presence of GSH with K(m) values of 130 microM for PGH2 and 37 microM for GSH, a turnover number of 600 min(-1), and a k(cat)/K(m) ratio of 4.6 min(-1) microM(-1). Dinoprostone 92-96 prostaglandin E synthase Mus musculus 45-52 11795891-7 2002 Taken together, these results demonstrate that mPGES-1 is an efficient downstream enzyme for the production of PGE2 in the activated macrophages treated by lipopolysaccharide. Dinoprostone 111-115 prostaglandin E synthase Mus musculus 47-54 12145315-10 2002 When mPGES is expressed in KAT-50 by transiently transfecting the cells, PGE(2) production is up-regulated substantially. Dinoprostone 73-79 prostaglandin E synthase Mus musculus 5-10 12233875-1 2002 OBJECTIVE: Recently, microsomal prostaglandin (PG) E synthase (mPGES) was cloned as a terminal enzyme catalyzing PGH2 to PGE2. Dinoprostone 121-125 prostaglandin E synthase Mus musculus 63-68 12034740-2 2002 Membrane-associated prostaglandin (PG) E2 synthase (mPGES) is an inducible terminal enzyme in the biosynthetic pathway for prostaglandin E2, which participates in many biological processes. Dinoprostone 123-139 prostaglandin E synthase Mus musculus 52-57 11704570-2 2001 One of the rate-limiting biosynthetic enzymes in PGE(2) synthesis is the terminal PGE(2) synthase (PGES). Dinoprostone 49-55 prostaglandin E synthase Mus musculus 82-97 11704570-2 2001 One of the rate-limiting biosynthetic enzymes in PGE(2) synthesis is the terminal PGE(2) synthase (PGES). Dinoprostone 49-55 prostaglandin E synthase Mus musculus 99-103 10869354-1 2000 Here we report the molecular identification of membrane-bound glutathione (GSH)-dependent prostaglandin (PG) E(2) synthase (mPGES), a terminal enzyme of the cyclooxygenase (COX)-2-mediated PGE(2) biosynthetic pathway. Dinoprostone 189-195 prostaglandin E synthase Mus musculus 124-129 11306620-3 2001 We herein cloned the rat glutathione-dependent microsomal prostaglandin E synthase (mPGES), the terminal enzyme for PGE(2) biosynthesis, and examined its induction in the rat brain after intraperitoneal injection of pyrogen lipopolysaccharide (LPS). Dinoprostone 116-122 prostaglandin E synthase Mus musculus 84-89 11584082-10 2001 The PGE(2) increase was associated with NOS2-mediated activation of COX and induction of mPGES. Dinoprostone 4-10 prostaglandin E synthase Mus musculus 89-94 11306620-9 2001 These results demonstrate that brain endothelial cells play an essential role in the PGE(2) production during fever by expressing COX-2 and mPGES. Dinoprostone 85-91 prostaglandin E synthase Mus musculus 140-145 10869354-10 2000 Thus, COX-2 and mPGES are essential components for delayed PGE(2) biosynthesis, which may be linked to inflammation, fever, osteogenesis, and even cancer. Dinoprostone 59-65 prostaglandin E synthase Mus musculus 16-21 33775835-0 2021 Discovery of N-Amido-Phenylsulfonamide Derivatives as Novel Microsomal Prostaglandin E2 Synthase-1 (mPGES-1) Inhibitors. Dinoprostone 71-87 prostaglandin E synthase Mus musculus 100-107 33775835-4 2021 Among them, MPO-0186 (scaffold C) inhibited the production of PGE2 (IC50: 0.24 muM) in A549 cells via inhibition of mPGES-1 (IC50: 0.49 muM in a cell-free assay) and was found to be approximately 9- and 8-fold more potent than MK-886 as a reference inhibitor, respectively. Dinoprostone 62-66 prostaglandin E synthase Mus musculus 116-123 33775835-5 2021 A molecular docking study theoretically suggests that MPO-0186 could inhibit PGE2 production by blocking the PGH2 binding site of mPGES-1 enzyme. Dinoprostone 77-81 prostaglandin E synthase Mus musculus 130-137 34877656-1 2022 BACKGROUND AND PURPOSE: Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible isomerase responsible for prostaglandin E2 production in inflammatory conditions. Dinoprostone 114-130 prostaglandin E synthase Mus musculus 24-61 33776573-3 2021 More specifically, TNFalpha/IL-1beta promotes expression of the prostaglandin E2- (PGE2-) producing enzymes, cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1). Dinoprostone 64-80 prostaglandin E synthase Mus musculus 177-184 23260349-1 2013 Inhibition of mPGES-1, the terminal enzyme in the arachidonic acid/COX pathway to regulate the production of pro-inflammatory prostaglandin PGE2, is considered an attractive new therapeutic target for safe and effective anti-inflammatory drugs. Dinoprostone 140-144 prostaglandin E synthase Mus musculus 14-21 33809724-5 2021 Inducible inflammatory key enzymatic pathways, as iNOS and COX-2/mPGES-1/PGE2, were upregulated by the cytokine mix while PBMT reverted their levels and activities. Dinoprostone 73-77 prostaglandin E synthase Mus musculus 65-72 33233853-1 2020 The dual inhibitor of the 5-lipoxygenase-activating protein (FLAP) and the microsomal prostaglandin E2 synthase-1 (mPGES-1), named BRP-187, represents a promising drug candidate due to its improved anti-inflammatory efficacy along with potentially reduced side effects in comparison to non-steroidal anti-inflammatory drugs (NSAIDs). Dinoprostone 86-102 prostaglandin E synthase Mus musculus 115-122 34798265-1 2022 Inflammation is closely linked to the abnormal phospholipid metabolism chain of cyclooxygenase-2/microsomal prostaglandin E2 synthase-1/prostaglandin E2 (COX-2/mPGES-1/PGE2). Dinoprostone 108-124 prostaglandin E synthase Mus musculus 160-167 34798265-1 2022 Inflammation is closely linked to the abnormal phospholipid metabolism chain of cyclooxygenase-2/microsomal prostaglandin E2 synthase-1/prostaglandin E2 (COX-2/mPGES-1/PGE2). Dinoprostone 136-152 prostaglandin E synthase Mus musculus 160-167 34798265-1 2022 Inflammation is closely linked to the abnormal phospholipid metabolism chain of cyclooxygenase-2/microsomal prostaglandin E2 synthase-1/prostaglandin E2 (COX-2/mPGES-1/PGE2). Dinoprostone 168-172 prostaglandin E synthase Mus musculus 160-167 34798265-4 2022 To avoid this, targeting downstream mPGES-1 instead of upstream COX is preferable to selectively block overexpressed PGE2 in inflammatory diseases. Dinoprostone 117-121 prostaglandin E synthase Mus musculus 36-43 34877656-1 2022 BACKGROUND AND PURPOSE: Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible isomerase responsible for prostaglandin E2 production in inflammatory conditions. Dinoprostone 114-130 prostaglandin E synthase Mus musculus 63-70 34766335-1 2022 BACKGROUND: Inhibition of the microsomal prostaglandin (PG) E2 synthase (mPGES-1) introduces a promising anti-inflammatory treatment approach by specifically reducing PGE2 . Dinoprostone 41-62 prostaglandin E synthase Mus musculus 73-80 34766335-1 2022 BACKGROUND: Inhibition of the microsomal prostaglandin (PG) E2 synthase (mPGES-1) introduces a promising anti-inflammatory treatment approach by specifically reducing PGE2 . Dinoprostone 167-171 prostaglandin E synthase Mus musculus 73-80 34766335-7 2022 In IL-1beta treated arteries, inhibition of mPGES-1 significantly reduced PGE2 levels while PGI2 levels remained unchanged. Dinoprostone 74-78 prostaglandin E synthase Mus musculus 44-51 34101620-2 2021 Deletion of mPges-1 in mice confers analgesia, restrains atherogenesis and fails to accelerate thrombogenesis, while suppressing PGE2, but increasing biosynthesis of PGI2. Dinoprostone 129-133 prostaglandin E synthase Mus musculus 12-19 34465013-2 2022 Enzymes involved in the metabolism of PGE2 include cyclooxygenase (COX)-2, microsomal prostaglandin E synthase-1 (mPGES-1), and 15-prostaglandin dehydrogenase (15-PGDH). Dinoprostone 38-42 prostaglandin E synthase Mus musculus 114-121 34465013-10 2022 In colon cancer cells, PGE2 was found to be upregulated upon stimulation by TNF-alpha, which led to strong induction of mPGES-1 without any change in the expression of COX-2 among the PGE2-related enzymes. Dinoprostone 23-27 prostaglandin E synthase Mus musculus 120-127 34465013-11 2022 Conclusion: These results demonstrated that PGE2 can be induced by stimuli such as TNF-alpha, and suggest that activation of mPGES-1 is more closely related than that of COX-2 in the induction of PGE2 on colon cancer. Dinoprostone 44-48 prostaglandin E synthase Mus musculus 125-132 34465013-11 2022 Conclusion: These results demonstrated that PGE2 can be induced by stimuli such as TNF-alpha, and suggest that activation of mPGES-1 is more closely related than that of COX-2 in the induction of PGE2 on colon cancer. Dinoprostone 196-200 prostaglandin E synthase Mus musculus 125-132 34405222-6 2021 Microsomal prostaglandin E synthase-1 (mPGES-1), the key terminal enzyme catalyzing the synthesis of inflammatory PGE2, and the four PGE2 receptors (EP1-4) have gained more attention as the promising alternative drug targets for the development of novel NSAIDs. Dinoprostone 114-118 prostaglandin E synthase Mus musculus 39-46 34405222-8 2021 In this review, we highlight the most recent advances from our and other studies on the role of PGE2, particularly mPGES-1 and the four PGE2 receptors, in cardiovascular diseases. Dinoprostone 96-100 prostaglandin E synthase Mus musculus 115-122 34320346-4 2021 Gain- and loss-of-function in vivo approaches further reveal that although provision of PGE2 amplifies psoriasiform inflammation, ablation of host mPGES1-dependent PGE2 synthesis is dispensable for cutaneous gammadelta17 T cell activation. Dinoprostone 164-168 prostaglandin E synthase Mus musculus 147-153 34242345-4 2021 By addition of exogenous PGE2, we found that the effect of KH176m on mPGES-1 expression and spheroid growth is due to the inhibition of a PGE2-driven positive feedback control-loop of mPGES-1 transcriptional regulation. Dinoprostone 25-29 prostaglandin E synthase Mus musculus 69-76 34242345-4 2021 By addition of exogenous PGE2, we found that the effect of KH176m on mPGES-1 expression and spheroid growth is due to the inhibition of a PGE2-driven positive feedback control-loop of mPGES-1 transcriptional regulation. Dinoprostone 25-29 prostaglandin E synthase Mus musculus 184-191 34242345-4 2021 By addition of exogenous PGE2, we found that the effect of KH176m on mPGES-1 expression and spheroid growth is due to the inhibition of a PGE2-driven positive feedback control-loop of mPGES-1 transcriptional regulation. Dinoprostone 138-142 prostaglandin E synthase Mus musculus 69-76 34242345-4 2021 By addition of exogenous PGE2, we found that the effect of KH176m on mPGES-1 expression and spheroid growth is due to the inhibition of a PGE2-driven positive feedback control-loop of mPGES-1 transcriptional regulation. Dinoprostone 138-142 prostaglandin E synthase Mus musculus 184-191 35105690-3 2022 Restricting PGE2 signaling via knockout of microsomal prostaglandin E synthase-1 (mPGES-1) in PyMT mice or of the prostanoid E receptor 3 (EP3) in CAFs stunted mammary carcinoma growth associated with strong CAF proliferation. Dinoprostone 12-16 prostaglandin E synthase Mus musculus 43-80 34084773-1 2021 Background: Microsomal prostaglandin E synthase-1 (mPGES-1)-derived prostaglandin E2 (PGE2) is a chief mediator of inflammation. Dinoprostone 86-90 prostaglandin E synthase Mus musculus 51-58 34084773-13 2021 Conclusion: These data demonstrate that mPGES-1-derived PGE2 plays a critical role in PD-associated peritoneal fibrosis through activation of the NLRP3 inflammasome. Dinoprostone 56-60 prostaglandin E synthase Mus musculus 40-47 35466565-2 2022 In our search for novel sEH inhibitors, we designed and synthesized novel analogs of the piperazine urea derivative 4, a previously discovered dual microsomal prostaglandin E2 synthase-1 (mPGES-1)/soluble epoxide hydrolase (sEH) inhibitor, to evaluate their potential as sEH inhibitors. Dinoprostone 159-175 prostaglandin E synthase Mus musculus 188-195 35417776-5 2022 Microsomal prostaglandin E synthase 1 (mPGES-1) catalyzes the final step of PGE2 biosynthesis. Dinoprostone 76-80 prostaglandin E synthase Mus musculus 39-46 35240529-9 2022 Therefore, it can be concluded that rutin hydrate reduces pyrexia in mice via downregulating PGE2 synthesis by inhibiting mPGES-1 activity. Dinoprostone 93-97 prostaglandin E synthase Mus musculus 122-129 34084773-1 2021 Background: Microsomal prostaglandin E synthase-1 (mPGES-1)-derived prostaglandin E2 (PGE2) is a chief mediator of inflammation. Dinoprostone 68-84 prostaglandin E synthase Mus musculus 51-58 34068550-10 2021 Moreover, MF6 suppressed the inflammation-associated prostaglandin E2 levels through microsomal prostaglandin E synthase-1 expression in the ischemic hemispheres. Dinoprostone 53-69 prostaglandin E synthase Mus musculus 85-122 35105690-3 2022 Restricting PGE2 signaling via knockout of microsomal prostaglandin E synthase-1 (mPGES-1) in PyMT mice or of the prostanoid E receptor 3 (EP3) in CAFs stunted mammary carcinoma growth associated with strong CAF proliferation. Dinoprostone 12-16 prostaglandin E synthase Mus musculus 82-89 33930567-3 2021 mPGES-1 is an inflammation-inducible enzyme that converts PGH2 into PGE2. Dinoprostone 68-72 prostaglandin E synthase Mus musculus 0-7 35152061-0 2022 Novel potent benzimidazole-based microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitors derived from BRP-201 that also inhibit leukotriene C4 synthase. Dinoprostone 44-60 prostaglandin E synthase Mus musculus 73-80 35152061-1 2022 Microsomal prostaglandin E2 synthase-1 (mPGES-1) is recognized as a promising therapeutic target for next-generation anti-inflammatory drugs to treat inflammatory diseases. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 35152061-2 2022 In this study, we report the identification of new, potent and selective inhibitors of human mPGES-1 such as compounds 10, 31 and 49 with IC50 of 0.03-0.09 muM in a cell-free assay of PGE2 production. Dinoprostone 184-188 prostaglandin E synthase Mus musculus 93-100 35056712-12 2022 In conclusion, green and black tea, and to a lesser extent Rooibos tea, are potent inhibitors of PGE2 formation in human monocytes, and mediate their effects by inhibiting the expression of the enzymes responsible for PGE2 formation, especially mPGES-1. Dinoprostone 218-222 prostaglandin E synthase Mus musculus 245-252 35069250-8 2021 Salt titration studies in an in vitro ASDN cell model, mouse CCD cell (mCCD-CL1), confirmed PGE2 synthesis is activated by low salt, and revealed that response is paralleled by induction of mPGES1 gene expression. Dinoprostone 92-96 prostaglandin E synthase Mus musculus 190-196 34983695-1 2022 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme that acts downstream of cyclooxygenase and plays a major role in inflammation by converting prostaglandin (PG) H2 to PGE2. Dinoprostone 193-197 prostaglandin E synthase Mus musculus 12-49 34983695-1 2022 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme that acts downstream of cyclooxygenase and plays a major role in inflammation by converting prostaglandin (PG) H2 to PGE2. Dinoprostone 193-197 prostaglandin E synthase Mus musculus 51-58 34983695-9 2022 In WT mice, the colonic expression of mPGES-1 was highly induced on both mRNA and protein levels and colonic PGE2 increased significantly after DSS administration. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 38-45 34983695-14 2022 CONCLUSIONS: These results demonstrate that mPGES-1 is the main enzyme responsible for colonic PGE2 production and deficiency of mPGES-1 facilitates the development of colitis by affecting the development of colonic T cell-mediated immunity. Dinoprostone 95-99 prostaglandin E synthase Mus musculus 44-51 35099767-1 2022 As the inducible terminal enzyme for prostaglandin E2 (PGE2) synthesis, microsomal PGE synthase-1 (mPGES-1) contributes to neuroinflammation and secondary brain injury after cerebral ischemia via producing excessive PGE2. Dinoprostone 37-53 prostaglandin E synthase Mus musculus 99-106 35099767-1 2022 As the inducible terminal enzyme for prostaglandin E2 (PGE2) synthesis, microsomal PGE synthase-1 (mPGES-1) contributes to neuroinflammation and secondary brain injury after cerebral ischemia via producing excessive PGE2. Dinoprostone 55-59 prostaglandin E synthase Mus musculus 99-106 35099767-1 2022 As the inducible terminal enzyme for prostaglandin E2 (PGE2) synthesis, microsomal PGE synthase-1 (mPGES-1) contributes to neuroinflammation and secondary brain injury after cerebral ischemia via producing excessive PGE2. Dinoprostone 216-220 prostaglandin E synthase Mus musculus 99-106 35099767-4 2022 In this study, blockade of mPGES-1 by our several novel compounds abolished the lipopolysaccharide (LPS)-induced PGE2 and pro-inflammatory cytokines interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor alpha (TNF-alpha) in mouse primary brain microglia. Dinoprostone 113-117 prostaglandin E synthase Mus musculus 27-34 35099767-5 2022 Inhibition of mPGES-1 also decreased PGE2 produced by neuronal cells under oxygen-glucose deprivation (OGD) stress. Dinoprostone 37-41 prostaglandin E synthase Mus musculus 14-21 35099767-6 2022 Among the five enzymes for PGE2 biosynthesis, mPGES-1 was the most induced one in cerebral ischemic lesions. Dinoprostone 27-31 prostaglandin E synthase Mus musculus 46-53 33582554-1 2021 Microsomal prostaglandin (PG) E synthase-1 (mPGES-1) and prostacyclin (PGI2) synthase (PGIS) are PG terminal synthases that work downstream of cyclooxygenase and synthesize PGE2 and PGI2, respectively. Dinoprostone 173-177 prostaglandin E synthase Mus musculus 44-51 33582554-7 2021 LC-MS analysis further showed that the increment in PGE2 levels in DNFB-treated ear tissue was reduced in mPGES-1 KO mice, and that 6-keto PGF1alpha (a stable metabolite of PGI2) was not detected in PGIS KO mice. Dinoprostone 52-56 prostaglandin E synthase Mus musculus 106-113 33582554-10 2021 mPGES-1-derived PGE2 and PGIS-derived PGI2 might coordinately promote acquired cutaneous immune responses. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 0-7 33596205-10 2021 We further found that PIC but not CHIKV increased the mRNA levels of cPLA2alpha and of mPGES-1, two other central enzymes in PGE2 production. Dinoprostone 125-129 prostaglandin E synthase Mus musculus 87-94 33788722-1 2021 BACKGROUND/AIM: Microsomal prostaglandin (PG) E synthase-1 (mPGES-1) is a terminal enzyme in PGE2 synthesis and highly expressed in several cancers. Dinoprostone 93-97 prostaglandin E synthase Mus musculus 60-67 33826984-1 2021 Microsomal prostaglandin E2 synthase-1 (mPGES-1), 5-lipoxygenase (5-LO) and 5- lipoxygenase-activating protein (FLAP) are key for biosynthesis of proinflammatory lipid mediators and pharmacologically relevant drug targets. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 33595097-1 2022 BACKGROUND AND PURPOSE: Recent biochemical and pharmacological studies have reported that in several tissues and cell types, microsomal prostaglandin E2 synthase (mPGES) and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) expression are modulated by a variety of inflammatory factors and stimuli Considering that very little is known about the biological effects promoted by IL-17 in the context of mPGES-1/PPAR-gamma modulation, we sought to investigate the contribution of this unique cytokine on this integrated pathway during the onset of inflammation. Dinoprostone 136-152 prostaglandin E synthase Mus musculus 413-420 33246032-2 2021 METHODS: We generated ligand-protein X-ray crystal structures of known inhibitors of microsomal prostaglandin E2 synthase-1 (mPGES-1) and the 5-Lipoxygenase Activating Protein (FLAP), with their respective proteins, to understand the overlapping pharmacophores. Dinoprostone 96-112 prostaglandin E synthase Mus musculus 125-132 33574423-1 2021 Microsomal prostaglandin E2 synthase 1 (mPGES-1) is recognized as a promising target for a next generation of anti-inflammatory drugs that are not expected to have the side effects of currently available anti-inflammatory drugs. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 33568930-9 2021 In this direction the options being explored are on synthesis of PGE2-mPGES-1; PGE2 degradation through a specific PG dehydrogenase, 15-PGDH, and by blocking its activity mediated through a specific PGE receptor, EP4. Dinoprostone 65-69 prostaglandin E synthase Mus musculus 70-77 33568930-9 2021 In this direction the options being explored are on synthesis of PGE2-mPGES-1; PGE2 degradation through a specific PG dehydrogenase, 15-PGDH, and by blocking its activity mediated through a specific PGE receptor, EP4. Dinoprostone 79-83 prostaglandin E synthase Mus musculus 70-77 33542207-3 2021 PGE2 is produced in an inducible manner in macrophages (Mphi) by microsomal PGE2-synthase-1 (mPGES-1), with the notion that it also conveys pro-resolving properties. