PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25452446-2 2015 Exploratory analyses of studies that used COX-2 inhibitors have demonstrated potentially superior outcome in patients in whom the urinary metabolite of PGE2 (PGE-M) is suppressed. Prostaglandins E 152-155 mitochondrially encoded cytochrome c oxidase II Homo sapiens 42-47 23682075-10 2013 Combining celecoxib and zileuton was associated with inhibition of both the COX-2 and 5-LO pathways manifested as reduced levels of urinary PGE-M and LTE4. Prostaglandins E 140-143 mitochondrially encoded cytochrome c oxidase II Homo sapiens 76-87 23398566-10 2013 Our results suggest that among many other mediators of eicosanoid signalling n-butyrate massively induces PGE(2) production by increasing the expression of PTGS2 (COX-2) in monocytes following TLR4 and TLR2 activation and induces secretion of LTB(4) and thromboxane B(2). Prostaglandins E 106-109 mitochondrially encoded cytochrome c oxidase II Homo sapiens 163-168 22923191-5 2013 Large amounts of COX-2-derived prostaglandin (PG)E(2) were secreted from LPS-stimulated A549 cells. Prostaglandins E 31-50 mitochondrially encoded cytochrome c oxidase II Homo sapiens 17-22 23636051-4 2013 Considering the importance of the proinflammatory COX-2-derived prostaglandin E2 (PGE2) in inflammation and cancer, Morris and colleagues found that urinary PGE-M is positively associated with obesity, smoking, and lung metastases in patients with breast cancer (4). Prostaglandins E 82-85 mitochondrially encoded cytochrome c oxidase II Homo sapiens 50-55 23059845-13 2013 Moreover, the protective effect observed in hCOX-2-transfected cells was suppressed by addition of DFU (COX-2 selective inhibitor), and mimicked by addition of PGE(2) in non-transfected cells. Prostaglandins E 160-163 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-50 22006370-8 2012 These findings indicate that the COX-2/PGE(2) /EP3 signaling pathway is involved in IGF-1-stimulated mammary tumorigenesis and that COX-2-selective inhibitors may be useful in the prevention or treatment of breast cancer associated with elevated IGF-1 levels in humans. Prostaglandins E 39-42 mitochondrially encoded cytochrome c oxidase II Homo sapiens 33-38 23163543-10 2013 Ex vivo inhibition of COX-1 (thromboxane A(2)) and COX-2 (PGE(2)) at the plasma concentrations of S(+)-ibuprofen corresponding to those found in the plasma following ingestion of 400 mg ibuprofen in dental and other inflammatory pain models provides evidence of the anti-inflammatory mechanism at OTC dosages. Prostaglandins E 58-61 mitochondrially encoded cytochrome c oxidase II Homo sapiens 51-56 22763855-8 2012 Here we show that tumor cells are able to elicit a strong induction of the COX-2/microsomal prostaglandin-E synthase-1 (mPGES-1)/PGE(2) axis in MSCs recruited to the tumor-associated stroma by releasing IL-1, which in turn elicits a mesenchymal/stem cell-like phenotype in the carcinoma cells. Prostaglandins E 121-124 mitochondrially encoded cytochrome c oxidase II Homo sapiens 75-80 22890791-11 2012 In contrast, production of MMP9, CCL4, COX-2, and IL-23 is solely regulated by PGE(2) , but not by LXR activation, offering new perspectives for therapeutic interventions. Prostaglandins E 79-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 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). Prostaglandins E 53-57 mitochondrially encoded cytochrome c oxidase II Homo sapiens 158-163 22696602-5 2012 Treatment of CD cells with either cyclooxygenase-1 (COX-1) or COX-2 inhibitors during exposure to FSS limited the increase in PGE(2) concentration to an equal extent, suggesting COX-1 and COX-2 contribute equally to FSS-induced PGE(2) release. Prostaglandins E 126-129 mitochondrially encoded cytochrome c oxidase II Homo sapiens 62-67 22373734-4 2012 Furthermore, COX-2 contribution to PGE(2) and PGI(2) production evokes and sustains systemic or peripheral inflammatory disease, but it is not involved in the COX-1-mediated GI tract events. Prostaglandins E 35-38 mitochondrially encoded cytochrome c oxidase II Homo sapiens 13-18 22486746-10 2012 The mRNA and protein expression of COX-2, along with production of PGE(2) and PGF(2alpha), are drastically raised by 2.5-5 mmol L(-1) TEGDMA. Prostaglandins E 67-70 mitochondrially encoded cytochrome c oxidase II Homo sapiens 35-40 22934275-2 2012 PGE(2) initiates an EP2/EP4-mediated positive feedback between COX2 and PGE(2) in monocytic precursors, redirecting dendritic cell differentiation to MDSCs. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-67 22626465-9 2012 This may be associated with the significant suppression of PGE(2) /IL-8 secretion via the down-regulated expression of COX-2 and IL-8 at the gene and/or protein levels. Prostaglandins E 59-62 mitochondrially encoded cytochrome c oxidase II Homo sapiens 119-124 22805469-13 2012 CONCLUSIONS AND CLINICAL RELEVANCE: These results suggest that the regulatory effects of LPS on eosinophilic airway inflammation are controlled via the COX-2/PGE(2) axis. Prostaglandins E 158-161 mitochondrially encoded cytochrome c oxidase II Homo sapiens 152-157 22262921-11 2012 In conclusion, inhibition of tumor COX-2-dependent PGE(2) by celecoxib may reduce tumor progression. Prostaglandins E 51-54 mitochondrially encoded cytochrome c oxidase II Homo sapiens 35-40 22308510-3 2012 We observed an enhanced production of PGE(2) in cocultures of HNSCC cell lines and fibroblasts, which was consistent with an upregulation of COX-2 and microsomal PGE-synthase-1 (mPGES-1) in fibroblasts. Prostaglandins E 38-41 mitochondrially encoded cytochrome c oxidase II Homo sapiens 141-146 22166248-2 2012 Most of the COX-2 tumor-inducing effects are believed to be mediated through overproduction of prostaglandin E(2) (PGE(2)), which can be measured using a urinary metabolite of PGE(2), PGE-M. Urinary PGE-M was assessed in a case-control study of colorectal adenoma. Prostaglandins E 115-118 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-17 22410675-1 2012 Five primary prostanoids are synthesized by the cyclooxygenase enzymes, COX-1 and COX-2: the prostaglandins PGE(2), PGF(2alpha), PGI(2), PGD(2) and thromboxane A2. Prostaglandins E 108-111 mitochondrially encoded cytochrome c oxidase II Homo sapiens 82-87 22166248-2 2012 Most of the COX-2 tumor-inducing effects are believed to be mediated through overproduction of prostaglandin E(2) (PGE(2)), which can be measured using a urinary metabolite of PGE(2), PGE-M. Urinary PGE-M was assessed in a case-control study of colorectal adenoma. Prostaglandins E 176-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-17 22166248-2 2012 Most of the COX-2 tumor-inducing effects are believed to be mediated through overproduction of prostaglandin E(2) (PGE(2)), which can be measured using a urinary metabolite of PGE(2), PGE-M. Urinary PGE-M was assessed in a case-control study of colorectal adenoma. Prostaglandins E 176-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-17 22166248-2 2012 Most of the COX-2 tumor-inducing effects are believed to be mediated through overproduction of prostaglandin E(2) (PGE(2)), which can be measured using a urinary metabolite of PGE(2), PGE-M. Urinary PGE-M was assessed in a case-control study of colorectal adenoma. Prostaglandins E 176-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-17 22135046-8 2012 Finally, levels of cervical COX-2 correlated with urinary PGE-M levels (P = 0.005). Prostaglandins E 58-61 mitochondrially encoded cytochrome c oxidase II Homo sapiens 28-33 21937683-1 2011 Prostaglandin E(2) (PGE(2)), the most abundant COX-2-derived prostaglandin found in colorectal