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 93-100 33542207-5 2021 Experimentally, we applied the mPGES-1 inhibitor compound III (CIII) once the inflammatory response was established and confirmed its potent PGE2-blocking efficacy. Dinoprostone 141-145 prostaglandin E synthase Mus musculus 31-38 33542207-10 2021 Our data suggest that mPGES-1-derived PGE2 contributes to the resolution of inflammation by preventing CX3CL1-mediated retention of activated myeloid cells at sites of injury. Dinoprostone 38-42 prostaglandin E synthase Mus musculus 22-29 33049240-12 2021 These results indicate that PGE2 is synthesized by COX-2/mPGES-1 in spinal endothelial cells after nerve injury. Dinoprostone 28-32 prostaglandin E synthase Mus musculus 57-64 33527033-1 2021 Microsomal prostaglandin E synthase 1 (mPGES-1) is the terminal synthase of prostaglandin E2 (PGE2) which plays a crucial role in inflammatory diseases. Dinoprostone 76-92 prostaglandin E synthase Mus musculus 39-46 33527033-1 2021 Microsomal prostaglandin E synthase 1 (mPGES-1) is the terminal synthase of prostaglandin E2 (PGE2) which plays a crucial role in inflammatory diseases. Dinoprostone 94-98 prostaglandin E synthase Mus musculus 39-46 33527033-2 2021 Thus, mPGES-1 inhibitors are promising agents for their better specificity in blocking the production of PGE2, a potent inflammatory mediator, compared with non-steroidal anti-inflammatory drugs (NSAIDs). Dinoprostone 105-109 prostaglandin E synthase Mus musculus 6-13 33441600-6 2021 Finally, we showed that the effect of KH176m on mPGES-1 expression is due to the inhibition of a PGE2-driven positive feedback control-loop of mPGES-1 transcriptional regulation. Dinoprostone 97-101 prostaglandin E synthase Mus musculus 48-55 33441600-6 2021 Finally, we showed that the effect of KH176m on mPGES-1 expression is due to the inhibition of a PGE2-driven positive feedback control-loop of mPGES-1 transcriptional regulation. Dinoprostone 97-101 prostaglandin E synthase Mus musculus 143-150 33292158-1 2021 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES-1) catalyzes the terminal step of prostaglandin E2 (PGE2) production, which plays an important role in the regulation of febrile response. Dinoprostone 91-107 prostaglandin E synthase Mus musculus 12-49 33473256-3 2020 Researchers have identified multiple signaling pathways involved in lung cancer chemoresistance, including cyclooxygenase-2 (COX-2)/microsomal prostaglandin E synthase-1 (mPGES-1) derived prostaglandin E2 (PGE2). Dinoprostone 188-204 prostaglandin E synthase Mus musculus 171-178 33473256-3 2020 Researchers have identified multiple signaling pathways involved in lung cancer chemoresistance, including cyclooxygenase-2 (COX-2)/microsomal prostaglandin E synthase-1 (mPGES-1) derived prostaglandin E2 (PGE2). Dinoprostone 206-210 prostaglandin E synthase Mus musculus 171-178 33053444-3 2021 Prostaglandin E2 (PGE2) is robustly synthesized in the ischemic cortex by quickly induced COX-2 and microsomal prostaglandin E synthase-1 (mPGES-1) following cerebral ischemia. Dinoprostone 0-16 prostaglandin E synthase Mus musculus 139-146 33053444-3 2021 Prostaglandin E2 (PGE2) is robustly synthesized in the ischemic cortex by quickly induced COX-2 and microsomal prostaglandin E synthase-1 (mPGES-1) following cerebral ischemia. Dinoprostone 18-22 prostaglandin E synthase Mus musculus 139-146 33408499-10 2020 Results: LFA-9 inhibited mPGES-1/5-LOX and their products PGE2 and LTB4, spared COX-1/2 and its product PGI2. Dinoprostone 58-62 prostaglandin E synthase Mus musculus 25-32 33292158-1 2021 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES-1) catalyzes the terminal step of prostaglandin E2 (PGE2) production, which plays an important role in the regulation of febrile response. Dinoprostone 91-107 prostaglandin E synthase Mus musculus 51-58 33292158-1 2021 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES-1) catalyzes the terminal step of prostaglandin E2 (PGE2) production, which plays an important role in the regulation of febrile response. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 12-49 33292158-1 2021 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES-1) catalyzes the terminal step of prostaglandin E2 (PGE2) production, which plays an important role in the regulation of febrile response. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 51-58 33292158-13 2021 CONCLUSIONS: PGE2 concentration reduction in hypothalamus, due to compound 1 central injection, is related to decreased mPGES-1 mRNA levels but not to COX-2 inhibition (IC50> 50 muM). Dinoprostone 13-17 prostaglandin E synthase Mus musculus 120-127 33273889-4 2020 Our results demonstrated that PGE2 and its processing enzymes COX-2 and mPGES-1 were highest in the synovial tissue of RA, followed by the synovial tissue of OA and JT patients. Dinoprostone 30-34 prostaglandin E synthase Mus musculus 72-79 33028694-1 2020 BACKGROUND: 2,5-dimethylcelecoxib (DMC) is a targeted inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1), a key enzyme in the PGE2 synthesis pathway of inflammatory mediators. Dinoprostone 136-140 prostaglandin E synthase Mus musculus 106-113 32583353-10 2020 Lowering the PGE2 levels through inhibition of human microsomal prostaglandin E synthase-1 (mPGES-1) can enhance the host immune response against COVID-19. Dinoprostone 13-17 prostaglandin E synthase Mus musculus 92-99 32449517-1 2020 BACKGROUND AND PURPOSE: mPGES-1 catalyzes the production of prostaglandin E2 (PGE2 ), the most abundant prostanoid related to inflammation and pain in arthritis. Dinoprostone 60-76 prostaglandin E synthase Mus musculus 24-31 32759273-1 2020 Deletion of microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibits inflammation and protects against atherosclerotic vascular diseases but displayed variable influence on pathologic cardiac remodeling. Dinoprostone 23-39 prostaglandin E synthase Mus musculus 52-59 32759273-9 2020 SIGNIFICANCE STATEMENT: Inhibitors of microsomal prostaglandin E2 synthase-1 (mPGES-1) are being developed as alternative analgesics that are less likely to elicit cardiovascular hazards than cyclooxygenase-2 selective nonsteroidal anti-inflammatory drugs. Dinoprostone 49-65 prostaglandin E synthase Mus musculus 78-85 32449517-1 2020 BACKGROUND AND PURPOSE: mPGES-1 catalyzes the production of prostaglandin E2 (PGE2 ), the most abundant prostanoid related to inflammation and pain in arthritis. Dinoprostone 78-82 prostaglandin E synthase Mus musculus 24-31 32410351-0 2020 Polysubstituted Pyrimidines as mPGES-1 Inhibitors: Discovery of Potent Inhibitors of PGE2 Production with a Strong Anti-inflammatory Effects in Carrageenan-Induced Rat Paw Edema. Dinoprostone 85-89 prostaglandin E synthase Mus musculus 31-38 32576928-1 2020 Microsomal prostaglandin E2 synthase-1 (mPGES-1) is known as an ideal target for next generation of anti-inflammatory drugs without the side effects of currently available anti-inflammatory drugs. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 32623799-4 2020 mPGES-1-derived prostaglandin E2 (PGE2 ) is known to promote tumor growth through increased proliferation and survival of tumor cells, immune suppression, angiogenesis, and therapy resistance, and we, therefore, hypothesize that mPGES-1 constitutes an interesting stromal target. Dinoprostone 16-32 prostaglandin E synthase Mus musculus 0-7 32623799-4 2020 mPGES-1-derived prostaglandin E2 (PGE2 ) is known to promote tumor growth through increased proliferation and survival of tumor cells, immune suppression, angiogenesis, and therapy resistance, and we, therefore, hypothesize that mPGES-1 constitutes an interesting stromal target. Dinoprostone 16-32 prostaglandin E synthase Mus musculus 229-236 32623799-4 2020 mPGES-1-derived prostaglandin E2 (PGE2 ) is known to promote tumor growth through increased proliferation and survival of tumor cells, immune suppression, angiogenesis, and therapy resistance, and we, therefore, hypothesize that mPGES-1 constitutes an interesting stromal target. Dinoprostone 34-38 prostaglandin E synthase Mus musculus 0-7 32623799-4 2020 mPGES-1-derived prostaglandin E2 (PGE2 ) is known to promote tumor growth through increased proliferation and survival of tumor cells, immune suppression, angiogenesis, and therapy resistance, and we, therefore, hypothesize that mPGES-1 constitutes an interesting stromal target. Dinoprostone 34-38 prostaglandin E synthase Mus musculus 229-236 32621176-7 2021 In this study, qRT-PCR and immunoblotting demonstrated that the key enzymes in PGE2 synthesis, including COX-1, COX-2, mPGES-1 and mPGES-2, were upregulated during cerebral I/R injury, but 15-PGDH, the main PGE2 degradation enzyme, was downregulated. Dinoprostone 79-83 prostaglandin E synthase Mus musculus 119-126 32655834-3 2020 One inflammatory pathway commonly dysregulated in cancer is the metabolism of arachidonic acid (AA) by Cyclooxygenase-2 (COX-2) and microsomal Prostaglandin E Synthase 1 (mPGES-1) into Prostaglandin E2 (PGE2). Dinoprostone 185-201 prostaglandin E synthase Mus musculus 171-178 32655834-3 2020 One inflammatory pathway commonly dysregulated in cancer is the metabolism of arachidonic acid (AA) by Cyclooxygenase-2 (COX-2) and microsomal Prostaglandin E Synthase 1 (mPGES-1) into Prostaglandin E2 (PGE2). Dinoprostone 203-207 prostaglandin E synthase Mus musculus 171-178 32655834-8 2020 miR-708 also represses PGE2 production by suppressing both COX-2 and mPGES-1 expression in lung cancer cells. Dinoprostone 23-27 prostaglandin E synthase Mus musculus 69-76 32295420-8 2020 mPGES-1-derived PGE2 critically regulates microcirculation via its receptor EP (receptor for prostanoid E) 4. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 0-7 32317963-1 2020 Rationale: The development of inhibitors of microsomal prostaglandin (PG)E2 synthase-1 (mPGES-1) was driven by the promise of attaining antiinflammatory agents with a safe cardiovascular profile because of the possible diversion of the accumulated substrate, PGH2, towards prostacyclin (PGI2). Dinoprostone 55-75 prostaglandin E synthase Mus musculus 88-95 32251289-0 2020 mPGES-1/PGE2 promotes the growth of T-ALL cells in vitro and in vivo by regulating the expression of MTDH via the EP3/cAMP/PKA/CREB pathway. Dinoprostone 8-12 prostaglandin E synthase Mus musculus 0-7 32251289-4 2020 Our previous studies found that mPGES-1/PGE2 was important for promoting the growth of leukaemia cells. Dinoprostone 40-44 prostaglandin E synthase Mus musculus 32-39 32251289-6 2020 Our results showed that mPGES-1/PGE2 regulates the expression of MTDH through the EP3/cAMP/PKA-CREB pathway in T-ALL cells. Dinoprostone 32-36 prostaglandin E synthase Mus musculus 24-31 32408877-1 2020 BACKGROUND: Dual inhibitors of the 5-lipoxygenase-activating protein (FLAP) and the microsomal prostaglandin E2 synthase-1 (mPGES-1) may exert better anti-inflammatory efficacy and lower risks of adverse effects versus non-steroidal anti-inflammatory drugs. Dinoprostone 95-111 prostaglandin E synthase Mus musculus 124-131 32060421-4 2020 Here, we showed that PTGES/PGE2 signaling was highly associated with lung tumorigenesis and metastasis in Gprc5a-ko mice. Dinoprostone 27-31 prostaglandin E synthase Mus musculus 21-26 31868102-1 2020 Prostaglandin E2 (PGE2), which is a potent pro-inflammatory lipid mediator, is biosynthesized from arachidonic acid by cyclooxygenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1). Dinoprostone 0-16 prostaglandin E synthase Mus musculus 175-182 31868102-1 2020 Prostaglandin E2 (PGE2), which is a potent pro-inflammatory lipid mediator, is biosynthesized from arachidonic acid by cyclooxygenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1). Dinoprostone 18-22 prostaglandin E synthase Mus musculus 175-182 32060421-8 2020 Importantly, targeting PGE2 signaling in Gprc5a-ko mice by PTGES inhibitor suppressed MDSC recruitment, restored T cells, and significantly repressed lung metastasis. Dinoprostone 23-27 prostaglandin E synthase Mus musculus 59-64 30897501-1 2019 OBJECTIVES: Microsomal prostaglandin E synthase-1 (mPGES-1) catalyses the formation of PGE2 in inflammatory tissues. Dinoprostone 87-91 prostaglandin E synthase Mus musculus 51-58 32022480-1 2020 Dual inhibition of microsomal prostaglandin E2 synthase-1 (mPGES-1) and 5-lipoxygenase (5-LO), two key enzymes involved in pro-inflammatory eicosanoid biosynthesis, represents a new strategy for treating inflammatory disorders. Dinoprostone 30-46 prostaglandin E synthase Mus musculus 59-66 32155782-8 2020 In the chronic infarction model, mice encoding endothelial NOX5 enhanced the cardiac mRNA expression of COX-2 and PGES, suggesting a COX-2/PGE2 response to NOX5 presence in an ischemic situation. Dinoprostone 139-143 prostaglandin E synthase Mus musculus 114-118 31732699-12 2020 EP2/4 receptors are involved in a positive feedback loop for COX-2 and mPGES-1 expression, thus enhancing PGE2 production. Dinoprostone 106-110 prostaglandin E synthase Mus musculus 71-78 32023904-7 2020 Quantitative RT-PCR analysis and protein detection showed that PGE2/COX-2 signaling was activated, shown by the upregulation of PGE2 production as well as COX-2 and microsomal PGE2 synthase (mPGES1) transcription in DCs specifically induced by M. bovis and BCG infection. Dinoprostone 63-67 prostaglandin E synthase Mus musculus 191-197 31404942-1 2019 BACKGROUND AND PURPOSE: Microsomal PGE synthase-1 (mPGES-1), the inducible synthase that catalyses the terminal step in PGE2 biosynthesis, is of high interest as therapeutic target to treat inflammation. Dinoprostone 120-124 prostaglandin E synthase Mus musculus 51-58 31638830-9 2019 Our data provide key signaling steps underlying seizure-induced P-gp up-regulation and suggest that mPGES-1 inhibitors could potentially prevent P-gp up-regulation in epilepsy.-Soldner, E. L. B., Hartz, A. M. S., Akanuma, S.-I., Pekcec, A., Doods, H., Kryscio, R. J., Hosoya, K.-I., Bauer, B. Inhibition of human microsomal PGE2 synthase-1 reduces seizure-induced increases of P-glycoprotein expression and activity at the blood-brain barrier. Dinoprostone 324-328 prostaglandin E synthase Mus musculus 100-107 30814036-1 2019 BACKGROUND: We previously studied the metabolomics, transcriptomics and proteomics of intestinal tissue of Hirschsprung disease (HSCR) patients; the results suggested that the expression of prostaglandin E2(PGE2), prostaglandin E receptor 2(PTGER2) and microsomal prostaglandin E synthase-1 (mPGES-1) notably increased in HSCR colon tissues. Dinoprostone 190-206 prostaglandin E synthase Mus musculus 292-299 30814036-1 2019 BACKGROUND: We previously studied the metabolomics, transcriptomics and proteomics of intestinal tissue of Hirschsprung disease (HSCR) patients; the results suggested that the expression of prostaglandin E2(PGE2), prostaglandin E receptor 2(PTGER2) and microsomal prostaglandin E synthase-1 (mPGES-1) notably increased in HSCR colon tissues. Dinoprostone 207-211 prostaglandin E synthase Mus musculus 292-299 30814036-2 2019 We already verified the differential expression of PGE2/EP2 in HSCR patients; therefore we investigate how mPGES-1 derived PGE2 affects the migration and the potential mechanism in cells, revealing the role of mPGES-1 derived PGE2 in the pathogenesis of Hirschsprung disease. Dinoprostone 51-55 prostaglandin E synthase Mus musculus 107-114 30814036-2 2019 We already verified the differential expression of PGE2/EP2 in HSCR patients; therefore we investigate how mPGES-1 derived PGE2 affects the migration and the potential mechanism in cells, revealing the role of mPGES-1 derived PGE2 in the pathogenesis of Hirschsprung disease. Dinoprostone 123-127 prostaglandin E synthase Mus musculus 107-114 30814036-2 2019 We already verified the differential expression of PGE2/EP2 in HSCR patients; therefore we investigate how mPGES-1 derived PGE2 affects the migration and the potential mechanism in cells, revealing the role of mPGES-1 derived PGE2 in the pathogenesis of Hirschsprung disease. Dinoprostone 123-127 prostaglandin E synthase Mus musculus 210-217 30814036-2 2019 We already verified the differential expression of PGE2/EP2 in HSCR patients; therefore we investigate how mPGES-1 derived PGE2 affects the migration and the potential mechanism in cells, revealing the role of mPGES-1 derived PGE2 in the pathogenesis of Hirschsprung disease. Dinoprostone 123-127 prostaglandin E synthase Mus musculus 107-114 30814036-2 2019 We already verified the differential expression of PGE2/EP2 in HSCR patients; therefore we investigate how mPGES-1 derived PGE2 affects the migration and the potential mechanism in cells, revealing the role of mPGES-1 derived PGE2 in the pathogenesis of Hirschsprung disease. Dinoprostone 123-127 prostaglandin E synthase Mus musculus 210-217 30814036-15 2019 Here we thoroughly inquire the role mPGES-1 derived PGE2 plays in cell migration which might provide a new thinking in the investigation interrelated to the pathogenesis of HSCR. Dinoprostone 52-56 prostaglandin E synthase Mus musculus 36-43 31229523-0 2019 A novel mPGES-1 inhibitor alleviates inflammatory responses by downregulating PGE2 in experimental models. Dinoprostone 78-82 prostaglandin E synthase Mus musculus 8-15 31229523-7 2019 Our data suggest that PBCH downregulates PGE2 production by interfering with the mPGES-1 activity, thus reducing edema and arthritis in rat models. Dinoprostone 41-45 prostaglandin E synthase Mus musculus 81-88 30349011-2 2019 In these inflammatory conditions, the release of prostaglandin E2 (PGE2) is increased via the activity of inducible microsomal PGE synthase-1 (mPGES-1). Dinoprostone 49-65 prostaglandin E synthase Mus musculus 143-150 30349011-2 2019 In these inflammatory conditions, the release of prostaglandin E2 (PGE2) is increased via the activity of inducible microsomal PGE synthase-1 (mPGES-1). Dinoprostone 67-71 prostaglandin E synthase Mus musculus 143-150 31136957-2 2019 Previous studies have shown that PGE2 accumulates in Escherichia coli-challenged ex vivo endometrial explants, increasing the expression of pro-inflammatory factors and aggravating tissue damage; these alterations are linked to key enzymes involved in the synthesis of PGE2, including cyclooxygenases-2 (COX-2) and microsomal PGES-1 (mPGES-1). Dinoprostone 33-37 prostaglandin E synthase Mus musculus 326-332 31136957-2 2019 Previous studies have shown that PGE2 accumulates in Escherichia coli-challenged ex vivo endometrial explants, increasing the expression of pro-inflammatory factors and aggravating tissue damage; these alterations are linked to key enzymes involved in the synthesis of PGE2, including cyclooxygenases-2 (COX-2) and microsomal PGES-1 (mPGES-1). Dinoprostone 33-37 prostaglandin E synthase Mus musculus 334-341 31059928-3 2019 In the present study, we aimed to determine the mRNA levels and immunolocalization of the enzymes responsible for PGE2 synthesis (PTGS2, mPGES1, mPGES2 and cPGES) in embryos at the 2-cell, 4-cell, 8-cell, 16-cell, morula, early blastocyst, blastocyst, expanded blastocyst and hatched blastocyst stages, using a well-defined bovine model of oocyte developmental competence based on the time of first cleavage. Dinoprostone 114-118 prostaglandin E synthase Mus musculus 137-143 30947012-11 2019 CONCLUSIONS: These results indicate that 5-ALA suppressed PGE2 production by macrophages via the downregulation of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 expression levels. Dinoprostone 58-62 prostaglandin E synthase Mus musculus 136-173 30930248-8 2019 These results indicate that PGE2 accumulates via PTGS-2 and mPGES-1 and induces tissue damage by upregulating pro-inflammatory factors and DAMPs in LPS-treated bovine endometrial explants. Dinoprostone 28-32 prostaglandin E synthase Mus musculus 60-67 31698145-5 2020 Selective inhibition of downstream mPGES-1 for reduction in only PGE2 biosynthesis is suggested as a safer therapeutic strategy. Dinoprostone 65-69 prostaglandin E synthase Mus musculus 35-42 32231562-2 2020 However, miR-574-5p has recently been shown to positively regulate the expression of microsomal prostaglandin E-synthase-1 (mPGES-1), a key enzyme in the prostaglandin E2 (PGE2) biosynthesis, by acting as decoy to the RNA-binding protein CUG-RNA binding protein 1 (CUGBP1) in human lung cancer. Dinoprostone 154-170 prostaglandin E synthase Mus musculus 124-131 32231562-2 2020 However, miR-574-5p has recently been shown to positively regulate the expression of microsomal prostaglandin E-synthase-1 (mPGES-1), a key enzyme in the prostaglandin E2 (PGE2) biosynthesis, by acting as decoy to the RNA-binding protein CUG-RNA binding protein 1 (CUGBP1) in human lung cancer. Dinoprostone 172-176 prostaglandin E synthase Mus musculus 124-131 32231562-3 2020 miR-574-5p exhibits oncogenic properties and promotes lung tumor growth in vivo via induction of mPGES-1-derived PGE2 synthesis. Dinoprostone 113-117 prostaglandin E synthase Mus musculus 97-104 32231562-8 2020 The specificity of miR-574-5p/CUGBP1 regulation on mPGES-1 expression supports the therapeutic strategy of pharmacological inhibition of PGE2 formation, which may provide significant therapeutic value for NSCLC patients with high miR-574-5p levels. Dinoprostone 137-141 prostaglandin E synthase Mus musculus 51-58 32435385-0 2020 Targeting mPGES-1 by a Combinatorial Approach: Identification of the Aminobenzothiazole Scaffold to Suppress PGE2 Levels. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 10-17 32435385-1 2020 Microsomal prostaglandin E2 synthase-1 (mPGES-1), the terminal enzyme responsible for the production of inducible prostaglandin E2, has become an attractive target for the treatment of inflammation and cancer pathologies. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 32435385-1 2020 Microsomal prostaglandin E2 synthase-1 (mPGES-1), the terminal enzyme responsible for the production of inducible prostaglandin E2, has become an attractive target for the treatment of inflammation and cancer pathologies. Dinoprostone 114-130 prostaglandin E synthase Mus musculus 40-47 31536727-8 2020 More interestingly, we found that NAN did not affect COX-2 expression and activity but reduced the PGE2 concentration by selective inhibition of microsomal prostaglandin E synthase-1 (mPGES-1). Dinoprostone 99-103 prostaglandin E synthase Mus musculus 184-191 32094439-2 2020 This study showed that the snake venom metalloprotease (SVMP) BaP1 activates FLSs to produce PGE2 by a mechanism dependent on COX-2, mPGES-1 and iPLA2s. Dinoprostone 93-97 prostaglandin E synthase Mus musculus 133-140 32094439-7 2020 Engagement of this receptor by PGE2 triggers a positive feedback loop for its production by up-regulating expression of key components of the PGE2 biosynthetic cascade (COX-2, mPGES-1 and the EP4 receptor), thus contributing to amplification of BaP1-induced effects in FLSs. Dinoprostone 31-35 prostaglandin E synthase Mus musculus 176-183 32094439-7 2020 Engagement of this receptor by PGE2 triggers a positive feedback loop for its production by up-regulating expression of key components of the PGE2 biosynthetic cascade (COX-2, mPGES-1 and the EP4 receptor), thus contributing to amplification of BaP1-induced effects in FLSs. Dinoprostone 142-146 prostaglandin E synthase Mus musculus 176-183 31638830-4 2019 Thus, we hypothesized that inhibiting microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), the enzyme generating PGE2, prevents blood-brain barrier P-gp up-regulation after status epilepticus (SE). Dinoprostone 49-65 prostaglandin E synthase Mus musculus 85-92 31638830-4 2019 Thus, we hypothesized that inhibiting microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), the enzyme generating PGE2, prevents blood-brain barrier P-gp up-regulation after status epilepticus (SE). Dinoprostone 67-71 prostaglandin E synthase Mus musculus 85-92 31638830-4 2019 Thus, we hypothesized that inhibiting microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), the enzyme generating PGE2, prevents blood-brain barrier P-gp up-regulation after status epilepticus (SE). Dinoprostone 117-121 prostaglandin E synthase Mus musculus 85-92 30879343-1 2019 mPGES-1 is a terminal rate-limiting enzyme responsible for inflammation-induced PGE2 production. Dinoprostone 80-84 prostaglandin E synthase Mus musculus 0-7 31392591-3 2019 Specifically, COX-2 overexpression accelerates the expression of microsomal PGE synthase-1 (mPGES-1) and lipocalin-type prostaglandin D synthase (L-PGDS), leading to the synthesis of PGE2 and 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) in 6-month-old APP/PS1 mice. Dinoprostone 183-187 prostaglandin E synthase Mus musculus 92-99 31207300-3 2019 Overexpression of mPGES-1/prostaglandin E-2 (PGE-2) signaling in GR cells was associated with acquisition of mesenchymal and stem-like cell properties, nuclear EGFR translocation and tolerance to cisplatin. Dinoprostone 26-43 prostaglandin E synthase Mus musculus 18-25 31231223-4 2019 Inhibition of mPGES-1 decreased PGE2 production and increased PGF2alpha and thromboxane B2 (TXB2) formation, while inhibition of COX-2 decreased the production of all three prostanoids. Dinoprostone 32-36 prostaglandin E synthase Mus musculus 14-21 31015404-3 2019 Here we report that COX-1 and mPGES-1 mediate production of substantial amounts of PGE2 and confer cardiac protection in MI/R. Dinoprostone 83-87 prostaglandin E synthase Mus musculus 30-37 30423474-2 2019 Although increased production of prostaglandin E2 (PGE2) has been implicated in tissue damage in several pathological settings, the role of microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal enzyme for PGE2 synthesis, in dopaminergic neurodegeneration remains unclear. Dinoprostone 222-226 prostaglandin E synthase Mus musculus 140-177 30423474-2 2019 Although increased production of prostaglandin E2 (PGE2) has been implicated in tissue damage in several pathological settings, the role of microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal enzyme for PGE2 synthesis, in dopaminergic neurodegeneration remains unclear. Dinoprostone 222-226 prostaglandin E synthase Mus musculus 179-186 30423474-5 2019 The genetic deletion of mPGES-1 not only abolished 6-OHDA-induced PGE2 production but also inhibited 6-OHDA-induced dopaminergic neurodegeneration both in vitro and in vivo. Dinoprostone 66-70 prostaglandin E synthase Mus musculus 24-31 30423474-7 2019 Furthermore, in cultured primary mesencephalic neurons, addition of PGE2 to compensate for the deficiency of 6-OHDA-induced PGE2 production in mPGES-1 KO neurons recovered 6-OHDA toxicity to almost the same extent as that seen in WT neurons. Dinoprostone 68-72 prostaglandin E synthase Mus musculus 143-150 30423474-7 2019 Furthermore, in cultured primary mesencephalic neurons, addition of PGE2 to compensate for the deficiency of 6-OHDA-induced PGE2 production in mPGES-1 KO neurons recovered 6-OHDA toxicity to almost the same extent as that seen in WT neurons. Dinoprostone 124-128 prostaglandin E synthase Mus musculus 143-150 30423474-8 2019 These results suggest that induction of mPGES-1 enhances 6-OHDA-induced dopaminergic neuronal death through excessive PGE2 production. Dinoprostone 118-122 prostaglandin E synthase Mus musculus 40-47 29599139-0 2018 Protective Role of mPGES-1 (Microsomal Prostaglandin E Synthase-1)-Derived PGE2 (Prostaglandin E2) and the Endothelial EP4 (Prostaglandin E Receptor) in Vascular Responses to Injury. Dinoprostone 75-79 prostaglandin E synthase Mus musculus 19-26 30867043-9 2019 Incubation of IL-1beta treated diseased tendon cells with selective mPGES-1 inhibitor Compound III, reduced PGE2, and simultaneously increased 6-keto PGF1alpha production. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 68-75 30506812-2 2019 The terminal enzyme, microsomal prostaglandin E synthase-1 (mPGES-1) regulating PGE2 synthesis is a promising therapeutic target to reduce inflammatory bone loss. Dinoprostone 80-84 prostaglandin E synthase Mus musculus 21-58 30506812-2 2019 The terminal enzyme, microsomal prostaglandin E synthase-1 (mPGES-1) regulating PGE2 synthesis is a promising therapeutic target to reduce inflammatory bone loss. Dinoprostone 80-84 prostaglandin E synthase Mus musculus 60-67 30506812-3 2019 The aim of this study was to investigate effects of mPGES-1 inhibitors, aminothiazoles TH-848 and TH-644, on PGE2 production and osteoclastogenesis in co-cultures of periodontal ligament (PDL) and osteoclast progenitor cells RAW 264.7, stimulated by lipopolysaccharide (LPS), and bone resorption in RANKL-mediated peripheral blood mononuclear cells (PBMCs). Dinoprostone 109-113 prostaglandin E synthase Mus musculus 52-59 30010723-9 2019 Treatment with the COX-2, mPGES-1, EP4, and protein kinase A (PKA) inhibitors decreased the production of PGE2, inflammatory factors, and DAMPs, simultaneously alleviating the E. coli-induced endometrial tissue damage. Dinoprostone 106-110 prostaglandin E synthase Mus musculus 26-33 30010723-10 2019 Therefore, the PGE2 that was generated by COX-2 and mPGES-1 accumulated, and this pathogenic PGE2 increased inflammatory damage by upregulating inflammatory factors and DAMPs in E. coli-infected bovine endometrial tissue. Dinoprostone 15-19 prostaglandin E synthase Mus musculus 52-59 30619314-0 2018 mPGES-1-Mediated Production of PGE2 and EP4 Receptor Sensing Regulate T Cell Colonic Inflammation. Dinoprostone 31-35 prostaglandin E synthase Mus musculus 0-7 30619314-5 2018 Absence of T cell autocrine mPGES1-dependent PGE2 reduces colitogenicity in association with an increase in CD4+RORgammat+ cells in the lamina propria. Dinoprostone 45-49 prostaglandin E synthase Mus musculus 28-34 30619314-7 2018 Thus, our research defines how mPGES-1-driven production of PGE2 by different cell types in distinct intestinal locations impacts T cell function during colitis. Dinoprostone 60-64 prostaglandin E synthase Mus musculus 31-38 30312760-5 2018 This study shows that 27-OH and HNE promote up-regulation of both the inducible enzymes COX-2 and mPGES-1, leading to increased production of prostaglandin (PG) E2 and inducible nitric oxide synthase, and the subsequent release of nitric oxide in human promonocytic U937 cells. Dinoprostone 142-163 prostaglandin E synthase Mus musculus 98-105 30312760-7 2018 This enhancement is presumably due to the induction of PGE2 synthesis, as a result of the up-regulation of the COX-2/mPGES-1, stimulated by the two oxidized lipids, 27-OH and HNE. Dinoprostone 55-59 prostaglandin E synthase Mus musculus 117-124 30453998-8 2018 The inhibition of LPS-induced PGE2 release by the most potent candidate KIT 17 was partially dependent on reduced protein synthesis of mPGES-1 and COX-2. Dinoprostone 30-34 prostaglandin E synthase Mus musculus 135-142 30382148-3 2018 Expression of the key enzymes of PGE2 synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Dinoprostone 33-37 prostaglandin E synthase Mus musculus 97-104 30382148-9 2018 In conclusion, attenuation of PGE2 production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH. Dinoprostone 30-34 prostaglandin E synthase Mus musculus 49-56 30333759-6 2018 Microsomal prostaglandin E synthase-1 (mPGES-1) is an enzyme, which specifically catalyzes the final step of PGE2 biosynthesis. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 0-37 30333759-6 2018 Microsomal prostaglandin E synthase-1 (mPGES-1) is an enzyme, which specifically catalyzes the final step of PGE2 biosynthesis. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 39-46 30333759-7 2018 Interestingly, mPGES-1 invalidation dramatically alters the production of PGE2 during inflammation. Dinoprostone 74-78 prostaglandin E synthase Mus musculus 15-22 30214544-6 2018 Microarray and western blot analyses revealed that c-Jun N-terminal kinase served a role in the mPGES-1/prostaglandin E2/EP4/MAPK positive feedback loops. Dinoprostone 104-120 prostaglandin E synthase Mus musculus 96-103 30053720-1 2018 Leukotrienes (LTs) and prostaglandin (PG)E2, produced by 5-lipoxygenase (5-LO) and microsomal prostaglandin E2 synthase-1 (mPGES-1), respectively, are key players in inflammation, and pharmacological suppression of these lipid mediators (LM) represents a strategy to intervene with inflammatory disorders. Dinoprostone 23-43 prostaglandin E synthase Mus musculus 123-130 29891646-1 2018 mPGES-1 (microsomal prostaglandin E synthase-1), the downstream enzyme responsible for PGE2 (prostaglandin E2) synthesis in inflammatory conditions and oxidative stress are increased in vessels from hypertensive animals. Dinoprostone 87-91 prostaglandin E synthase Mus musculus 0-7 29891646-1 2018 mPGES-1 (microsomal prostaglandin E synthase-1), the downstream enzyme responsible for PGE2 (prostaglandin E2) synthesis in inflammatory conditions and oxidative stress are increased in vessels from hypertensive animals. Dinoprostone 93-109 prostaglandin E synthase Mus musculus 0-7 29891646-2 2018 We evaluated the role of mPGES-1-derived PGE2 in the vascular dysfunction and remodeling in hypertension and the possible contribution of oxidative stress. Dinoprostone 41-45 prostaglandin E synthase Mus musculus 25-32 29891646-7 2018 In conclusion, mPGES-1-derived PGE2 is involved in vascular remodeling, stiffness, and endothelial dysfunction in hypertension likely through an increase of oxidative stress produced by NADPH oxidase and mitochondria. Dinoprostone 31-35 prostaglandin E synthase Mus musculus 15-22 29458169-2 2018 This study aims to examine the role of endogenous prostaglandin E2 (PGE2) produced by inducible microsomal PGE synthase-1 (mPGES-1), a terminal enzyme of PGE2 generation, in liver injury and repair following hepatic I/R. Dinoprostone 50-66 prostaglandin E synthase Mus musculus 123-130 29458169-2 2018 This study aims to examine the role of endogenous prostaglandin E2 (PGE2) produced by inducible microsomal PGE synthase-1 (mPGES-1), a terminal enzyme of PGE2 generation, in liver injury and repair following hepatic I/R. Dinoprostone 68-72 prostaglandin E synthase Mus musculus 123-130 29458169-2 2018 This study aims to examine the role of endogenous prostaglandin E2 (PGE2) produced by inducible microsomal PGE synthase-1 (mPGES-1), a terminal enzyme of PGE2 generation, in liver injury and repair following hepatic I/R. Dinoprostone 154-158 prostaglandin E synthase Mus musculus 123-130 29458169-16 2018 Herein, we demonstrated that inducible prostaglandin E2 synthase (mPGES-1), an enzyme involved in synthesizing prostaglandin E2, worsens the injury and delays liver repair through accumulation of proinflammatory macrophages. Dinoprostone 39-55 prostaglandin E synthase Mus musculus 66-73 29804818-5 2018 By specifically targeting microsomal prostaglandin E synthase-1 (mPGES-1) activity with a small molecule inhibitor we could block CAF-derived PGE2 production leading to reduced tumor growth, impaired angiogenesis, inhibited CAF migration and infiltration, reduced tumor cell proliferation and a favorable shift in the M1/M2 macrophage ratio. Dinoprostone 142-146 prostaglandin E synthase Mus musculus 65-72 30538110-1 2019 PURPOSE: Microsomal prostaglandin E2 synthase 1 (mPGES1) was evaluated as an important downstream effector of the COX2 pathway responsible for tumor-mediated immunosuppression in melanoma. Dinoprostone 20-36 prostaglandin E synthase Mus musculus 49-55 30537167-0 2019 A Multi-step Virtual Screening Protocol for the Identification of Novel Non-acidic Microsomal Prostaglandin E2 Synthase-1 (mPGES-1) Inhibitors. Dinoprostone 94-110 prostaglandin E synthase Mus musculus 123-130 30537167-1 2019 Microsomal prostaglandin E2 synthase-1 (mPGES-1) is a potential therapeutic target for the treatment of inflammatory diseases and certain types of cancer. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 30463256-1 2018 Microsomal prostaglandin E synthetase-1 (mPGES-1) is an inducible terminal enzyme for the production of prostaglandin E2 (PGE2). Dinoprostone 104-120 prostaglandin E synthase Mus musculus 41-48 30463256-1 2018 Microsomal prostaglandin E synthetase-1 (mPGES-1) is an inducible terminal enzyme for the production of prostaglandin E2 (PGE2). Dinoprostone 122-126 prostaglandin E synthase Mus musculus 41-48 30027346-12 2018 Our data suggest that an activation of the COX-2/mPGES-1 synthetic pathway is responsible for the increased renal formation of PGE2 in response to LPS and that the vasodilatory effect of PGE2 and PGI2 is enhanced during endotoxemia. Dinoprostone 127-131 prostaglandin E synthase Mus musculus 49-56 30205824-10 2018 CONCLUSIONS: CGRP expression in the IFP of KOA patients is regulated by the COX-2/mPGES-1/PGE2 pathway. Dinoprostone 90-94 prostaglandin E synthase Mus musculus 82-89 29569150-9 2018 Based on the discussed data, the positive correlation between PGE2, COX-2, and mPGES-1 confirm the role of PGE2 pathway and neuroinflammation in the etiology of ASD, and the possibility of using PGE2, COX-2 and mPGES-1 as biomarkers of autism severity. Dinoprostone 62-66 prostaglandin E synthase Mus musculus 79-86 29569150-9 2018 Based on the discussed data, the positive correlation between PGE2, COX-2, and mPGES-1 confirm the role of PGE2 pathway and neuroinflammation in the etiology of ASD, and the possibility of using PGE2, COX-2 and mPGES-1 as biomarkers of autism severity. Dinoprostone 107-111 prostaglandin E synthase Mus musculus 79-86 29569150-9 2018 Based on the discussed data, the positive correlation between PGE2, COX-2, and mPGES-1 confirm the role of PGE2 pathway and neuroinflammation in the etiology of ASD, and the possibility of using PGE2, COX-2 and mPGES-1 as biomarkers of autism severity. Dinoprostone 107-111 prostaglandin E synthase Mus musculus 79-86 30015253-2 2018 New dual inhibitors of 5-lipoxygenase (5-LO) and microsomal prostaglandin E2 synthase-1 (mPGES-1), that block, at the same time, the formation of PGE2 and LTs, are currently emerged as a highly interesting drug candidates for better pharmacotherapie of inflammation-related disorders. Dinoprostone 146-150 prostaglandin E synthase Mus musculus 89-96 29891860-3 2018 We hypothesized that PGE2 may exert autocrine effect in SMC to induce microsomal prostaglandin E synthase-1 (mPGES-1), which contributes to motility dysfunction after obstruction is resolved. Dinoprostone 21-25 prostaglandin E synthase Mus musculus 109-116 29891860-9 2018 Expression of mPGES-1 in colon SMC was inducible by stretch or PGE2. Dinoprostone 63-67 prostaglandin E synthase Mus musculus 14-21 29891860-10 2018 Administration of mPGES-1 inhibitor Cay 10526 either before or after the release of obstruction normalized PGE2 levels and improved motility in the post-BO rats. Dinoprostone 107-111 prostaglandin E synthase Mus musculus 18-25 29895492-8 2018 The inhibition of LPS-induced PGE2 release in primary microglia was partially dependent on reduced protein synthesis of mPGES-1 and the reduction in the activation of cytosolic phospholipase A2 (cPLA2) without altering COX-2 enzymatic activity, inhibitor of kappa B alpha (IkappaBalpha) degradation, and the activation of multiple mitogen activated protein kinases (MAPKs). Dinoprostone 30-34 prostaglandin E synthase Mus musculus 120-127 29599139-0 2018 Protective Role of mPGES-1 (Microsomal Prostaglandin E Synthase-1)-Derived PGE2 (Prostaglandin E2) and the Endothelial EP4 (Prostaglandin E Receptor) in Vascular Responses to Injury. Dinoprostone 75-79 prostaglandin E synthase Mus musculus 28-65 29599139-0 2018 Protective Role of mPGES-1 (Microsomal Prostaglandin E Synthase-1)-Derived PGE2 (Prostaglandin E2) and the Endothelial EP4 (Prostaglandin E Receptor) in Vascular Responses to Injury. Dinoprostone 81-97 prostaglandin E synthase Mus musculus 19-26 29599139-0 2018 Protective Role of mPGES-1 (Microsomal Prostaglandin E Synthase-1)-Derived PGE2 (Prostaglandin E2) and the Endothelial EP4 (Prostaglandin E Receptor) in Vascular Responses to Injury. Dinoprostone 81-97 prostaglandin E synthase Mus musculus 28-65 29599139-3 2018 To examine the role of mPGES-1-derived PGE2 (prostaglandin E2) in vascular remodeling without the IP. Dinoprostone 39-43 prostaglandin E synthase Mus musculus 23-30 29599139-3 2018 To examine the role of mPGES-1-derived PGE2 (prostaglandin E2) in vascular remodeling without the IP. Dinoprostone 45-61 prostaglandin E synthase Mus musculus 23-30 29599139-12 2018 CONCLUSIONS: Removal of the IP receptors unmasks a protective role of mPGES-1-derived PGE2 in limiting injury-induced vascular hyperplasia. Dinoprostone 86-90 prostaglandin E synthase Mus musculus 70-77 29470537-3 2018 Recently, we discovered that VNS mediated splenic acetylcholine (ACh) release and subsequent immunosuppression in response to LPS associated inflammation is impaired in mice lacking microsomal prostaglandin E synthase-1 (mPGES-1) expression, a key enzyme responsible for prostaglandin E2 synthesis. Dinoprostone 271-287 prostaglandin E synthase Mus musculus 182-219 28991413-6 2018 It inhibited the production of the mPGES-1 product, prostaglandin E2 (PGE2) by 97.8+-1.6 % at 50 muM in HeLa cells and can be a starting point for designing molecules inhibiting all three targets simultaneously. Dinoprostone 52-68 prostaglandin E synthase Mus musculus 35-42 28991413-6 2018 It inhibited the production of the mPGES-1 product, prostaglandin E2 (PGE2) by 97.8+-1.6 % at 50 muM in HeLa cells and can be a starting point for designing molecules inhibiting all three targets simultaneously. Dinoprostone 70-74 prostaglandin E synthase Mus musculus 35-42 29440395-7 2018 Cyclooxygenase 2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1) are enzymes up-regulated at the site of inflammation and account for the bulk of PGE2 biosynthesis. Dinoprostone 158-162 prostaglandin E synthase Mus musculus 29-66 29440395-7 2018 Cyclooxygenase 2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1) are enzymes up-regulated at the site of inflammation and account for the bulk of PGE2 biosynthesis. Dinoprostone 158-162 prostaglandin E synthase Mus musculus 68-75 29456107-1 2018 Human mPGES-1 has emerged as a promising target in exploring a next generation of anti-inflammatory drugs, as selective mPGES-1 inhibitors are expected to discriminatively suppress the production of induced PGE2 without blocking the normal biosynthesis of other prostanoids including homeostatic PGE2. Dinoprostone 207-211 prostaglandin E synthase Mus musculus 6-13 29456107-1 2018 Human mPGES-1 has emerged as a promising target in exploring a next generation of anti-inflammatory drugs, as selective mPGES-1 inhibitors are expected to discriminatively suppress the production of induced PGE2 without blocking the normal biosynthesis of other prostanoids including homeostatic PGE2. Dinoprostone 207-211 prostaglandin E synthase Mus musculus 120-127 29456107-1 2018 Human mPGES-1 has emerged as a promising target in exploring a next generation of anti-inflammatory drugs, as selective mPGES-1 inhibitors are expected to discriminatively suppress the production of induced PGE2 without blocking the normal biosynthesis of other prostanoids including homeostatic PGE2. Dinoprostone 296-300 prostaglandin E synthase Mus musculus 6-13 29456107-1 2018 Human mPGES-1 has emerged as a promising target in exploring a next generation of anti-inflammatory drugs, as selective mPGES-1 inhibitors are expected to discriminatively suppress the production of induced PGE2 without blocking the normal biosynthesis of other prostanoids including homeostatic PGE2. Dinoprostone 296-300 prostaglandin E synthase Mus musculus 120-127 29470537-3 2018 Recently, we discovered that VNS mediated splenic acetylcholine (ACh) release and subsequent immunosuppression in response to LPS associated inflammation is impaired in mice lacking microsomal prostaglandin E synthase-1 (mPGES-1) expression, a key enzyme responsible for prostaglandin E2 synthesis. Dinoprostone 271-287 prostaglandin E synthase Mus musculus 221-228 29511436-5 2018 Interestingly, DHA also inactivated the COX-2/mPGES-1/PGE2 cascade which has been shown to play a critical role in promoting the mesangial cell cycle progression by our previous studies. Dinoprostone 54-58 prostaglandin E synthase Mus musculus 46-53 29133047-1 2018 mPGES-1, a glutathione-dependent membrane protein is involved in the last step of PGE2 production and has been well recognized as a strategic target for the development of anti-inflammatory and anti-cancer agents. Dinoprostone 82-86 prostaglandin E synthase Mus musculus 0-7 29237778-0 2018 mPGES1-Dependent Prostaglandin E2 (PGE2) Controls Antigen-Specific Th17 and Th1 Responses by Regulating T Autocrine and Paracrine PGE2 Production. Dinoprostone 17-33 prostaglandin E synthase Mus musculus 0-6 29237778-0 2018 mPGES1-Dependent Prostaglandin E2 (PGE2) Controls Antigen-Specific Th17 and Th1 Responses by Regulating T Autocrine and Paracrine PGE2 Production. Dinoprostone 35-39 prostaglandin E synthase Mus musculus 0-6 29237778-0 2018 mPGES1-Dependent Prostaglandin E2 (PGE2) Controls Antigen-Specific Th17 and Th1 Responses by Regulating T Autocrine and Paracrine PGE2 Production. Dinoprostone 130-134 prostaglandin E synthase Mus musculus 0-6 29237778-3 2018 Microsomal PGE synthase 1 (mPGES1) is an integral membrane enzyme whose regulated expression controls PGE2 levels and is highly expressed at sites of inflammation. Dinoprostone 102-106 prostaglandin E synthase Mus musculus 27-33 29237778-10 2018 Furthermore, we uncover a coordination of autocrine and paracrine mPGES1-driven PGE2 production that impacts effector T cell IL-17A and IFN-gamma responses. Dinoprostone 80-84 prostaglandin E synthase Mus musculus 66-72 29507686-0 2018 Mitochondrial oxidative stress activates COX-2/mPGES-1/PGE2 cascade induced by albumin in renal proximal tubular cells. Dinoprostone 55-59 prostaglandin E synthase Mus musculus 47-54 29507686-1 2018 COX-2/mPGES-1/PGE2 cascade is of importance in the pathogenesis of kidney injury. Dinoprostone 14-18 prostaglandin E synthase Mus musculus 6-13 29507686-3 2018 The present study was undertaken to investigate the role of mitochondrial oxidative stress in albumin-induced activation of COX-2/mPGES-1/PGE2 cascade in renal proximal tubular cells. Dinoprostone 138-142 prostaglandin E synthase Mus musculus 130-137 29507686-8 2018 Similarly, COX-2/mPGES-1/PGE2 cascade was significantly activated by albumin in dose- and time-dependent manners, which was abolished by MnTBAP treatment in parallel with a blockade of oxidative stress. Dinoprostone 25-29 prostaglandin E synthase Mus musculus 17-24 29507686-9 2018 Collectively, the findings from current study demonstrated that mitochondrial oxidative stress could activate COX-2/mPGES-1/PGE2 cascade in proximal tubular cells under the proteinuria condition. Dinoprostone 124-128 prostaglandin E synthase Mus musculus 116-123 29226622-2 2017 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme synthesizing PGE2 , the most abundant prostanoid related to inflammation and inflammatory pain. Dinoprostone 84-88 prostaglandin E synthase Mus musculus 0-37 29257087-1 2017 Microsomal prostaglandin synthetase-1 (mPGES-1) is an inducible terminal enzyme that produces prostaglandin E2 (PGE2). Dinoprostone 94-110 prostaglandin E synthase Mus musculus 39-46 29257087-1 2017 Microsomal prostaglandin synthetase-1 (mPGES-1) is an inducible terminal enzyme that produces prostaglandin E2 (PGE2). Dinoprostone 112-116 prostaglandin E synthase Mus musculus 39-46 29104159-4 2018 Multiple enzymes are involved in renal PGE2 biosynthesis, including the three main PGE2 terminal synthases, i.e. microsomal PGE2 synthase-1 (mPGES-1), mPGES-2 and cytosolic PGE2 synthase (cPGES). Dinoprostone 39-43 prostaglandin E synthase Mus musculus 141-148 29104159-4 2018 Multiple enzymes are involved in renal PGE2 biosynthesis, including the three main PGE2 terminal synthases, i.e. microsomal PGE2 synthase-1 (mPGES-1), mPGES-2 and cytosolic PGE2 synthase (cPGES). Dinoprostone 83-87 prostaglandin E synthase Mus musculus 141-148 29104159-5 2018 In the kidney, mPGES-1 is highly expressed in the collecting duct where it is the dominant contributor of PGE2 biosynthesis and participates in blood pressure regulation and renal hemodynamic maintenance. Dinoprostone 106-110 prostaglandin E synthase Mus musculus 15-22 29100801-1 2017 This letter describes the synthesis and biological evaluation of furan and dihydrofuran-fused tricyclic benzo[d]imidazole derivatives as novel mPGES-1 inhibitors, capable of inhibiting an increased PGE2 production in the disease state. Dinoprostone 198-202 prostaglandin E synthase Mus musculus 143-150 29226622-2 2017 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme synthesizing PGE2 , the most abundant prostanoid related to inflammation and inflammatory pain. Dinoprostone 84-88 prostaglandin E synthase Mus musculus 39-46 29042013-12 2017 mPGES-1 inhibition also preserved higher basal levels of PGE2 production when compared to either COX inhibitor, which might be beneficial in a clinical setting. Dinoprostone 57-61 prostaglandin E synthase Mus musculus 0-7 28675448-2 2017 Microsomal PGE synthase-1 (mPGES-1) catalyses the formation of PGE2 from COX-derived PGH2 . Dinoprostone 63-67 prostaglandin E synthase Mus musculus 27-34 29042013-13 2017 In conclusion, this work identifies mPGES-1 as a key regulator of PGE2 production and a PGE2-selective target in equine leukocytes. Dinoprostone 66-70 prostaglandin E synthase Mus musculus 36-43 29042013-0 2017 Inhibition of microsomal prostaglandin E-synthase-1 (mPGES-1) selectively suppresses PGE2 in an in vitro equine inflammation model. Dinoprostone 85-89 prostaglandin E synthase Mus musculus 53-60 29042013-3 2017 One potential target is microsomal prostaglandin E-synthase-1 (mPGES-1), which is the terminal enzyme downstream of COX-2 in the inducible PGE2 synthesis cascade. Dinoprostone 139-143 prostaglandin E synthase Mus musculus 63-70 29042013-13 2017 In conclusion, this work identifies mPGES-1 as a key regulator of PGE2 production and a PGE2-selective target in equine leukocytes. Dinoprostone 88-92 prostaglandin E synthase Mus musculus 36-43 29042013-5 2017 The objective of this study was to determine if mPGES-1 is a PGE2-selective anti-inflammatory target in equine leukocytes. Dinoprostone 61-65 prostaglandin E synthase Mus musculus 48-55 28954232-0 2017 Inflammatory Resolution Triggers a Prolonged Phase of Immune Suppression through COX-1/mPGES-1-Derived Prostaglandin E2. Dinoprostone 103-119 prostaglandin E synthase Mus musculus 87-94 28954232-5 2017 IFNgamma upregulated microsomal prostaglandin E synthase-1 (mPGES-1) alongside cyclo-oxygenase (COX-1) within macrophage populations, resulting in sustained prostaglandin (PG)E2 biosynthesis. Dinoprostone 157-177 prostaglandin E synthase Mus musculus 60-67 28983247-1 2017 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme situated downstream of cyclo-oxygenase-2, promoting the excessive PGE2 production in inflammation. Dinoprostone 137-141 prostaglandin E synthase Mus musculus 0-37 28983247-1 2017 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme situated downstream of cyclo-oxygenase-2, promoting the excessive PGE2 production in inflammation. Dinoprostone 137-141 prostaglandin E synthase Mus musculus 39-46 28979673-2 2017 Some studies also reported that COX-2/mPGES-1/PGE2 cascade played a pathogenic role in vascular injury. Dinoprostone 46-50 prostaglandin E synthase Mus musculus 38-45 28979673-8 2017 As expected, mPGES-1 protein was markedly increased by PM2.5 exposure in line with a significant increment of PGE2 release in medium. Dinoprostone 110-114 prostaglandin E synthase Mus musculus 13-20 28979673-11 2017 Taken together, these results suggested that PM2.5 could activate inflammatory axis of COX-2/PGES/PGE2 in vascular endothelial cells to promote cell apoptosis and inflammatory response. Dinoprostone 98-102 prostaglandin E synthase Mus musculus 93-97 28565823-1 2017 The aim of the present study was to investigate the correlation between glucocorticoid activity regulation, prostaglandin E2 (PGE2) synthesis, and synovial inflammation inhibition activity, through microsomal prostaglandin E synthase-1 (mPGES-1) expression regulated by the glucocorticoid pre-receptor regulator, 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD1). Dinoprostone 108-124 prostaglandin E synthase Mus musculus 237-244 28627961-1 2017 INTRODUCTION: Microsomal prostaglandin E2 synthase-1 (mPGES-1) catalyzes the terminal step of prostaglandin E2 (PGE2) generation. Dinoprostone 25-41 prostaglandin E synthase Mus musculus 54-61 28627961-1 2017 INTRODUCTION: Microsomal prostaglandin E2 synthase-1 (mPGES-1) catalyzes the terminal step of prostaglandin E2 (PGE2) generation. Dinoprostone 112-116 prostaglandin E synthase Mus musculus 54-61 28257996-8 2017 Indeed, we show that through its downstream effectors (PGE-2, PKA, PI3K/Akt), mPGES-1 recruits non-canonical transcription factors, thus facilitating iNOS production. Dinoprostone 55-60 prostaglandin E synthase Mus musculus 78-85 28341741-2 2017 LPS, a TLR4 ligand, induces macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and microsomal PGE2 synthase 1 (mPGES-1) (1). Dinoprostone 52-68 prostaglandin E synthase Mus musculus 132-139 28341741-2 2017 LPS, a TLR4 ligand, induces macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and microsomal PGE2 synthase 1 (mPGES-1) (1). Dinoprostone 70-74 prostaglandin E synthase Mus musculus 132-139 28341741-10 2017 The ubiquitous induction of mPGES-1-dependent PGE2 may be crucial for innate immune system activation during various IL-33 driven pathologic disorders. Dinoprostone 46-50 prostaglandin E synthase Mus musculus 28-35 28565823-1 2017 The aim of the present study was to investigate the correlation between glucocorticoid activity regulation, prostaglandin E2 (PGE2) synthesis, and synovial inflammation inhibition activity, through microsomal prostaglandin E synthase-1 (mPGES-1) expression regulated by the glucocorticoid pre-receptor regulator, 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD1). Dinoprostone 126-130 prostaglandin E synthase Mus musculus 237-244 28273917-6 2017 Inhibition of PGE2 was partially dependent on the reduced levels of PGE2 synthesising enzymes, COX-2 and mPGES-1. Dinoprostone 14-18 prostaglandin E synthase Mus musculus 105-112 28487024-2 2017 Placental PGE2 synthesis might be mediated by microsomal PGE synthase-1 (mPGES-1), in addition to cyclooxygenase (COX) isoforms. Dinoprostone 10-14 prostaglandin E synthase Mus musculus 73-80 28052039-8 2017 Furthermore, inhibiting mPGES-1 by a siRNA approach in MCs also ameliorated UA-induced MC proliferation in line with a significant blockade of PGE2 secretion. Dinoprostone 143-147 prostaglandin E synthase Mus musculus 24-31 28052039-0 2017 COX-2/mPGES-1/PGE2 cascade activation mediates uric acid-induced mesangial cell proliferation. Dinoprostone 14-18 prostaglandin E synthase Mus musculus 6-13 28052039-10 2017 In conclusion, our findings indicated that COX-2/mPGES-1/PGE2 cascade activation mediated UA-induced MC proliferation. Dinoprostone 57-61 prostaglandin E synthase Mus musculus 49-56 27375005-1 2017 From experiments in mice in which the prostaglandin E2 (PGE2) synthesizing enzyme mPGES-1 was genetically deleted, as well as from experiments in which PGE2 was injected directly into the brain, PGE2 has been implicated as a mediator of inflammatory induced anorexia. Dinoprostone 38-54 prostaglandin E synthase Mus musculus 82-89 27827823-5 2017 Mobilization efficiency was twice as high in chimeric mice lacking mPGES-1, specifically in hematopoietic cells, suggesting that prostaglandin E2 (PGE2) from hematopoietic cells modulated the bone marrow (BM) microenvironment. Dinoprostone 129-145 prostaglandin E synthase Mus musculus 67-74 27827823-5 2017 Mobilization efficiency was twice as high in chimeric mice lacking mPGES-1, specifically in hematopoietic cells, suggesting that prostaglandin E2 (PGE2) from hematopoietic cells modulated the bone marrow (BM) microenvironment. Dinoprostone 147-151 prostaglandin E synthase Mus musculus 67-74 27375005-1 2017 From experiments in mice in which the prostaglandin E2 (PGE2) synthesizing enzyme mPGES-1 was genetically deleted, as well as from experiments in which PGE2 was injected directly into the brain, PGE2 has been implicated as a mediator of inflammatory induced anorexia. Dinoprostone 56-60 prostaglandin E synthase Mus musculus 82-89 27375005-1 2017 From experiments in mice in which the prostaglandin E2 (PGE2) synthesizing enzyme mPGES-1 was genetically deleted, as well as from experiments in which PGE2 was injected directly into the brain, PGE2 has been implicated as a mediator of inflammatory induced anorexia. Dinoprostone 152-156 prostaglandin E synthase Mus musculus 82-89 27375005-1 2017 From experiments in mice in which the prostaglandin E2 (PGE2) synthesizing enzyme mPGES-1 was genetically deleted, as well as from experiments in which PGE2 was injected directly into the brain, PGE2 has been implicated as a mediator of inflammatory induced anorexia. Dinoprostone 152-156 prostaglandin E synthase Mus musculus 82-89 28096371-0 2017 COX2/mPGES1/PGE2 pathway regulates PD-L1 expression in tumor-associated macrophages and myeloid-derived suppressor cells. Dinoprostone 12-16 prostaglandin E synthase Mus musculus 5-11 28096371-7 2017 Tumor-infiltrating PD-L1+ cells isolated from tumor-bearing mice also exerted morphology of tumor-associated macrophages and expressed high levels of prostaglandin E2 (PGE2)-forming enzymes microsomal PGE2 synthase 1 (mPGES1) and COX2. Dinoprostone 168-172 prostaglandin E synthase Mus musculus 218-224 28096371-9 2017 Together, our study demonstrates that the COX2/mPGES1/PGE2 pathway involved in the regulation of PD-L1 expression in tumor-infiltrating myeloid cells and, therefore, reprogramming of PGE2 metabolism in tumor microenvironment provides an opportunity to reduce immune suppression in tumor host. Dinoprostone 54-58 prostaglandin E synthase Mus musculus 47-53 28096371-9 2017 Together, our study demonstrates that the COX2/mPGES1/PGE2 pathway involved in the regulation of PD-L1 expression in tumor-infiltrating myeloid cells and, therefore, reprogramming of PGE2 metabolism in tumor microenvironment provides an opportunity to reduce immune suppression in tumor host. Dinoprostone 183-187 prostaglandin E synthase Mus musculus 47-53 28086912-11 2017 WWL70 attenuated the expression of COX-2 and PGES-1/2 leading to the downregulation of the biosynthetic pathways of PGE2 and PGE2-G. Dinoprostone 116-120 prostaglandin E synthase Mus musculus 45-51 28086912-11 2017 WWL70 attenuated the expression of COX-2 and PGES-1/2 leading to the downregulation of the biosynthetic pathways of PGE2 and PGE2-G. Dinoprostone 125-129 prostaglandin E synthase Mus musculus 45-51 27784694-1 2017 Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 to prostaglandin E2 (PGE2), plays an important role in a variety of inflammatory diseases. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 27784694-1 2017 Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 to prostaglandin E2 (PGE2), plays an important role in a variety of inflammatory diseases. Dinoprostone 104-120 prostaglandin E synthase Mus musculus 40-47 27784694-1 2017 Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 to prostaglandin E2 (PGE2), plays an important role in a variety of inflammatory diseases. Dinoprostone 122-126 prostaglandin E synthase Mus musculus 40-47 28628921-7 2017 Albumin markedly activated cyclooxygenase-2 (COX-2)/ microsomal prostaglandin E synthase-1 (mPGES-1)/PGE2 pathway in this cell line, an effect largely abolished by NLRP3 silencing at both mRNA and protein levels. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 92-99 28458341-4 2017 Therefore, to elucidate the role of PGE2, studies of microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal enzyme for PGE2 synthesis, have recently been an active area of research. Dinoprostone 135-139 prostaglandin E synthase Mus musculus 92-99 28628921-9 2017 CONCLUSIONS: The findings suggest that COX-2/mPGES-1/PGE2 axis could be activated by albumin in the proximal tubular cells via a NLRP3 inflammasome-mediated mechanism and could thus contribute to proteinuria-related renal tubular cell injury. Dinoprostone 53-57 prostaglandin E synthase Mus musculus 45-52 27453433-0 2016 Inhibition of GSK-3 reduces prostaglandin E2 production by decreasing the expression levels of COX-2 and mPGES-1 in monocyte/macrophage lineage cells. Dinoprostone 28-44 prostaglandin E synthase Mus musculus 105-112 28854439-0 2017 mPGES-1-Derived PGE2 Contributes to Indoxyl Sulfate-Induced Mesangial Cell Proliferation. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 0-7 28854439-3 2017 Thus, the present study was undertaken to examine the role of microsomal prostaglandin E synthase-1 (mPGES-1)-derived Prostaglandin E2 (PGE2) in IS-induced MC proliferation. Dinoprostone 118-134 prostaglandin E synthase Mus musculus 101-108 28854439-3 2017 Thus, the present study was undertaken to examine the role of microsomal prostaglandin E synthase-1 (mPGES-1)-derived Prostaglandin E2 (PGE2) in IS-induced MC proliferation. Dinoprostone 136-140 prostaglandin E synthase Mus musculus 101-108 28854439-7 2017 Interestingly, silencing mPGES-1 reduced cell number in S and G2 phases and blocked the upregulation of cyclin A2 and cyclin D1 in parallel with blunted PGE2 release after IS treatment, indicating that mPGES-1-derived PGE2 could contribute to MC proliferation. Dinoprostone 153-157 prostaglandin E synthase Mus musculus 25-32 28854439-7 2017 Interestingly, silencing mPGES-1 reduced cell number in S and G2 phases and blocked the upregulation of cyclin A2 and cyclin D1 in parallel with blunted PGE2 release after IS treatment, indicating that mPGES-1-derived PGE2 could contribute to MC proliferation. Dinoprostone 218-222 prostaglandin E synthase Mus musculus 25-32 28854439-7 2017 Interestingly, silencing mPGES-1 reduced cell number in S and G2 phases and blocked the upregulation of cyclin A2 and cyclin D1 in parallel with blunted PGE2 release after IS treatment, indicating that mPGES-1-derived PGE2 could contribute to MC proliferation. Dinoprostone 218-222 prostaglandin E synthase Mus musculus 202-209 28854439-10 2017 CONCLUSION: mPGES-1-derived PGE2 contributed to IS-induced mesangial cell proliferation. Dinoprostone 28-32 prostaglandin E synthase Mus musculus 12-19 27720548-1 2016 In our previous research, a novel series of phenylsulfonyl hydrazide derivatives were found to reduce LPS-induced PGE2 levels in RAW 264.7 macrophage cells via an inhibition of mPGES-1 enzyme. Dinoprostone 114-118 prostaglandin E synthase Mus musculus 177-184 27645308-14 2016 PGE2 which is the end product of mPGES-1 was measured by using ELISA kit. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 33-40 28239316-10 2017 CONCLUSIONS: Early inactivation of 15-PGDH, followed by activation of COX-2 and mPGEs-1, contributes to PGE2 production, leading to colon carcinogenesis. Dinoprostone 104-108 prostaglandin E synthase Mus musculus 80-87 27597418-1 2016 The biosynthesis of leukotrienes in one of the arachidonic acid pathways and PGE2 in the other by 5-LOX and mPGES1 respectively, play pivotal roles in augmenting inflammatory responses. Dinoprostone 77-81 prostaglandin E synthase Mus musculus 108-114 27554445-4 2016 These data are consistent with selective mPGES-1-mediated reduction of PGE2. Dinoprostone 71-75 prostaglandin E synthase Mus musculus 41-48 27453433-1 2016 Inflammatory stimuli induce prostaglandin E2 (PGE2) synthesis by upregulating cycloxgenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1). Dinoprostone 28-44 prostaglandin E synthase Mus musculus 132-139 27453433-1 2016 Inflammatory stimuli induce prostaglandin E2 (PGE2) synthesis by upregulating cycloxgenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1). Dinoprostone 46-50 prostaglandin E synthase Mus musculus 132-139 27453433-9 2016 These results suggested that GSK-3 plays a key role in PGE2 production by increasing COX-2 and mPGES-1 probably through Egr-1-mediated transcription and GSK-3 inhibitors may be potential as novel anti-inflammatory drugs. Dinoprostone 55-59 prostaglandin E synthase Mus musculus 95-102 27482714-4 2016 Mechanistically, we discovered that upon A. phagocytophilum infection, cytosolic phospholipase A2 cleaves arachidonic acid from phospholipids, which is converted to the eicosanoid prostaglandin E2 (PGE2) via cyclooxygenase 2 (COX2) and the membrane associated prostaglandin E synthase-1 (mPGES-1). Dinoprostone 180-196 prostaglandin E synthase Mus musculus 288-295 24824420-2 2016 PG E2 (PGE2 ) tumour-promoting activity has been confirmed and its production is controlled by Cyclooxygenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1). Dinoprostone 0-5 prostaglandin E synthase Mus musculus 151-158 27177970-0 2016 Identification of the two-phase mechanism of arachidonic acid regulating inflammatory prostaglandin E2 biosynthesis by targeting COX-2 and mPGES-1. Dinoprostone 86-102 prostaglandin E synthase Mus musculus 139-146 27177970-1 2016 Through linking inducible cyclooxygenase (COX)-2 with microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), a Single-Chain Enzyme Complex (SCEC, COX-2-10aa-mPGES-1) was engineered to mimic a specific inflammatory PGE2 biosynthesis from omega-6 fatty acid, arachidonic acid (AA), by eliminating involvements of non-inducible COX-1 and other PGE2 synthases. Dinoprostone 65-81 prostaglandin E synthase Mus musculus 101-108 27177970-1 2016 Through linking inducible cyclooxygenase (COX)-2 with microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), a Single-Chain Enzyme Complex (SCEC, COX-2-10aa-mPGES-1) was engineered to mimic a specific inflammatory PGE2 biosynthesis from omega-6 fatty acid, arachidonic acid (AA), by eliminating involvements of non-inducible COX-1 and other PGE2 synthases. Dinoprostone 83-87 prostaglandin E synthase Mus musculus 101-108 27177970-1 2016 Through linking inducible cyclooxygenase (COX)-2 with microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), a Single-Chain Enzyme Complex (SCEC, COX-2-10aa-mPGES-1) was engineered to mimic a specific inflammatory PGE2 biosynthesis from omega-6 fatty acid, arachidonic acid (AA), by eliminating involvements of non-inducible COX-1 and other PGE2 synthases. Dinoprostone 83-87 prostaglandin E synthase Mus musculus 159-166 27177970-1 2016 Through linking inducible cyclooxygenase (COX)-2 with microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), a Single-Chain Enzyme Complex (SCEC, COX-2-10aa-mPGES-1) was engineered to mimic a specific inflammatory PGE2 biosynthesis from omega-6 fatty acid, arachidonic acid (AA), by eliminating involvements of non-inducible COX-1 and other PGE2 synthases. Dinoprostone 216-220 prostaglandin E synthase Mus musculus 101-108 27177970-1 2016 Through linking inducible cyclooxygenase (COX)-2 with microsomal prostaglandin E2 (PGE2) synthase-1 (mPGES-1), a Single-Chain Enzyme Complex (SCEC, COX-2-10aa-mPGES-1) was engineered to mimic a specific inflammatory PGE2 biosynthesis from omega-6 fatty acid, arachidonic acid (AA), by eliminating involvements of non-inducible COX-1 and other PGE2 synthases. Dinoprostone 216-220 prostaglandin E synthase Mus musculus 101-108 27177970-2 2016 Using the SCEC, we characterized coupling reactions between COX-2 and mPGES-1 at 1:1 ratio of inflammatory PGE2 production. Dinoprostone 107-111 prostaglandin E synthase Mus musculus 70-77 27159620-6 2016 Furthermore, pharmacological inhibition or siRNA-mediated knockdown of microsomal prostaglandin E synthase-1 (mPGES-1), the enzyme that functions downstream of COX-2 during the synthesis of PGE2, significantly increased expression of characteristics of the differentiated SMC phenotype. Dinoprostone 190-194 prostaglandin E synthase Mus musculus 110-117 27159620-7 2016 Therefore, our findings suggest that COX-2 and mPGES-1-dependent synthesis of PGE2 contributes to a dedifferentiated hASMC phenotype and that mPGES-1 may provide a novel pharmacological target for treatment of cardiovascular diseases where altered SMC differentiation has a causative role. Dinoprostone 78-82 prostaglandin E synthase Mus musculus 47-54 27440004-3 2016 By contrast, deletion of microsomal prostaglandin E synthase 1 (mPGES-1) confers analgesia, attenuates atherogenesis, and fails to accelerate thrombogenesis, while suppressing prostaglandin E2, but increasing biosynthesis of PGI2. Dinoprostone 176-192 prostaglandin E synthase Mus musculus 25-62 27440004-3 2016 By contrast, deletion of microsomal prostaglandin E synthase 1 (mPGES-1) confers analgesia, attenuates atherogenesis, and fails to accelerate thrombogenesis, while suppressing prostaglandin E2, but increasing biosynthesis of PGI2. Dinoprostone 176-192 prostaglandin E synthase Mus musculus 64-71 27440004-7 2016 CONCLUSIONS: Although suppression of prostaglandin E2 accounts for the protective effect of mPGES-1 deletion in atherosclerosis, augmentation of PGI2 is the dominant contributor to its favorable thrombogenic profile. Dinoprostone 37-53 prostaglandin E synthase Mus musculus 92-99 29100270-4 2017 Meanwhile, NLRP3 and mPGES-1 were stimulated in NKCC2 positive tubules (thick ascending limb, TAL) paralleled with increased urinary PGE2 excretion. Dinoprostone 133-137 prostaglandin E synthase Mus musculus 21-28 27012893-1 2016 Microsomal prostaglandin E synthase-1 (mPGES-1) is a membrane protein which plays crucial role in arachidonic acid metabolism, in the catalysis of PGH2 to PGE2. Dinoprostone 155-159 prostaglandin E synthase Mus musculus 39-46 27301644-11 2016 Inhibition of PGE2 by RBE was dependent on reduced COX-2 and mPGES-1 immunoreactivity in microglia. Dinoprostone 14-18 prostaglandin E synthase Mus musculus 61-68 27059285-2 2016 Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme involved in the synthesis of PGE2, and its expression is enhanced during bacterial infections. Dinoprostone 93-97 prostaglandin E synthase Mus musculus 0-37 27059285-2 2016 Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme involved in the synthesis of PGE2, and its expression is enhanced during bacterial infections. Dinoprostone 93-97 prostaglandin E synthase Mus musculus 39-46 27059285-3 2016 Genetic deletion of mPGES-1 in mice results in diminished PGE2 production and elevated levels of other prostaglandins after infection. Dinoprostone 58-62 prostaglandin E synthase Mus musculus 20-27 27059285-10 2016 These results suggest that specific inhibition of PGE2 synthesis by targeting mPGES-1 may weaken host defense against bacterial infections. Dinoprostone 50-54 prostaglandin E synthase Mus musculus 78-85 27102561-1 2016 Microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme for the synthesis of prostaglandin E2 (PGE2), a proproliferative and antiapoptotic lipid molecule important for tissue regeneration and injury repair. Dinoprostone 92-108 prostaglandin E synthase Mus musculus 0-37 26915684-1 2016 A small library of 2,3-dihydroxybenzamide- and N-(2,3-dihydroxyphenyl)-4-sulfonamide-based microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitors was identified following a step-by-step optimization of small aromatic fragments selected to interact in focused regions in the active site of mPGES-1. Dinoprostone 102-118 prostaglandin E synthase Mus musculus 131-138 27102561-1 2016 Microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme for the synthesis of prostaglandin E2 (PGE2), a proproliferative and antiapoptotic lipid molecule important for tissue regeneration and injury repair. Dinoprostone 92-108 prostaglandin E synthase Mus musculus 39-46 27102561-1 2016 Microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme for the synthesis of prostaglandin E2 (PGE2), a proproliferative and antiapoptotic lipid molecule important for tissue regeneration and injury repair. Dinoprostone 110-114 prostaglandin E synthase Mus musculus 0-37 27102561-1 2016 Microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme for the synthesis of prostaglandin E2 (PGE2), a proproliferative and antiapoptotic lipid molecule important for tissue regeneration and injury repair. Dinoprostone 110-114 prostaglandin E synthase Mus musculus 39-46 27102561-6 2016 Our findings provide novel evidence that mPGES-1 prevents Fas-induced liver injury through activation of Akt and related signaling and suggest that induction of mPGES-1 or treatment with PGE2 may represent important therapeutic strategy for the prevention and treatment of Fas-associated liver injuries. Dinoprostone 187-191 prostaglandin E synthase Mus musculus 41-48 26987561-2 2016 The aim of this study was to investigate the effect of aminothiazoles targeting prostaglandin E synthase-1 (mPGES-1) on RANKL- and lipopolysaccharide (LPS)-mediated osteoclastogenesis and prostaglandin E2 (PGE2 ) production in vitro using the osteoclast precursor RAW 264.7 cells. Dinoprostone 188-204 prostaglandin E synthase Mus musculus 108-115 26987561-2 2016 The aim of this study was to investigate the effect of aminothiazoles targeting prostaglandin E synthase-1 (mPGES-1) on RANKL- and lipopolysaccharide (LPS)-mediated osteoclastogenesis and prostaglandin E2 (PGE2 ) production in vitro using the osteoclast precursor RAW 264.7 cells. Dinoprostone 206-210 prostaglandin E synthase Mus musculus 108-115 27064015-13 2016 The IMP extract increased PGE2 and PGF2alpha levels qRT-PCR revealed that transcripts of rate-limiting PGE2- and PGF2alpha-biosynthetic enzymes - COX-1, mPGES1 and AKR1C3 were notably up-regulated. Dinoprostone 103-107 prostaglandin E synthase Mus musculus 153-159 27015117-10 2016 Moreover, the expressions of microsomal PGE2 synthase (mPGES-1), PGE2, PGE2 receptor (EP) 2 and EP4 were increased and EP3 expression was decreased in APP/PS1 mice, while misoprostol reversed these changes. Dinoprostone 40-44 prostaglandin E synthase Mus musculus 55-62 26915684-1 2016 A small library of 2,3-dihydroxybenzamide- and N-(2,3-dihydroxyphenyl)-4-sulfonamide-based microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitors was identified following a step-by-step optimization of small aromatic fragments selected to interact in focused regions in the active site of mPGES-1. Dinoprostone 102-118 prostaglandin E synthase Mus musculus 294-301 26585956-7 2016 Culture of WT endothelial cells with M27 increases the secretion of prostaglandin E2 (PGE2), the enzymatic product of Ptges, in WT but not in Gas6(-/-) endothelial cells. Dinoprostone 68-84 prostaglandin E synthase Mus musculus 118-123 26739892-0 2016 mPGES-1-derived PGE2 contributes to adriamycin-induced podocyte injury. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 0-7 26739892-8 2016 More importantly, in mPGES-1-deficient mice, albuminuria induced by ADR showed a remarkable attenuation in line with decreased urinary output of PGE2 and TNF-alpha, highly suggesting an in vivo role of mPGES-1 in mediating podocyte injury. Dinoprostone 145-149 prostaglandin E synthase Mus musculus 21-28 27174800-0 2016 A positive feedback loop between progesterone and microsomal prostaglandin E synthase-1-mediated PGE2 promotes production of both in mouse granulosa cells. Dinoprostone 97-101 prostaglandin E synthase Mus musculus 50-87 27174800-8 2016 Taken together, P4 may regulate mPGES-1 expression to increase PGE2 secretion and in turn P4 production. Dinoprostone 63-67 prostaglandin E synthase Mus musculus 32-39 26585956-7 2016 Culture of WT endothelial cells with M27 increases the secretion of prostaglandin E2 (PGE2), the enzymatic product of Ptges, in WT but not in Gas6(-/-) endothelial cells. Dinoprostone 86-90 prostaglandin E synthase Mus musculus 118-123 26611322-1 2015 Prostacyclin synthase (PGIS) and microsomal prostaglandin E synthase-1 (mPGES-1) are prostaglandin (PG) terminal synthases that function downstream of inducible cyclooxygenase (COX)-2 in the PGI2 and PGE2 biosynthetic pathways, respectively. Dinoprostone 200-204 prostaglandin E synthase Mus musculus 33-70 26755582-1 2016 Microsomal prostaglandin E2 synthase type 1 (mPGES-1) is responsible for the formation of the potent lipid mediator prostaglandin E2 under proinflammatory conditions, and this enzyme has received considerable attention as a drug target. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 45-52 26602278-4 2016 Molecular docking suggests that compound 8n could inhibit PGE2 production by blocking the PGH2 binding site of human mPGES-1 enzyme. Dinoprostone 58-62 prostaglandin E synthase Mus musculus 117-124 27594972-7 2016 In this review, we highlight the most recent advances from our and other studies on the regulation of PGE2, particularly mPGES-1 and the four PGE2 receptors, in cardiovascular function, with a particular emphasis on blood pressure regulation, atherosclerosis, thrombosis, and myocardial infarction. Dinoprostone 102-106 prostaglandin E synthase Mus musculus 121-128 26673392-4 2016 Membrane-associated prostaglandin E synthase-1 (mPGES-1) is an enzyme responsible for the production of prostaglandin E2 (PGE2) that is the best-characterized immune modulatory lipid in vitro and in vivo models of inflammation. Dinoprostone 104-120 prostaglandin E synthase Mus musculus 48-55 26673392-4 2016 Membrane-associated prostaglandin E synthase-1 (mPGES-1) is an enzyme responsible for the production of prostaglandin E2 (PGE2) that is the best-characterized immune modulatory lipid in vitro and in vivo models of inflammation. Dinoprostone 122-126 prostaglandin E synthase Mus musculus 48-55 26673392-10 2016 Our results showed that this selective mPGES-1 inhibitor has anti-influenza effects by inhibiting PGE2 production, which suppresses the induction of pro-inflammatory genes. Dinoprostone 98-102 prostaglandin E synthase Mus musculus 39-46 26543101-10 2016 CONCLUSIONS: Our data revealed the pivotal role of COX-2-mPGES-1-PGE2 axis in vascular calcification. Dinoprostone 65-69 prostaglandin E synthase Mus musculus 57-64 26611322-1 2015 Prostacyclin synthase (PGIS) and microsomal prostaglandin E synthase-1 (mPGES-1) are prostaglandin (PG) terminal synthases that function downstream of inducible cyclooxygenase (COX)-2 in the PGI2 and PGE2 biosynthetic pathways, respectively. Dinoprostone 200-204 prostaglandin E synthase Mus musculus 72-79 26352871-5 2015 The results showed that mPGES-1-dependent release of PGE2 was markedly induced in colon cancer cells after transient transfection with mPGES-1 overexpression vector, accompanied by elevated CCR7 expression. Dinoprostone 53-57 prostaglandin E synthase Mus musculus 135-142 26123522-8 2015 Moreover, we (i) present current strategies for interfering with mPGES-1-mediated PGE2 synthesis, (ii) summarize bioanalytical approaches for mPGES-1 drug discovery and (iii) describe preclinical test systems for the characterization of mPGES-1 inhibitors. Dinoprostone 82-86 prostaglandin E synthase Mus musculus 65-72 26352871-3 2015 Induction of COX-2 and membrane-associated PGE synthase 1 (mPGES-1), which are overexpressed in numerous cancer types, cooperatively enhance PGE2 expression, which contributes to carcinogenesis and cancer progression. Dinoprostone 141-145 prostaglandin E synthase Mus musculus 59-66 26352871-6 2015 PGE2 levels and CCR7 expression were markedly attenuated in colon cancer cells in which mPGES-1 was blocked, which identified mPGES-1 as a potential therapeutic target for the regulation of CCR7 expression. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 88-95 26352871-4 2015 The present study investigated whether CCR7 expression is associated with the levels of mPGES-1-derived PGE2. Dinoprostone 104-108 prostaglandin E synthase Mus musculus 88-95 26352871-5 2015 The results showed that mPGES-1-dependent release of PGE2 was markedly induced in colon cancer cells after transient transfection with mPGES-1 overexpression vector, accompanied by elevated CCR7 expression. Dinoprostone 53-57 prostaglandin E synthase Mus musculus 24-31 26352871-6 2015 PGE2 levels and CCR7 expression were markedly attenuated in colon cancer cells in which mPGES-1 was blocked, which identified mPGES-1 as a potential therapeutic target for the regulation of CCR7 expression. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 126-133 26352871-7 2015 Finally, overexpression of CCR7 was partly mediated through the AKT/glycogen synthase kinase 3beta signaling pathway dependent on the binding of mPGES-1-derived PGE2 to the prostaglandin EP4 receptor. Dinoprostone 161-165 prostaglandin E synthase Mus musculus 145-152 26276006-9 2015 The downregulation of mPGES-1 was associated with inhibition of prostaglandin E2 production. Dinoprostone 64-80 prostaglandin E synthase Mus musculus 22-29 26134597-2 2015 Expression of microsomal prostaglandin E2 (PGE2) synthase type 1 (mPGES-1) is increased in the wall of intracranial aneurysms in humans. Dinoprostone 25-41 prostaglandin E synthase Mus musculus 66-73 26134597-2 2015 Expression of microsomal prostaglandin E2 (PGE2) synthase type 1 (mPGES-1) is increased in the wall of intracranial aneurysms in humans. Dinoprostone 43-47 prostaglandin E synthase Mus musculus 66-73 26134597-3 2015 PGE2, a by-product of mPGES-1, is associated with inflammation and cerebrovascular dysfunction. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 22-29 25817443-4 2015 The microsomal prostaglandin E synthase-1 (mPGES-1) gene product, mPGES-1, participates in prostaglandin E2 (PGE2) production. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 66-73 26150361-0 2015 Role of microsomal prostaglandin E synthase-1 (mPGES-1)-derived prostaglandin E2 in colon carcinogenesis. Dinoprostone 64-80 prostaglandin E synthase Mus musculus 47-54 26150361-3 2015 Microsomal prostaglandin E (PGE) synthase-1 (mPGES-1) and mPGES-1-derived PGE2 have gained attention recently as alternative targets to COX-2 for colorectal cancer chemoprevention and chemotherapy. Dinoprostone 74-78 prostaglandin E synthase Mus musculus 58-65 26088337-1 2015 Microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitors are considered as potential therapeutic agents for the treatment of inflammatory pain and certain types of cancer. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 25817443-4 2015 The microsomal prostaglandin E synthase-1 (mPGES-1) gene product, mPGES-1, participates in prostaglandin E2 (PGE2) production. Dinoprostone 91-107 prostaglandin E synthase Mus musculus 43-50 26100239-4 2015 Genetic deletion of microsomal prostaglandin E synthase-1 (mPGES-1), the enzyme responsible for the second step of the PGE2 biosynthesis, has resulted in reduced tumor progression in mouse models of colon cancer. Dinoprostone 119-123 prostaglandin E synthase Mus musculus 20-57 25817443-4 2015 The microsomal prostaglandin E synthase-1 (mPGES-1) gene product, mPGES-1, participates in prostaglandin E2 (PGE2) production. Dinoprostone 91-107 prostaglandin E synthase Mus musculus 66-73 25817443-4 2015 The microsomal prostaglandin E synthase-1 (mPGES-1) gene product, mPGES-1, participates in prostaglandin E2 (PGE2) production. Dinoprostone 109-113 prostaglandin E synthase Mus musculus 43-50 26379884-12 2015 The findings indicate that the therapy with prostaglandin E2 (PGE2)-blocking agents may decrease the PGE2 production not only by direct inhibition of COX-2 activity, but also by down-regulating the expression of genes encoding for COX-2, microsomal prostaglandin-endoperoxide synthase 1 (mPGES-1) and prostaglandin E receptors 4 (EP4) in the articular chondrocytes. Dinoprostone 44-60 prostaglandin E synthase Mus musculus 288-295 26379884-12 2015 The findings indicate that the therapy with prostaglandin E2 (PGE2)-blocking agents may decrease the PGE2 production not only by direct inhibition of COX-2 activity, but also by down-regulating the expression of genes encoding for COX-2, microsomal prostaglandin-endoperoxide synthase 1 (mPGES-1) and prostaglandin E receptors 4 (EP4) in the articular chondrocytes. Dinoprostone 62-66 prostaglandin E synthase Mus musculus 288-295 26379884-12 2015 The findings indicate that the therapy with prostaglandin E2 (PGE2)-blocking agents may decrease the PGE2 production not only by direct inhibition of COX-2 activity, but also by down-regulating the expression of genes encoding for COX-2, microsomal prostaglandin-endoperoxide synthase 1 (mPGES-1) and prostaglandin E receptors 4 (EP4) in the articular chondrocytes. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 288-295 26100239-4 2015 Genetic deletion of microsomal prostaglandin E synthase-1 (mPGES-1), the enzyme responsible for the second step of the PGE2 biosynthesis, has resulted in reduced tumor progression in mouse models of colon cancer. Dinoprostone 119-123 prostaglandin E synthase Mus musculus 59-66 25961169-1 2015 Microsomal prostaglandin E synthase 1 (mPGES-1) is an alpha-helical homotrimeric integral membrane inducible enzyme that catalyzes the formation of prostaglandin E2 (PGE2) from prostaglandin H2 (PGH2). Dinoprostone 148-164 prostaglandin E synthase Mus musculus 39-46 25988363-1 2015 In vascular inflammation, prostaglandin E2 (PGE2) is largely biosynthesized by microsomal PGE2 synthase-1 (mPGES-1), competing with other downstream eicosanoid-synthesizing enzymes, such as PGIS, a synthase of a vascular protector prostacyclin (PGI2), to isomerize the cyclooxygenase (COX)-2-derived prostaglandin H2 (PGH2). Dinoprostone 26-42 prostaglandin E synthase Mus musculus 107-114 25988363-1 2015 In vascular inflammation, prostaglandin E2 (PGE2) is largely biosynthesized by microsomal PGE2 synthase-1 (mPGES-1), competing with other downstream eicosanoid-synthesizing enzymes, such as PGIS, a synthase of a vascular protector prostacyclin (PGI2), to isomerize the cyclooxygenase (COX)-2-derived prostaglandin H2 (PGH2). Dinoprostone 44-48 prostaglandin E synthase Mus musculus 107-114 25988363-2 2015 In this study, we found that a majority of the product from the cells co-expressing human COX-2, mPGES-1, and PGIS was PGE2. Dinoprostone 119-123 prostaglandin E synthase Mus musculus 97-104 25988363-6 2015 When COX-2-10aa-PGIS (with a 14.4 A separation) was co-expressed with mPGES-1 on the ER membrane, a major product was PGE2, but not PGI2. Dinoprostone 118-122 prostaglandin E synthase Mus musculus 70-77 25988363-7 2015 However, expression of COX-2-10aa-PGIS and mPGES-1 on a separated ER with a distance of >>30.8 A reduced the level of PGE2 production. Dinoprostone 124-128 prostaglandin E synthase Mus musculus 43-50 25961169-1 2015 Microsomal prostaglandin E synthase 1 (mPGES-1) is an alpha-helical homotrimeric integral membrane inducible enzyme that catalyzes the formation of prostaglandin E2 (PGE2) from prostaglandin H2 (PGH2). Dinoprostone 166-170 prostaglandin E synthase Mus musculus 39-46 26226733-13 2015 Moreover, the expression of IL-1beta and mPGES-1 was decreased after Guizhi Fuling capsule and active complex treatment, which might contribute to the inhibitory effect of Guizhi Fuling capsule in the releasing of IL-1beta, TNF-alpha and PGE2. Dinoprostone 238-242 prostaglandin E synthase Mus musculus 41-48 25871398-0 2015 MPGES-1-derived PGE2 suppresses CD80 expression on tumor-associated phagocytes to inhibit anti-tumor immune responses in breast cancer. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 0-7 25634334-1 2015 Microsomal PGE2 synthase-1 (mPGES-1), the terminal enzyme in the formation of inducible PGE2, represents a potential target for cancer chemoprevention. Dinoprostone 11-15 prostaglandin E synthase Mus musculus 28-35 25634334-1 2015 Microsomal PGE2 synthase-1 (mPGES-1), the terminal enzyme in the formation of inducible PGE2, represents a potential target for cancer chemoprevention. Dinoprostone 88-92 prostaglandin E synthase Mus musculus 28-35 25634334-8 2015 Given that mPGES-1 is highly expressed within the intestinal stroma under the inflammatory conditions of DSS-induced ulceration, we propose a complex and dual role for inducible PGE2 synthesis within the colonic mucosa. Dinoprostone 178-182 prostaglandin E synthase Mus musculus 11-18 25634334-12 2015 Inducible PGE2 production by mPGES-1 is critical for the colonic mucosal homeostasis. Dinoprostone 10-14 prostaglandin E synthase Mus musculus 29-36 25729216-1 2015 COX-2/mPGES-1/PGE2 cascade plays critical roles in modulating many physiological and pathological actions in different organs. Dinoprostone 14-18 prostaglandin E synthase Mus musculus 6-13 25548276-14 2015 We propose that cytosolic phospholipase A2alpha, COX-2, and mPGES-1 in the Golgi comprise a dedicated system for COX-2-dependent PGE2 biosynthesis. Dinoprostone 129-133 prostaglandin E synthase Mus musculus 60-67 24974175-1 2015 The increase in PGE2 production by microsomal PGE synthase-1 (mPGES-1) in CNS contributes to the severity of the inflammatory and pain responses in the model of edema formation and hyperalgesia induced by carrageenan. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 62-69 25967073-8 2015 Walls of ruptured human intracranial aneurysms have higher levels of COX-2 and microsomal prostaglandin E2 synthase 1 (mPGES-1), both of which are known to be inhibited by aspirin. Dinoprostone 90-106 prostaglandin E synthase Mus musculus 119-126 25729216-5 2015 The new insights from this review not only increase the understanding of the pathological role of the COX-2/mPGES-1/PGE2 pathway in kidney injuries, but also shed new light on the innovation of the strategies for the treatment of kidney diseases. Dinoprostone 116-120 prostaglandin E synthase Mus musculus 108-115 25314295-1 2015 OBJECTIVES: Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal enzyme in the production of prostaglandin E2 (PGE2) and its expression is upregulated during inflammation. Dinoprostone 102-118 prostaglandin E synthase Mus musculus 51-58 26538827-0 2015 Downregulation of mPGES-1 Expression via EGR1 Plays an Important Role in Inhibition of Caffeine on PGE2 Synthesis of HBx(+) Hepatocytes. Dinoprostone 99-103 prostaglandin E synthase Mus musculus 18-25 25460828-6 2015 We further assessed the precise role of PGE2 synthesis on mucosal injury and repair by utilizing mice with a genetic deletion of microsomal PGE synthase-1 (mPGES-1), the terminal synthase in the formation of inducible PGE2. Dinoprostone 218-222 prostaglandin E synthase Mus musculus 156-163 25314295-1 2015 OBJECTIVES: Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal enzyme in the production of prostaglandin E2 (PGE2) and its expression is upregulated during inflammation. Dinoprostone 120-124 prostaglandin E synthase Mus musculus 51-58 25139833-0 2014 Prostaglandin E2 produced by inducible COX-2 and mPGES-1 promoting cancer cell proliferation in vitro and in vivo. Dinoprostone 0-16 prostaglandin E synthase Mus musculus 49-56 25453800-6 2014 Molecular docking study provides the possibility that compound 7i could inhibit PGE2 production by blocking the PGH2 binding site of mPGES-1 instead of COX-2 enzyme. Dinoprostone 80-84 prostaglandin E synthase Mus musculus 133-140 25139833-3 2014 MAIN METHODS: In this study, a chronic inflammation pathway was mimicked with a stable cell line that over-expressed a novel human enzyme consisting of cyclooxygenase isoform-2 (COX-2) linked to microsomal (PGE2 synthase-1 (mPGES-1)) for the overproduction of pathogenic PGE2. Dinoprostone 207-211 prostaglandin E synthase Mus musculus 224-231 25108236-1 2014 Microsomal prostaglandin E synthase 1 (mPGES-1) is the terminal regulator of PGE2 synthesis. Dinoprostone 77-81 prostaglandin E synthase Mus musculus 39-46 25260492-1 2014 mPGES-1 is inducible terminal synthase acting downstream of COX enzymes in arachidonic acid pathway, regulates the biosynthesis of pro-inflammatory prostaglandin PGE2. Dinoprostone 162-166 prostaglandin E synthase Mus musculus 0-7 25108236-8 2014 In the presence of 15d-PGJ2, the expression of COX-2 was unaffected, but that of the EGR1-mPGES-1-PGE2 axis was inhibited. Dinoprostone 98-102 prostaglandin E synthase Mus musculus 90-97 24668417-1 2014 Previous studies in rats have demonstrated that microsomal prostaglandin E synthase-1 (mPGES-1) is induced in brain vascular cells that also express inducible cyclooxygenase-2, suggesting that such cells are the source of the increased PGE2 levels that are seen in the brain following peripheral immune stimulation, and that are associated with sickness responses such as fever, anorexia, and stress hormone release. Dinoprostone 236-240 prostaglandin E synthase Mus musculus 48-85 24909729-9 2014 Furthermore, COX-2 upregulation resulted in an increase in mPGES-1, an enzyme responsible for PGE2 production. Dinoprostone 94-98 prostaglandin E synthase Mus musculus 59-66 24668417-1 2014 Previous studies in rats have demonstrated that microsomal prostaglandin E synthase-1 (mPGES-1) is induced in brain vascular cells that also express inducible cyclooxygenase-2, suggesting that such cells are the source of the increased PGE2 levels that are seen in the brain following peripheral immune stimulation, and that are associated with sickness responses such as fever, anorexia, and stress hormone release. Dinoprostone 236-240 prostaglandin E synthase Mus musculus 87-94 24668417-6 2014 These data imply a widespread synthesis of PGE2 or other mPGES-1-dependent products in the mouse brain that may be related to inflammation-induced sickness symptom as well as other functions, such as blood flow regulation. Dinoprostone 43-47 prostaglandin E synthase Mus musculus 57-64 24794772-1 2014 Agents targeting microsomal prostaglandin E2 synthase-1 (mPGES-1) would inhibit only PGE2 production induced by inflammatory stimuli and thus could represent a valuable alternative to non-steroidal anti-inflammatory drugs (NSAIDs) as they should be free from the severe side effects of the classic anti-inflammatory drugs. Dinoprostone 85-89 prostaglandin E synthase Mus musculus 57-64 25069917-8 2014 CONCLUSION: Pgt, Mrp4, and mPGES expression was detected in the endothelial cells of normal and LPS-inflamed rat incisor pulp tissue, suggesting that these cells are associated with the biosynthesis and transmembrane transport of PGE2. Dinoprostone 230-234 prostaglandin E synthase Mus musculus 27-32 25164664-2 2014 The febrile response is triggered by prostaglandin E2 synthesis mediated by induced expression of the enzymes cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1). Dinoprostone 37-53 prostaglandin E synthase Mus musculus 139-176 25164664-2 2014 The febrile response is triggered by prostaglandin E2 synthesis mediated by induced expression of the enzymes cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1). Dinoprostone 37-53 prostaglandin E synthase Mus musculus 178-185 24866789-2 2014 We previously demonstrated that PGE(2) synthesis by F. tularensis-infected macrophages requires cytosolic phospholipase A2 (cPLA(2)), cyclooxygenase 2 (COX-2), and microsomal prostaglandin E synthase 1 (mPGES1). Dinoprostone 32-38 prostaglandin E synthase Mus musculus 203-209 25019142-6 2014 Microsomal prostaglandin E2 synthase-1 (mPGES-1), a downstream PG synthase, specifically catalyzes the biosynthesis of COX-2-derived PGE2 from PGH2, and describes itself as a valuable therapeutic target for the treatment of acute and chronic inflammatory disease conditions. Dinoprostone 133-137 prostaglandin E synthase Mus musculus 40-47 24753592-1 2014 Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vascular cells differentially regulates the response to vascular injury, reflecting distinct effects of mPGES-1-derived PGE2 in these cell types on discrete cellular components of the vasculature. Dinoprostone 183-187 prostaglandin E synthase Mus musculus 0-37 24886859-1 2014 INTRODUCTION: Microsomal prostaglandin E synthase 1 (mPGES-1) catalyzes the terminal step in the biosynthesis of PGE2, a critical mediator in the pathophysiology of osteoarthritis (OA). Dinoprostone 113-117 prostaglandin E synthase Mus musculus 53-60 24753592-1 2014 Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vascular cells differentially regulates the response to vascular injury, reflecting distinct effects of mPGES-1-derived PGE2 in these cell types on discrete cellular components of the vasculature. Dinoprostone 183-187 prostaglandin E synthase Mus musculus 39-46 24753592-1 2014 Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vascular cells differentially regulates the response to vascular injury, reflecting distinct effects of mPGES-1-derived PGE2 in these cell types on discrete cellular components of the vasculature. Dinoprostone 183-187 prostaglandin E synthase Mus musculus 167-174 24756129-1 2014 Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), plays an important role in a variety of diseases. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 24756129-1 2014 Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), plays an important role in a variety of diseases. Dinoprostone 111-127 prostaglandin E synthase Mus musculus 40-47 24756129-1 2014 Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), plays an important role in a variety of diseases. Dinoprostone 129-133 prostaglandin E synthase Mus musculus 40-47 24756129-4 2014 We found that mPGES-1 deficient (mPGES-1-/-) mice exhibited more severe fibrotic lesions with a decrease in PGE2 content in lungs after bleomycin treatment when compared with wild type (mPGES-1+/+) mice. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 14-21 24756129-4 2014 We found that mPGES-1 deficient (mPGES-1-/-) mice exhibited more severe fibrotic lesions with a decrease in PGE2 content in lungs after bleomycin treatment when compared with wild type (mPGES-1+/+) mice. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 33-40 24756129-4 2014 We found that mPGES-1 deficient (mPGES-1-/-) mice exhibited more severe fibrotic lesions with a decrease in PGE2 content in lungs after bleomycin treatment when compared with wild type (mPGES-1+/+) mice. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 33-40 24756129-5 2014 The mPGES-1 expression levels and PGE2 content were also decreased in bleomycin-treated mPGES-1+/+ mice compared to saline-treated mPGES-1+/+ mice. Dinoprostone 34-38 prostaglandin E synthase Mus musculus 88-95 24756129-5 2014 The mPGES-1 expression levels and PGE2 content were also decreased in bleomycin-treated mPGES-1+/+ mice compared to saline-treated mPGES-1+/+ mice. Dinoprostone 34-38 prostaglandin E synthase Mus musculus 88-95 24756129-7 2014 In cultured human lung fibroblast cells (MRC-5), siRNA-mediated knockdown of mPGES-1 augmented transforming growth factor-beta1 (TGF-beta1)-induced alpha-smooth muscle actin (alpha-SMA) protein expression, and the increase was reversed by treatment of PGE2, selective EP2 agonist and focal adhesion kinase (FAK) inhibitor. Dinoprostone 252-256 prostaglandin E synthase Mus musculus 77-84 24756129-8 2014 In conclusion, these findings revealed mPGES-1 exerts an essential effect against pulmonary fibrogenesis via EP2-mediated signaling transduction, and activation of mPGES-1-PGE2-EP2-FAK signaling pathway may represent a new therapeutic strategy for treatment of IPF patients. Dinoprostone 172-176 prostaglandin E synthase Mus musculus 164-171 24138533-1 2014 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible terminal synthase in PGE2 biosynthesis by inflammatory and cancer cells. Dinoprostone 85-89 prostaglandin E synthase Mus musculus 39-46 24726877-4 2014 Targeted PGE2 suppression via genetic ablation of microsomal prostaglandin E-synthase 1 (mPGES-1) or by the pharmacological inhibition of PGE2 receptors EP2 and EP4 substantially improved survival against lethal IAV infection whereas PGE2 administration reversed this phenotype. Dinoprostone 9-13 prostaglandin E synthase Mus musculus 89-96 24505358-10 2014 These variations in mPGES-1 and 15-PGDH density account for the decreased PGE2 level observed in varicose veins. Dinoprostone 74-78 prostaglandin E synthase Mus musculus 20-27 24127557-1 2013 Microsomal PGE synthase-1 (mPGES-1) is an inducible enzyme that specifically catalyzes the conversion of PGH2 to PGE2. Dinoprostone 113-117 prostaglandin E synthase Mus musculus 27-34 24045148-7 2013 As opposed to mPGES-1 genetic deletion, which attenuated PGE2 production and caused a shunt to the thromboxane pathway, mPGES-1 inhibition with compound III reduced PGE2 production and tended to decrease the levels of other prostanoids. Dinoprostone 165-169 prostaglandin E synthase Mus musculus 120-127 23916744-2 2013 mPGES-1 depletion not only suppresses inflammation via absence of inducible PGE2 but might also cause an activation of anti-inflammatory pathways. Dinoprostone 76-80 prostaglandin E synthase Mus musculus 0-7 23916744-4 2013 In LPS-induced peritoneal macrophages from mPGES-1 knock-out (mPGES-1-/-, KO) mice PGE2 production was markedly attenuated, whereas levels of PGD2 metabolites (15-deoxy-Delta(12,14) PGJ2 and 15-deoxy-Delta(12,14) PGD2) were increased compared to wild type mice. Dinoprostone 83-87 prostaglandin E synthase Mus musculus 43-50 23916744-4 2013 In LPS-induced peritoneal macrophages from mPGES-1 knock-out (mPGES-1-/-, KO) mice PGE2 production was markedly attenuated, whereas levels of PGD2 metabolites (15-deoxy-Delta(12,14) PGJ2 and 15-deoxy-Delta(12,14) PGD2) were increased compared to wild type mice. Dinoprostone 83-87 prostaglandin E synthase Mus musculus 62-69 23624019-8 2013 Loss of mPGES-1 was associated with a substantial reduction in intramammary PGE2 levels, aromatase activity, and angiogenesis in mammary glands from HER2/neu transgenic mice. Dinoprostone 76-80 prostaglandin E synthase Mus musculus 8-15 24130900-5 2013 Our results showed that the inhibition of sPLA2-IIA alleviated the release of PGE2 by suppressing the activation of ERK1/2, cPLA2alpha, COX-2 and mPGES-1. Dinoprostone 78-82 prostaglandin E synthase Mus musculus 146-153 23893854-1 2013 The eicosanoid prostaglandin E2 (PGE2 ) plays important roles in neuroinflammation and it is produced by the sequential action of the enzymes cyclooxygenase-2 (COX-2) and prostaglandin E synthase (PTGES). Dinoprostone 15-31 prostaglandin E synthase Mus musculus 171-195 23893854-1 2013 The eicosanoid prostaglandin E2 (PGE2 ) plays important roles in neuroinflammation and it is produced by the sequential action of the enzymes cyclooxygenase-2 (COX-2) and prostaglandin E synthase (PTGES). Dinoprostone 15-31 prostaglandin E synthase Mus musculus 197-202 23893854-1 2013 The eicosanoid prostaglandin E2 (PGE2 ) plays important roles in neuroinflammation and it is produced by the sequential action of the enzymes cyclooxygenase-2 (COX-2) and prostaglandin E synthase (PTGES). Dinoprostone 33-37 prostaglandin E synthase Mus musculus 171-195 23893854-1 2013 The eicosanoid prostaglandin E2 (PGE2 ) plays important roles in neuroinflammation and it is produced by the sequential action of the enzymes cyclooxygenase-2 (COX-2) and prostaglandin E synthase (PTGES). Dinoprostone 33-37 prostaglandin E synthase Mus musculus 197-202 23536473-0 2013 Necrosis in DU145 prostate cancer spheroids induces COX-2/mPGES-1-derived PGE2 to promote tumor growth and to inhibit T cell activation. Dinoprostone 74-78 prostaglandin E synthase Mus musculus 58-65 23536473-3 2013 Therefore, targeting microsomal PGE synthase 1 (mPGES-1), the downstream enzyme in the COX-2-dependent pathway of PGE2 production might be attractive, although conflicting data regarding a potential tumor-supporting function of mPGES-1 were reported. Dinoprostone 114-118 prostaglandin E synthase Mus musculus 48-55 23536473-7 2013 Pharmacological inhibition of COX-2 and mPGES-1 supported the crucial role of PGE2 for growth of MCTS. Dinoprostone 78-82 prostaglandin E synthase Mus musculus 40-47 24055573-0 2013 Anti-inflammatory properties of prostaglandin E2: deletion of microsomal prostaglandin E synthase-1 exacerbates non-immune inflammatory arthritis in mice. Dinoprostone 32-48 prostaglandin E synthase Mus musculus 62-99 24055573-4 2013 180 (2008) 8361-8368) that microsomal prostaglandin E synthase-1 (mPGES-1) deletion, which regulates PGE2 production, resulted in the suppression of collagen-induced arthritis (CIA) in mice. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 27-64 24055573-4 2013 180 (2008) 8361-8368) that microsomal prostaglandin E synthase-1 (mPGES-1) deletion, which regulates PGE2 production, resulted in the suppression of collagen-induced arthritis (CIA) in mice. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 66-73 23900502-2 2013 Cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) induced by inflammation are believed to mediate prostaglandin E2 (PGE2) production thereby promoting carcinogenesis. Dinoprostone 125-141 prostaglandin E synthase Mus musculus 68-75 23900502-2 2013 Cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) induced by inflammation are believed to mediate prostaglandin E2 (PGE2) production thereby promoting carcinogenesis. Dinoprostone 143-147 prostaglandin E synthase Mus musculus 68-75 24198734-5 2013 Arzanol has been reported to inhibit inflammatory transcription factor NF kappaB activation, HIV replication in T cells, releases of IL-1 beta , IL-6, IL-8, and TNF-alpha , and biosynthesis of PGE2 by potentially inhibiting mPGES-1 enzyme. Dinoprostone 193-197 prostaglandin E synthase Mus musculus 224-231 23943621-2 2013 Microsomal prostaglandin E (PGE) synthase-1 (mPGES-1) is an inducible enzyme that couples with cyclooxygenase-2 for the biosynthesis of PGE2. Dinoprostone 136-140 prostaglandin E synthase Mus musculus 45-52 23943621-12 2013 Taken together, these findings identify PGE2 as a key regulator of white-to-brown adipogenesis and suggest the existence of a coordinate regulation of adipogenesis between PPARgamma and mPGES-1. Dinoprostone 40-44 prostaglandin E synthase Mus musculus 186-193 23913682-8 2013 Both KLF5 and mPGES1 promoted prostaglandin E2 production; regulated p21, p27, and Survivin downstream gene expression; and likewise stimulated cell proliferation. Dinoprostone 30-46 prostaglandin E synthase Mus musculus 14-20 23439561-7 2013 Knockdown of mPGES1 by mPGES1 small interfering RNA (siRNA) blocked acid-induced increase in PGE2 production and thymidine incorporation. Dinoprostone 93-97 prostaglandin E synthase Mus musculus 13-19 24101387-8 2013 NF-kappaB and MAPK cascades-activated transcription factor activator protein 1 (AP-1) and CREB-binding protein (CBP/p300) lead to expression of cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2) and membrane-bound prostaglandin E synthase 1 (mPGES-1), and thus to increased release of arachidonic acid and production of prostaglandins, particularly prostaglandin E2 (PGE2). Dinoprostone 359-375 prostaglandin E synthase Mus musculus 252-259 24101387-8 2013 NF-kappaB and MAPK cascades-activated transcription factor activator protein 1 (AP-1) and CREB-binding protein (CBP/p300) lead to expression of cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2) and membrane-bound prostaglandin E synthase 1 (mPGES-1), and thus to increased release of arachidonic acid and production of prostaglandins, particularly prostaglandin E2 (PGE2). Dinoprostone 377-381 prostaglandin E synthase Mus musculus 252-259 23759445-4 2013 EP4 antagonist addition to H37Ra-infected Mphis inhibited the expression of cyclooxygenase 2 (COX2) and microsomal prostaglandin E synthase-1 (mPGES-1), which are involved in PGE2 production. Dinoprostone 175-179 prostaglandin E synthase Mus musculus 143-150 23791007-1 2013 Microsomal prostaglandin E2 synthase-1 (mPGES1), an inducible enzyme similar to cyclooxygenase-2, functions downstream of cyclooxygenase-2 in the synthesis of prostaglandin E2. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-46 23791007-1 2013 Microsomal prostaglandin E2 synthase-1 (mPGES1), an inducible enzyme similar to cyclooxygenase-2, functions downstream of cyclooxygenase-2 in the synthesis of prostaglandin E2. Dinoprostone 159-175 prostaglandin E synthase Mus musculus 40-46 23789712-1 2013 Microsomal prostaglandin E synthase-1 (mPGES-1) constitutes an inducible glutathione-dependent integral membrane protein that catalyzes the oxido-reduction of cyclooxygenase derived PGH2 into PGE2. Dinoprostone 192-196 prostaglandin E synthase Mus musculus 39-46 23684692-0 2013 Cysteinyl leukotriene-receptor-1 antagonists interfere with PGE2 synthesis by inhibiting mPGES-1 activity. Dinoprostone 60-64 prostaglandin E synthase Mus musculus 89-96 23447581-2 2013 The inducible enzyme microsomal prostaglandin E synthase-1 (mPGES-1), catalyzing the terminal step of PGE2 biosynthesis, is an attractive target for selective PGE2 inhibition. Dinoprostone 102-106 prostaglandin E synthase Mus musculus 60-67 23447581-2 2013 The inducible enzyme microsomal prostaglandin E synthase-1 (mPGES-1), catalyzing the terminal step of PGE2 biosynthesis, is an attractive target for selective PGE2 inhibition. Dinoprostone 159-163 prostaglandin E synthase Mus musculus 60-67 23447581-6 2013 In summary, these results demonstrate that the aminothiazoles represent novel mPGES-1 inhibitors for inhibition of PGE2 production and reduction of bone resorption in experimental periodontitis, and may be used as potential anti-inflammatory drugs for treatment of chronic inflammatory diseases, including periodontitis. Dinoprostone 115-119 prostaglandin E synthase Mus musculus 78-85 23439561-7 2013 Knockdown of mPGES1 by mPGES1 small interfering RNA (siRNA) blocked acid-induced increase in PGE2 production and thymidine incorporation. Dinoprostone 93-97 prostaglandin E synthase Mus musculus 23-29 23439561-12 2013 We conclude that mPGES1 mediates acid-induced increase in PGE2 production and cell proliferation. Dinoprostone 58-62 prostaglandin E synthase Mus musculus 17-23 23266396-1 2013 Microsomal prostaglandin synthetase-1 (mPGES-1) is an inducible terminal enzyme required for prostaglandin E(2) (PGE(2)) biosynthesis. Dinoprostone 93-111 prostaglandin E synthase Mus musculus 39-46 23488692-2 2013 Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal enzyme of the PGE2 pathway inducible by proinflammatory cytokines. Dinoprostone 76-80 prostaglandin E synthase Mus musculus 39-46 23591846-6 2013 In in vitro experiments, mPGES-1 produces PGE2, which enhances astrocytic Ca2+ levels via the EP3 receptor and increases Ca2+-dependent glutamate release, thus aggravating neuronal injury. Dinoprostone 42-46 prostaglandin E synthase Mus musculus 25-32 23431194-2 2013 The main source of inducible PGE2, microsomal PGE2 synthase-1 (mPGES-1), has emerged as an interesting drug target for treatment of pain. Dinoprostone 29-33 prostaglandin E synthase Mus musculus 63-70 24237030-1 2013 The PGE2 pathway is important in inflammation-driven diseases and specific targeting of the inducible mPGES-1 is warranted due to the cardiovascular problems associated with the long-term use of COX-2 inhibitors. Dinoprostone 4-8 prostaglandin E synthase Mus musculus 102-109 23266396-1 2013 Microsomal prostaglandin synthetase-1 (mPGES-1) is an inducible terminal enzyme required for prostaglandin E(2) (PGE(2)) biosynthesis. Dinoprostone 113-118 prostaglandin E synthase Mus musculus 39-46 23171554-0 2013 mPGES-1-derived PGE2 mediates dehydration natriuresis. Dinoprostone 16-20 prostaglandin E synthase Mus musculus 0-7 23142196-13 2013 It is also suggested that mPGES-1 inhibition contributes to the effect of ANE on PGE(2) production in the microglia. Dinoprostone 81-87 prostaglandin E synthase Mus musculus 26-33 23042097-0 2013 Hypoxia-inducible factor-2alpha is essential in activating the COX2/mPGES-1/PGE2 signaling axis in colon cancer. Dinoprostone 76-80 prostaglandin E synthase Mus musculus 68-75 23042097-8 2013 Further examination revealed that the terminal PGE(2) synthesis enzyme microsomal prostaglandin E synthase 1 (mPGES-1) was overexpressed in the colon of Vhl(DeltaIE)/Apc(min/+) mice. Dinoprostone 47-53 prostaglandin E synthase Mus musculus 71-108 23042097-8 2013 Further examination revealed that the terminal PGE(2) synthesis enzyme microsomal prostaglandin E synthase 1 (mPGES-1) was overexpressed in the colon of Vhl(DeltaIE)/Apc(min/+) mice. Dinoprostone 47-53 prostaglandin E synthase Mus musculus 110-117 23042097-10 2013 Together, our findings demonstrate that HIF-2alpha is a major regulator of COX2/mPGES-1/PGE(2) pathway in colon tumors. Dinoprostone 88-94 prostaglandin E synthase Mus musculus 80-87 22964849-4 2012 The PGE2-generating capacity was enhanced in various obese mouse models by the induction of cyclooxygenase 2 and microsomal prostaglandin E-synthases (mPGES1, mPGES2). Dinoprostone 4-8 prostaglandin E synthase Mus musculus 151-157 24489534-3 2013 Strikingly, urinary PGE2 was remarkably elevated in db/db mice paralleled with the increased protein expressions of COX-2 and mPGES-1. Dinoprostone 20-24 prostaglandin E synthase Mus musculus 126-133 24489534-8 2013 Collectively, the present study demonstrated an inhibitory effect of PPAR gamma activation on renal mPGES-1/PGE2/EP4 pathway in type-2 diabetes and suggested that mPGES-1 may potentially serve as a therapeutic target for treating type-2 diabetes-associated DN. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 100-107 24489534-8 2013 Collectively, the present study demonstrated an inhibitory effect of PPAR gamma activation on renal mPGES-1/PGE2/EP4 pathway in type-2 diabetes and suggested that mPGES-1 may potentially serve as a therapeutic target for treating type-2 diabetes-associated DN. Dinoprostone 108-112 prostaglandin E synthase Mus musculus 163-170 22978524-3 2012 The purpose of this study was to investigate the cellular system of PGE(2) production via microsomal PGE synthetase-1 (mPGES-1), the inducible PGE(2) -generating enzyme, and PGE(2) elimination from the CSF via the blood-CSF barrier (BCSFB). Dinoprostone 68-74 prostaglandin E synthase Mus musculus 120-127 22978524-4 2012 Immunohistochemical analysis revealed that mPGES-1 was expressed in the soma and perivascular sheets of astrocytes, pia mater, and brain blood vessel endothelial cells, suggesting that these cells are local production sites of PGE(2) in the CSF. Dinoprostone 227-233 prostaglandin E synthase Mus musculus 43-50 23995802-2 2013 We recently identified the microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal enzyme for prostaglandin E2 synthesis, as a critical factor in stroke-reperfusion injury. Dinoprostone 109-125 prostaglandin E synthase Mus musculus 27-64 23995802-2 2013 We recently identified the microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal enzyme for prostaglandin E2 synthesis, as a critical factor in stroke-reperfusion injury. Dinoprostone 109-125 prostaglandin E synthase Mus musculus 66-73 23995802-3 2013 Co-induction of mPGES-1 and cyclooxygenase (COX)-2, an upstream enzyme for PGE2 production, was observed after brain ischemia. Dinoprostone 75-79 prostaglandin E synthase Mus musculus 16-23 23995802-4 2013 In mPGES-1 knockout (KO) mice, in which the postischemic PGE2 production in the cortex was completely absent, the ischemic injuries were less severe compared to those in wild-type (WT) mice. Dinoprostone 57-61 prostaglandin E synthase Mus musculus 3-10 23995802-11 2013 These results suggest that mPGES-1 and COX-2 are co-induced by excessive glutamate in the ischemic brain and act together to exacerbate stroke injury through PGE2 production followed by activation of EP3 receptors. Dinoprostone 158-162 prostaglandin E synthase Mus musculus 27-34 22872578-2 2012 The production of PGE2 depends on cyclooxygenase-2 and microsomal prostaglandin E synthase-1 (mPGES-1), but the identity of the cells involved has been a matter of controversy. Dinoprostone 18-22 prostaglandin E synthase Mus musculus 55-92 22872578-2 2012 The production of PGE2 depends on cyclooxygenase-2 and microsomal prostaglandin E synthase-1 (mPGES-1), but the identity of the cells involved has been a matter of controversy. Dinoprostone 18-22 prostaglandin E synthase Mus musculus 94-101 22872578-4 2012 Mice lacking mPGES-1 in hematopoietic cells displayed an intact febrile response to lipopolysaccharide, associated with elevated levels of PGE2 in the cerebrospinal fluid. Dinoprostone 139-143 prostaglandin E synthase Mus musculus 13-20 22872578-5 2012 In contrast, mice that expressed mPGES-1 only in hematopoietic cells, although displaying elevated PGE2 levels in plasma but not in the cerebrospinal fluid, showed no febrile response to lipopolysaccharide, thus pointing to the critical role of brain-derived PGE2 for fever. Dinoprostone 99-103 prostaglandin E synthase Mus musculus 33-40 22872578-5 2012 In contrast, mice that expressed mPGES-1 only in hematopoietic cells, although displaying elevated PGE2 levels in plasma but not in the cerebrospinal fluid, showed no febrile response to lipopolysaccharide, thus pointing to the critical role of brain-derived PGE2 for fever. Dinoprostone 259-263 prostaglandin E synthase Mus musculus 33-40 22822059-1 2012 Arachidonic acid is converted to prostaglandin E(2) (PGE(2)) by a sequential enzymatic reaction performed by two isoenzyme groups, cyclooxygenases (COX-1 and COX-2) and terminal prostaglandin E synthases (cPGES, mPGES-1, and mPGES-2). Dinoprostone 33-51 prostaglandin E synthase Mus musculus 212-219 22822059-2 2012 mPGES-1 is widely considered to be the final enzyme regulating COX-2-dependent PGE(2) synthesis. Dinoprostone 79-85 prostaglandin E synthase Mus musculus 0-7 22537108-0 2012 Concurrent blockade of free radical and microsomal prostaglandin E synthase-1-mediated PGE2 production improves safety and efficacy in a mouse model of amyotrophic lateral sclerosis. Dinoprostone 87-91 prostaglandin E synthase Mus musculus 40-77 22537108-4 2012 AAD-2004 completely removed free radicals at 50 nM as a potent spin-trapping molecule and inhibited microsomal PGE(2) synthase-1 (mPGES-1) activity in response to both lipopolysaccharide-treated BV2 cell with IC(50) of 230 nM and recombinant human mPGES-1 protein with IC(50) of 249 nM in vitro. Dinoprostone 111-117 prostaglandin E synthase Mus musculus 130-137 22537108-9 2012 Targeting both mPGES-1-mediated PGE(2) and free radicals may be a promising approach to reduce neurodegeneration in ALS and possibly other neurodegenerative diseases. Dinoprostone 32-38 prostaglandin E synthase Mus musculus 15-22 22795900-2 2012 mPGES-1 catalyzes the synthesis of the inducible prostaglandin E(2) in response to pro-inflammatory stimuli, rendering this enzyme extremely interesting in drug discovery process owing to the drastic reduction of the severe side effects typical for traditional non-steroidal anti-inflammatory drugs. Dinoprostone 49-67 prostaglandin E synthase Mus musculus 0-7 22081067-1 2012 In this report we describe the contribution of prostaglandin E(2) (PGE(2)) derived from the inducible microsomal PGE-synthase type-1 (mPGES-1) to the epidermal growth factor receptor (EGFR) oncogenic drive in tumor epithelial cells and in tumor-bearing mice. Dinoprostone 47-65 prostaglandin E synthase Mus musculus 134-141 22081067-1 2012 In this report we describe the contribution of prostaglandin E(2) (PGE(2)) derived from the inducible microsomal PGE-synthase type-1 (mPGES-1) to the epidermal growth factor receptor (EGFR) oncogenic drive in tumor epithelial cells and in tumor-bearing mice. Dinoprostone 67-73 prostaglandin E synthase Mus musculus 134-141 22573380-13 2012 We assume that mPGES-1 is coregulated with COX-2 for PGE(2) synthesis to orchestrate postnatal kidney development and growth. Dinoprostone 53-59 prostaglandin E synthase Mus musculus 15-22 22466648-7 2012 LPS exposure induced expression of microsomal PGE synthase-1 (mPGES-1), a key enzyme in PGE2 biosynthesis. Dinoprostone 88-92 prostaglandin E synthase Mus musculus 62-69 22511203-8 2012 Together, S. officinalis extracts and its ingredients carnosol and carnosic acid inhibit PGE(2) formation by selectively targeting mPGES-1. Dinoprostone 89-95 prostaglandin E synthase Mus musculus 131-138 22588264-1 2012 BACKGROUND AND PURPOSE: Cyclooxygenase-2 (COX-2) and Microsomal Prostaglandin E2 Synthase-1 (mPGES-1) catalyze isomerization of the cyclooxygenase product PGH2 into PGE2. Dinoprostone 165-169 prostaglandin E synthase Mus musculus 93-100 22589381-1 2012 BACKGROUND: Microsomal prostaglandin E(2) synthase-1 (mPGES-1), encoded by the Ptges gene, catalyzes prostaglandin E(2) biosynthesis and is expressed by leukocytes, cardiac myocytes, and cardiac fibroblasts. Dinoprostone 23-41 prostaglandin E synthase Mus musculus 54-61 22589381-9 2012 CONCLUSIONS: Lack of mPGES-1 in bone marrow-derived leukocytes negatively regulates COX-1 expression, prostaglandin E(2) biosynthesis, and inflammation in the infarct and leads to impaired LV function, adverse LV remodeling, and decreased survival after acute myocardial infarction. Dinoprostone 102-120 prostaglandin E synthase Mus musculus 21-28 21986945-2 2012 However, the precise contribution of microsomal PGE synthase (mPGES)-1, a terminal enzyme that acts downstream of COX-2 in the PGE(2)-biosynthetic pathway, to multiple processes of tumor development is not yet fully understood. Dinoprostone 127-133 prostaglandin E synthase Mus musculus 37-70 22237797-12 2012 Taken together, these results suggest that mPGES-1-derived PGE(2) reduces urine concentrating ability through suppression of renal medullary expression of V(2) receptors and AQP2 but may enhance it by mediating the central AVP response. Dinoprostone 59-65 prostaglandin E synthase Mus musculus 43-50 22803375-2 2012 Prostaglandin E2 (PGE2) plays a key role in generation of these pathological states, while PGE, synthase-1 (mPGES-1) is one of crucial biological elements in the process of PGE2 production. Dinoprostone 173-177 prostaglandin E synthase Mus musculus 108-115 21743491-6 2012 Mechanistically, mPGES-1-induced HCC cell proliferation, invasion and migration involve PGE(2) production and activation of early growth response 1 (EGR1) and beta-catenin. Dinoprostone 88-94 prostaglandin E synthase Mus musculus 17-24 22260630-2 2012 Efforts have shifted towards the specific PGE2 terminal synthases, particularly mPGES-1 (microsomal PGE synthase 1), which has emerged as the crucial inducible synthase with roles in pain, cancer and inflammation. Dinoprostone 42-46 prostaglandin E synthase Mus musculus 80-87 22268508-0 2012 Involvement of PGE2 and the cAMP signalling pathway in the up-regulation of COX-2 and mPGES-1 expression in LPS-activated macrophages. Dinoprostone 15-19 prostaglandin E synthase Mus musculus 86-93 22268508-2 2012 In the present study, we describe a PGE2 positive feedback for COX (cyclo-oxygenase)-2 and mPGES-1 [microsomal PGES (PGE synthase)-1] expression in the macrophage cell line RAW 264.7. Dinoprostone 36-40 prostaglandin E synthase Mus musculus 91-98 22268508-3 2012 Our results show that PGE2 induces COX-2 and mPGES-1 expression, an effect mimicked by dbcAMP (dibutyryl-cAMP) or forskolin. Dinoprostone 22-26 prostaglandin E synthase Mus musculus 45-52 22268508-8 2012 Activation of the PGE2/EP2/PKA signalling pathway induced the phosphorylation of CREB [CRE (cAMP-response element)-binding protein] in macrophages and stimulated the specific binding of this transcription factor to COX2 and mPGES-1 promoters. Dinoprostone 18-22 prostaglandin E synthase Mus musculus 224-231 22268508-10 2012 In summary, the results of the present study demonstrate that activation of PKA/CREB signalling through the EP2 receptor by PGE2 plays a key role in the expression of COX-2 and mPGES-1 in activated macrophages. Dinoprostone 124-128 prostaglandin E synthase Mus musculus 177-184 22089456-10 2012 GS inhibits PGE(2) synthesis through reduction in the activity of COX-2 and the production and activity of mPGES-1. Dinoprostone 12-18 prostaglandin E synthase Mus musculus 107-114 22116053-11 2012 In the brain, an expression of cytokines (TNFalpha, IL-1beta, and IL-6) and inducible forms of enzymes for prostaglandin E2 synthesis (COX-2 and mPGES) occurred, which was accompanied by a moderate activation of the transcription factors NFkappaB and STAT3, and a strong activation of the transcription factor NF-IL6, in cells of specific areas with an open blood-brain barrier. Dinoprostone 107-123 prostaglandin E synthase Mus musculus 145-150 22227567-7 2012 Finally, the induction of mPGES-1 was regulated, in part, through a positive feedback loop dependent on PGE(2) binding to EP4. Dinoprostone 104-110 prostaglandin E synthase Mus musculus 26-33 23226252-0 2012 Lipopolysaccharide-induced expression of microsomal prostaglandin E synthase-1 mediates late-phase PGE2 production in bone marrow derived macrophages. Dinoprostone 99-103 prostaglandin E synthase Mus musculus 41-78 22106404-1 2012 Microsomal prostaglandin E synthase 1 (mPGES-1) is a cytokine-inducible enzyme responsible for generation of prostaglandin E(2) (PGE(2)) during the inflammatory response. Dinoprostone 109-127 prostaglandin E synthase Mus musculus 0-37 22106404-1 2012 Microsomal prostaglandin E synthase 1 (mPGES-1) is a cytokine-inducible enzyme responsible for generation of prostaglandin E(2) (PGE(2)) during the inflammatory response. Dinoprostone 109-127 prostaglandin E synthase Mus musculus 39-46 21742035-5 2012 In these DM1 cells, PGE(2) production is increased through up-regulation of cyclooxygenase 2 (Cox-2), mPGES-1 and prostaglandin EP2/EP4 receptors. Dinoprostone 20-26 prostaglandin E synthase Mus musculus 102-109 21856412-9 2011 LPS-induced activation of redox-sensitive signaling intermediates such as MAPKs, transcription factor NF-kappaB, and EGR-1, a transcriptional regulator of mPGES-1, which in collaboration with COX-2 leads to the production of PGE2, was also significantly prevented by AR inhibition. Dinoprostone 225-229 prostaglandin E synthase Mus musculus 155-162 23166763-3 2012 We found that SFN indeed blocked PGE2 production in human A549 cancer cells not by inhibiting COX-2, but rather by suppressing the expression of microsomal prostaglandin E synthase (mPGES-1), the enzyme that directly synthesizes PGE2. Dinoprostone 229-233 prostaglandin E synthase Mus musculus 182-189 22815767-1 2012 BACKGROUND: Blockade of Prostaglandin (PG) E(2) production via deletion of microsomal Prostaglandin E synthase-1 (mPGES-1) gene reduces tumor cell proliferation in vitro and in vivo on xenograft tumors. Dinoprostone 24-47 prostaglandin E synthase Mus musculus 114-121 22815767-10 2012 CONCLUSION: Our work demonstrates that the pharmacological inhibition of mPGES-1 reduces squamous carcinoma growth by suppressing PGE(2) mediated-EGFR signalling and by impairing tumor associated angiogenesis. Dinoprostone 130-136 prostaglandin E synthase Mus musculus 73-80 22038016-4 2011 Cytotoxicity assays and flow cytometry showed that MK886, an inhibitor of mPGES-1, inhibits proliferation of HL-60 cells and induces apoptosis in a dose- and time-dependent manner, which may result from down-regulation of mPGES-1 expression and PGE2 synthesis. Dinoprostone 245-249 prostaglandin E synthase Mus musculus 74-81 21341175-2 2011 In inflammation, bacterial products and cytokines enhance the expression of COX-2 and inducible microsomal prostaglandin E synthase-1 (mPGES-1) which are functionally coupled to result in increased PGE2 formation in macrophages and tissue cells. Dinoprostone 198-202 prostaglandin E synthase Mus musculus 135-142 22038016-1 2011 Microsomal prostaglandin E synthase-1 (mPGES-1), an inducible enzyme that specifically catalyzes the conversion of prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), has been reported to be over-expressed in a variety of solid tumor cells and tissues, but not in normal tissues. Dinoprostone 142-158 prostaglandin E synthase Mus musculus 39-46 22038016-1 2011 Microsomal prostaglandin E synthase-1 (mPGES-1), an inducible enzyme that specifically catalyzes the conversion of prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), has been reported to be over-expressed in a variety of solid tumor cells and tissues, but not in normal tissues. Dinoprostone 160-164 prostaglandin E synthase Mus musculus 39-46 21873375-8 2011 However, silencing prostaglandins E2 signaling pathways using mPGES-1 knockout mice, which are resistant to cytokine-induced sickness behavior, did not modify the responses to the toxin. Dinoprostone 19-36 prostaglandin E synthase Mus musculus 62-69 21784115-0 2011 Prostaglandin E2 produced by microsomal prostaglandin E synthase-1 regulates the onset and the maintenance of wakefulness. Dinoprostone 0-16 prostaglandin E synthase Mus musculus 29-66 21784115-1 2011 This study examined the effect of prostaglandin E(2) (PGE(2)) produced by microsomal prostaglandin E synthase-1 (mPGES-1) on circadian rhythm. Dinoprostone 34-52 prostaglandin E synthase Mus musculus 74-111 21784115-1 2011 This study examined the effect of prostaglandin E(2) (PGE(2)) produced by microsomal prostaglandin E synthase-1 (mPGES-1) on circadian rhythm. Dinoprostone 34-52 prostaglandin E synthase Mus musculus 113-120 21801310-1 2011 Microsomal prostaglandin E synthase-1 (mPGES-1) is the key enzyme for prostaglandin E2 (PGE2) generation during inflammation and is a potential target for designing anti-inflammatory drugs. Dinoprostone 70-86 prostaglandin E synthase Mus musculus 39-46 21801310-1 2011 Microsomal prostaglandin E synthase-1 (mPGES-1) is the key enzyme for prostaglandin E2 (PGE2) generation during inflammation and is a potential target for designing anti-inflammatory drugs. Dinoprostone 88-92 prostaglandin E synthase Mus musculus 39-46 21497116-6 2011 PGE2 expression was markedly reduced in PGE synthase-deficient (Ptges-/-) macrophages, and Ptges-/- mice displayed reduced antigen-specific serum IgE concentrations after immunization with alum or silica. Dinoprostone 0-4 prostaglandin E synthase Mus musculus 64-69 21466167-1 2011 Microsomal prostaglandin E(2) synthase-1 (mPGES-1) catalyzes prostaglandin E(2) formation and is considered as a potential anti-inflammatory pharmacological target. Dinoprostone 11-29 prostaglandin E synthase Mus musculus 42-49 21576350-2 2011 PGE(2) is generated from arachidonic acid by the sequential actions of the COX and terminal synthases (PGES). Dinoprostone 0-6 prostaglandin E synthase Mus musculus 103-107 21448233-1 2011 Microsomal PGE synthase 1 (mPGES-1) is the terminal enzyme in the induced state of prostaglandin E(2) (PGE(2)) synthesis and constitutes a therapeutic target for rheumatoid arthritis (RA) treatment. Dinoprostone 83-101 prostaglandin E synthase Mus musculus 27-34 21354147-1 2011 BACKGROUND & AIMS: Microsomal prostaglandin E synthase-1 (mPGES-1) is a rate-limiting enzyme that is coupled with cyclooxygenase (COX)-2 in the synthesis of prostaglandin E2. Dinoprostone 161-177 prostaglandin E synthase Mus musculus 62-69 21277871-4 2011 The present work was conducted to evaluate the expression of PGE(2)-pathway-related enzymes in human microvascular endothelial cells (HMVEC) in culture and to test the hypothesis that the tumor cell-HMVEC cross talk could increase mPGES-1 expression in HMVEC. Dinoprostone 61-67 prostaglandin E synthase Mus musculus 231-238 21190819-0 2011 Genetic deletion of mPGES-1 abolishes PGE2 production in murine dendritic cells and alters the cytokine profile, but does not affect maturation or migration. Dinoprostone 38-42 prostaglandin E synthase Mus musculus 20-27 21435451-8 2011 Furthermore, PGE(2) production was diminished in gingival fibroblasts derived from mPGES-1 knockout mice, compared with wild-type fibroblasts. Dinoprostone 13-19 prostaglandin E synthase Mus musculus 83-90 21435451-9 2011 These results suggest that fibroblasts and smooth muscle cells are important sources of mPGES-1, which may contribute to increased PGE(2) production in the inflammatory condition periodontitis. Dinoprostone 131-137 prostaglandin E synthase Mus musculus 88-95 21193590-1 2011 Our laboratory previously reported that inducible PGE(2) synthase, mPGES-1, contributes to micromolar production of PGE(2) in neonatal ventricular myocytes in vitro, which stimulates their growth. Dinoprostone 50-56 prostaglandin E synthase Mus musculus 67-74 21435451-1 2011 The inflammatory mediator prostaglandin E(2) (PGE(2)) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. Dinoprostone 26-44 prostaglandin E synthase Mus musculus 223-230 21435451-1 2011 The inflammatory mediator prostaglandin E(2) (PGE(2)) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. Dinoprostone 46-52 prostaglandin E synthase Mus musculus 223-230 21190819-1 2011 We undertook this study to determine the role of Microsomal PGE Synthase-1 (mPGES-1), and mPGES-1-generated Prostaglandin (PG) E2 on Dendritic Cell (DC) phenotype and function. Dinoprostone 108-129 prostaglandin E synthase Mus musculus 90-97 21190819-4 2011 Compared to wild-type, mPGES-1 deficient DCs exhibited a markedly attenuated increase in PGE2 production upon LPS stimulation, and displayed preferential shunting towards PGD2 production. Dinoprostone 89-93 prostaglandin E synthase Mus musculus 23-30 21190819-6 2011 However, mPGES-1 deficient DCs generated reduced amounts of the Th1 cytokine IL-12, which may in part be due to increased PGD2 rather than decreased PGE2. Dinoprostone 149-153 prostaglandin E synthase Mus musculus 9-16 21282500-8 2011 Consistent with in vivo rediversion of PG biosynthesis, mPGES-1-deleted vascular smooth muscle cells generated less PGE2 but more PGI2 and expressed reduced tenascin-C compared with wild-type cells. Dinoprostone 116-120 prostaglandin E synthase Mus musculus 56-63 21687502-8 2011 We conclude that the suppression of PGE(2) biosynthesis in vitro and in vivo by acting on mPGES-1 critically contributes to the anti-inflammatory efficiency of Hyp. Dinoprostone 36-42 prostaglandin E synthase Mus musculus 90-97 21266028-1 2011 INTRODUCTION: Microsomal prostaglandin E2 synthase-1 (mPGES-1) is an inducible enzyme that acts downstream of cyclooxygenase (COX) to specifically catalyze the conversion of prostaglandin (PG) H2 to PGE2. Dinoprostone 199-203 prostaglandin E synthase Mus musculus 54-61 20933508-5 2011 In fact, arzanol could block COX-2/mPGES-1-mediated PGE(2) biosynthesis in lipopolysaccharide-stimulated human monocytes and human whole blood, but not the concomitant COX-2-derived biosynthesis of thromboxane B(2) or of 6-keto PGF(1alpha), and the expression of COX-2 or mPGES-1 protein was not affected. Dinoprostone 52-58 prostaglandin E synthase Mus musculus 35-42 21247731-3 2011 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme downstream of COX-2 in prostaglandin E(2) biosynthesis. Dinoprostone 94-112 prostaglandin E synthase Mus musculus 0-37 21247731-3 2011 Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme downstream of COX-2 in prostaglandin E(2) biosynthesis. Dinoprostone 94-112 prostaglandin E synthase Mus musculus 39-46 20587000-12 2010 CONCLUSION: The findings confirm a key function of COX2 and mPGES1 for the synthesis of pyrogenic PGE2 and, at the same time, document their early response to LPS. Dinoprostone 98-102 prostaglandin E synthase Mus musculus 60-66 21372596-1 2011 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES1) is critical for prostaglandin E(2) formation in ductus arteriosus (DA) and, accordingly, in its patency. Dinoprostone 75-93 prostaglandin E synthase Mus musculus 12-49 21372596-1 2011 BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES1) is critical for prostaglandin E(2) formation in ductus arteriosus (DA) and, accordingly, in its patency. Dinoprostone 75-93 prostaglandin E synthase Mus musculus 51-57 21224505-8 2010 This study demonstrates that IL-1beta activates expression of mPGES-1 mRNA in uterine tissues to stimulate synthesis and secretion of PGE2 on days 10 to 13 of both pregnancy and the estrous cycle. Dinoprostone 134-138 prostaglandin E synthase Mus musculus 62-69 20171718-6 2010 Decreased PGE(2) content in ULFs of gonadotropin-treated pigs was preceded by lower endometrial mPGES-1 gene expression in hormonally-stimulated animals in comparison to control gilts (P<0.01). Dinoprostone 10-16 prostaglandin E synthase Mus musculus 96-103 20546888-3 2010 Functional coupling of the inducible enzymes COX-2 and mPGES-1 has been proposed for increased production of PGE(2) in different cell types. Dinoprostone 109-115 prostaglandin E synthase Mus musculus 55-62 20546888-12 2010 Our findings point out to Egr-1 and NF-kappaB cooperation as determinant for PGE2 synthesis by macrophages in inflammatory processes through the coordinated regulation of COX-2 and mPGES-1. Dinoprostone 77-81 prostaglandin E synthase Mus musculus 181-188 20954326-1 2010 Prostaglandin E2 (PGE2) is a proinflammatory mediator that is synthesized by cyclooxygenases (COX-1 and COX-2) and prostaglandin E synthases (cPGES-1 and mPGES-1); PGE2 exerts its biological effects by binding to specific receptors. Dinoprostone 0-16 prostaglandin E synthase Mus musculus 154-161 20954326-1 2010 Prostaglandin E2 (PGE2) is a proinflammatory mediator that is synthesized by cyclooxygenases (COX-1 and COX-2) and prostaglandin E synthases (cPGES-1 and mPGES-1); PGE2 exerts its biological effects by binding to specific receptors. Dinoprostone 18-22 prostaglandin E synthase Mus musculus 154-161 20682710-7 2010 PGE-2 triggers a feed-forward loop involving HIF-1alpha, which impinges on mPGEs-1 and VEGF expression, events prevented by DPE via extracellular signal-related kinase 1/2. Dinoprostone 0-5 prostaglandin E synthase Mus musculus 75-82 20338073-11 2010 The mechanism of action implicated seems to be via the inhibition of activation of NF-kappaB and MAPK, down-regulation of COX-2 and mPGES-1 expressions, and consequently,via the reduction of PGE2 production. Dinoprostone 191-195 prostaglandin E synthase Mus musculus 132-139 20222108-14 2010 CONCLUSION: Our findings indicate that adiponectin induces COX-2 and mPGES-1 expression, resulting in the enhancement of PGE(2) production by RASFs. Dinoprostone 121-127 prostaglandin E synthase Mus musculus 69-76 20492447-5 2010 This optimization process led to the identification of three strictly correlated compounds 14g, 16g, and 18 with higher inhibitory potency on PGE(2) production on mouse macrophage cell line RAW264.7 through the selective modulation of mPGES-1 enzyme expression. Dinoprostone 142-148 prostaglandin E synthase Mus musculus 235-242 20412387-2 2010 Downstream actions of IL-1beta include production of prostaglandin (PG) E(2) by increasing expression of cyclooxygenase (COX) enzymes and prostaglandin E synthase (PGES) isoforms. Dinoprostone 53-76 prostaglandin E synthase Mus musculus 138-162 20412387-2 2010 Downstream actions of IL-1beta include production of prostaglandin (PG) E(2) by increasing expression of cyclooxygenase (COX) enzymes and prostaglandin E synthase (PGES) isoforms. Dinoprostone 53-76 prostaglandin E synthase Mus musculus 164-168 20025057-5 2010 However, in cells treated with LPS coupled with COX-2 neutralization, the mRNA expression levels of COX-2, mPGES-1, tumor necrosis factor-alpha, interleukin-1beta and inducible nitric oxide synthase were significantly suppressed; production of prostaglandin E(2) and reactive oxygen species also decreased. Dinoprostone 244-262 prostaglandin E synthase Mus musculus 107-143 20067770-1 2010 Inflammation-induced microsomal prostaglandin E synthase-1 (mPGES-1) is the terminal enzyme that synthesizes prostaglandin E(2) (PGE(2)) downstream of cyclooxygenase-2 (COX-2). Dinoprostone 109-127 prostaglandin E synthase Mus musculus 60-67 20067770-5 2010 In inflammation and clinically relevant biological systems, mPGES-1 expression, like COX-2 expression was induced in cell context- and time-dependent manner, consistent with the kinetics of PGE(2) synthesis. Dinoprostone 190-196 prostaglandin E synthase Mus musculus 60-67 19739114-4 2010 In OAC cells, reduction of mPGES-1 with RNA interference blocked PGE2 production, inhibited serum-induced proliferation and enhanced apoptosis in the COX-2 expressing cell lines (OE33 and FLO) but had no effect in COX-2 deficient BIC-1 cells. Dinoprostone 65-69 prostaglandin E synthase Mus musculus 27-34 20110555-8 2010 The prostaglandin E synthase (mPGES-1) gene has multiple EGR1 binding sites on its promoter, and induction of mPGES-1 mRNA (as well as the prostanoid product, PGE2) by injurious ventilation was highly dependent on the presence of the Egr1 gene. Dinoprostone 159-163 prostaglandin E synthase Mus musculus 4-28 20110555-8 2010 The prostaglandin E synthase (mPGES-1) gene has multiple EGR1 binding sites on its promoter, and induction of mPGES-1 mRNA (as well as the prostanoid product, PGE2) by injurious ventilation was highly dependent on the presence of the Egr1 gene. Dinoprostone 159-163 prostaglandin E synthase Mus musculus 30-37 19739114-5 2010 Three different methods of inhibiting mPGES-1 (RNA interference, a novel small molecule inhibitor and the endogenous inhibitor 15-deoxy-Delta(12,14)-PGJ(2)) also blocked leptin induced mPGES-1 expression and PGE2 production and abolished the leptin-induced proliferative and anti-apoptotic effects in OE33 cells, without affecting COX-2 expression. Dinoprostone 208-212 prostaglandin E synthase Mus musculus 38-45 20398340-4 2010 RESULTS: Microarray and western blot analyses showed that the mRNA and protein expression of the inflammatory induced microsomal prostaglandin E synthase-1 (mPGES-1) was up-regulated by the cytokine TNFalpha, accompanied by enhanced expression of COX-2 and increased production of PGE2. Dinoprostone 281-285 prostaglandin E synthase Mus musculus 157-164 20025212-2 2010 Inhibitors of mPGES-1 mimicking prostaglandin E(2) often interact with cyclooxygenases (COXs) 1 and 2, leading to unwanted side effects. Dinoprostone 32-50 prostaglandin E synthase Mus musculus 14-21 19948080-7 2010 We conclude that the inhibitory effect of ellagic acid on PGE2 release from monocytes is due to a suppressed expression of COX-2, mPGEs-1 and cPLA2alpha, rather than a direct effect on the activities of these enzymes. Dinoprostone 58-62 prostaglandin E synthase Mus musculus 130-137 19995978-0 2009 Targeted lipidomics reveals mPGES-1-PGE2 as a therapeutic target for multiple sclerosis. Dinoprostone 36-40 prostaglandin E synthase Mus musculus 28-35 19845504-1 2009 mPGES-1 (microsomal prostaglandin E synthase-1) is a stimulus-inducible enzyme that functions downstream of COX (cyclo-oxygenase)-2 in the PGE2 (prostaglandin E2)-biosynthesis pathway. Dinoprostone 139-143 prostaglandin E synthase Mus musculus 0-7 19845504-1 2009 mPGES-1 (microsomal prostaglandin E synthase-1) is a stimulus-inducible enzyme that functions downstream of COX (cyclo-oxygenase)-2 in the PGE2 (prostaglandin E2)-biosynthesis pathway. Dinoprostone 139-143 prostaglandin E synthase Mus musculus 9-46 19845504-1 2009 mPGES-1 (microsomal prostaglandin E synthase-1) is a stimulus-inducible enzyme that functions downstream of COX (cyclo-oxygenase)-2 in the PGE2 (prostaglandin E2)-biosynthesis pathway. Dinoprostone 145-161 prostaglandin E synthase Mus musculus 0-7 19845504-1 2009 mPGES-1 (microsomal prostaglandin E synthase-1) is a stimulus-inducible enzyme that functions downstream of COX (cyclo-oxygenase)-2 in the PGE2 (prostaglandin E2)-biosynthesis pathway. Dinoprostone 145-161 prostaglandin E synthase Mus musculus 9-46 19845504-4 2009 We found that siRNA (small interfering RNA) silencing of mPGES-1 in LLC cells decreased PGE2 synthesis markedly, accompanied by reduced cell proliferation, attenuated Matrigel invasiveness and increased extracellular matrix adhesion. Dinoprostone 88-92 prostaglandin E synthase Mus musculus 57-64 19845504-9 2009 Thus our present approaches provide unequivocal evidence for critical roles of the mPGES-1-dependent PGE2 biosynthetic pathway in both cancer cells and host microenvironments in tumour growth and metastasis. Dinoprostone 101-105 prostaglandin E synthase Mus musculus 83-90 19298395-8 2009 CONCLUSIONS AND IMPLICATIONS: MC is the first natural product to inhibit mPGES-1 that efficiently suppresses PGE(2) formation without significant inhibition of the COX enzymes. Dinoprostone 109-115 prostaglandin E synthase Mus musculus 73-80 19884011-1 2009 Selective inhibition of pro-inflammatory prostaglandin (PG)E(2) formation via microsomal PGE(2) synthase-1 (mPGES-1) might be superior over inhibition of all cyclooxygenase (COX)-derived products by non-steroidal anti-inflammatory drugs (NSAIDs) and coxibs. Dinoprostone 41-63 prostaglandin E synthase Mus musculus 108-115 19524423-6 2009 The deletion of mPGES-1 in mice results in increased prostacyclin I(2) (PGI(2)) formation and marginal effects on the circulatory prostaglandin E(2) (PGE(2)) level. Dinoprostone 130-148 prostaglandin E synthase Mus musculus 16-23 19428335-9 2009 The production of PGE(2) was decreased by HO-1 induction as a result of diminished mPGES-1 protein and mRNA expression. Dinoprostone 18-24 prostaglandin E synthase Mus musculus 83-90 19754408-3 2009 Two inducible enzymes, COX-2 and microsomal prostaglandin E synthase (mPGES), regulate PGE(2) production. Dinoprostone 87-93 prostaglandin E synthase Mus musculus 70-75 19426689-3 2009 In cell-free assays, garcinol inhibited the activity of purified 5-lipoxygenase and blocked the mPGES-1-mediated conversion of PGH2 to PGE2 with IC50 values of 0.1 and 0.3 microM, respectively. Dinoprostone 135-139 prostaglandin E synthase Mus musculus 96-103 19010065-11 2009 These data underline the complexity of the pathways regulating PGE(2) synthesis and suggest the existence of a compensatory mechanism whereby mPGES1 expression can be diminished, potentially reducing the stimulus for further PGE(2) production. Dinoprostone 63-69 prostaglandin E synthase Mus musculus 142-148 19022895-5 2009 Immune-challenged IL-6 knockout mice did not produce fever, in contrast to wild-type mice, but the expression of the inducible PGE(2)-synthesizing enzymes, cyclooxygenase-2 and microsomal prostaglandin E synthase-1, was similarly up-regulated in the hypothalamus of both genotypes, which also displayed similarly elevated PGE(2) levels in the cerebrospinal fluid. Dinoprostone 322-328 prostaglandin E synthase Mus musculus 177-214 19347995-2 2009 The terminal prostaglandin synthases mPGES-1, mPGES-2, and cPGES convert PGH2 into prostaglandin E2. Dinoprostone 83-99 prostaglandin E synthase Mus musculus 37-44 19486608-5 2009 Expression of prostaglandin-E2 synthase (mPGES-1) mRNA in the endometrium was upregulated during the oestrous cycle, while protein expression presented a similar pattern to that of PGE2 concentration in the uterine flushings. Dinoprostone 181-185 prostaglandin E synthase Mus musculus 41-48 18984580-1 2009 Microsomal prostaglandin E synthase type 1 (mPGES-1) converts prostaglandin endoperoxides, generated from arachidonic acid by cyclooxygenases, into prostaglandin E2. Dinoprostone 148-164 prostaglandin E synthase Mus musculus 44-51 19034132-12 2008 CONCLUSIONS: alpha-SMA-positive cells and myofibroblasts express mPGES-1 mRNA and protein, and in addition, mPGES-1 colocalized with COX-2, suggesting that myofibroblasts synthesize prostaglandin E2 and may act on and accelerate corneal wound healing. Dinoprostone 182-198 prostaglandin E synthase Mus musculus 108-115 18614967-0 2008 Role of microsomal prostaglandin E synthase-1 (mPGES1)-derived PGE2 in patency of the ductus arteriosus in the mouse. Dinoprostone 63-67 prostaglandin E synthase Mus musculus 8-45 18547825-11 2008 These data suggest that prolonged therapy with PGE2 blocking agents decreases PGE2 production not only by direct inhibition of COX-2 activity, but also by down-regulating COX-2 and mPGES-1 synthesis in the cartilage. Dinoprostone 47-51 prostaglandin E synthase Mus musculus 181-188 18803240-6 2008 Interestingly, the induction of cyclooxygenase 2 and microsomal prostaglandin E synthase (mPGES), the rate-limiting enzymes for synthesis of PGE2 by LPS, was diminished to a degree that correlated with the absence of IL-6 but not entirely with leptin. Dinoprostone 141-145 prostaglandin E synthase Mus musculus 90-95 18614967-0 2008 Role of microsomal prostaglandin E synthase-1 (mPGES1)-derived PGE2 in patency of the ductus arteriosus in the mouse. Dinoprostone 63-67 prostaglandin E synthase Mus musculus 47-53 18614967-8 2008 We conclude that mPGES1 is critical for PGE2 formation in the ductus but its loss does not entail compensatory up-regulation of other relaxing mechanisms. Dinoprostone 40-44 prostaglandin E synthase Mus musculus 17-23 18626113-1 2008 Microsomal prostaglandin E2 synthase-1 (mPGES-1) catalyzes the formation of prostaglandin E2 (PGE2) from the endoperoxide prostaglandin H2 (PGH2). Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47 18642283-7 2008 CONCLUSIONS: COX-2, functionally coordinated with mPGES-1, is likely to be the limiting enzyme in PGE(2) biosynthesis in HNSCC. Dinoprostone 98-104 prostaglandin E synthase Mus musculus 50-57 18642283-9 2008 Our results support the notion that mPGES-1, cPGES, and EP-1 could be the targets for the development of specific PGE(2)-modifier drugs for HNSCC treatment that could avoid negative side effects of COX-2 selective inhibitors. Dinoprostone 114-120 prostaglandin E synthase Mus musculus 36-43 18524979-1 2008 Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal prostaglandin E(2) (PGE(2)) synthase in the cyclooxygenase pathway. Dinoprostone 62-80 prostaglandin E synthase Mus musculus 0-37 18524979-1 2008 Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal prostaglandin E(2) (PGE(2)) synthase in the cyclooxygenase pathway. Dinoprostone 62-80 prostaglandin E synthase Mus musculus 39-46 18524979-2 2008 Inhibitors of mPGES-1 may block PGE(2) production and relieve inflammatory symptoms. Dinoprostone 32-38 prostaglandin E synthase Mus musculus 14-21 18479189-0 2008 GPx2 counteracts PGE2 production by dampening COX-2 and mPGES-1 expression in human colon cancer cells. Dinoprostone 17-21 prostaglandin E synthase Mus musculus 56-63 18626113-1 2008 Microsomal prostaglandin E2 synthase-1 (mPGES-1) catalyzes the formation of prostaglandin E2 (PGE2) from the endoperoxide prostaglandin H2 (PGH2). Dinoprostone 76-92 prostaglandin E synthase Mus musculus 40-47 18626113-1 2008 Microsomal prostaglandin E2 synthase-1 (mPGES-1) catalyzes the formation of prostaglandin E2 (PGE2) from the endoperoxide prostaglandin H2 (PGH2). Dinoprostone 94-98 prostaglandin E synthase Mus musculus 40-47 19087588-10 2008 Pg-LPS-induced PGE2 synthesis was mainly due to enhanced expression of COX-2 and mPGES-1, whereas cPLA2 played an insignificant role. Dinoprostone 15-19 prostaglandin E synthase Mus musculus 81-88 18484512-4 2008 The downstream enzymes in PG synthesis pathway are: microsomal PGE synthase-1 (mPGES-1), PGF synthase (PGFS) and prostaglandin 9-ketoreductase/carbonyl reductase (CBR1) which catalyzes conversion of PGE 2 into PGF2 alpha. Dinoprostone 199-204 prostaglandin E synthase Mus musculus 79-86 18459759-0 2008 Microsomal prostaglandin E2 synthase-1 (mPGES-1): a novel anti-inflammatory therapeutic target. Dinoprostone 11-27 prostaglandin E synthase Mus musculus 40-47