cancer, promotes tumor cell proliferation and survival via multiple signaling pathways. Prostaglandins E 20-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-52 22346776-5 2011 RESULTS: Both PGE(2) and PGI(2) productions were almost completely inhibited by the depletion of COX-2. Prostaglandins E 14-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-102 21840302-2 2011 Non-steroidal anti-inflammatory drugs are considered to have chemo-preventive effects on these diseases by reducing the biosynthesis of PGE(2) via their inhibition of COX-2. Prostaglandins E 136-139 mitochondrially encoded cytochrome c oxidase II Homo sapiens 167-172 22002714-2 2011 Prostaglandin E2 (PGE(2)) is the most abundant prostanoid in the human body, and synthesis of PGE(2) is driven by cyclooxygenase enzymes including COX-2. Prostaglandins E 18-21 mitochondrially encoded cytochrome c oxidase II Homo sapiens 147-152 22002714-2 2011 Prostaglandin E2 (PGE(2)) is the most abundant prostanoid in the human body, and synthesis of PGE(2) is driven by cyclooxygenase enzymes including COX-2. Prostaglandins E 94-97 mitochondrially encoded cytochrome c oxidase II Homo sapiens 147-152 21926111-0 2011 Colon tumour cells increase PGE(2) by regulating COX-2 and 15-PGDH to promote survival during the microenvironmental stress of glucose deprivation. Prostaglandins E 28-31 mitochondrially encoded cytochrome c oxidase II Homo sapiens 49-54 21964530-2 2011 Overexpression of COX-2 or 5-LOX increases levels of PGE-2 and 5-HETE, respectively. Prostaglandins E 53-56 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 22122764-4 2011 Among upregulated genes in tumour tissue is COX-2 which synthesises large amounts of PGE(2). Prostaglandins E 85-88 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-49 21807015-4 2011 Our results showed that among the tested molecules, all sensitizers specifically prevent the production of PMA/LPS-induced COX-2 metabolites (PGE(2,) TxB(2) and PGD(2)), eugenol and cinnamaldehyde inhibiting also the production of IL-1beta and TNF-alpha. Prostaglandins E 142-145 mitochondrially encoded cytochrome c oxidase II Homo sapiens 123-128 22066110-7 2011 CONCLUSION: These results demonstrate that COX-2 derived PGE(2) is up-regulated and COX-2 inhibitor may have an anti-angiogenic effect in the colon cancer cells resistant to 5-FU. Prostaglandins E 57-60 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-48 21147091-5 2011 The expression of COX-2, iNOS, and their products PGE(2) and NO also increased. Prostaglandins E 50-53 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-23 21868314-7 2011 Both the non-selective COX inhibitor indomethacin and the selective COX-2 inhibitor SC-236 completely abolished EGF-induced PGE(2) release, and suppressed the mitogenic effect of EGF. Prostaglandins E 124-127 mitochondrially encoded cytochrome c oxidase II Homo sapiens 68-73 21699992-1 2011 Cultured preadipocytes enhance the synthesis of prostaglandin (PG) E(2) and PGF(2alpha) involving the induction of cyclooxygenase (COX)-2 during the growth phase upon stimulation with a mixture of phorbol 12-myristate 13-acetate, a mitogenic factor, and calcium ionophore A23187. Prostaglandins E 48-68 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-137 21209362-4 2011 The present results show that progressive accumulation of collagen I in the extracellular medium induces a significant increase of COX-2 expression in human mesangial cells, resulting in an enhancement in PGE(2) production. Prostaglandins E 205-208 mitochondrially encoded cytochrome c oxidase II Homo sapiens 131-136 20082309-5 2010 Higher concentrations of IL-1beta-induced COX-2 mRNA and protein associated with an increase in PGE(2) and cAMP, and all of these parameters were potentiated by bFGF. Prostaglandins E 96-99 mitochondrially encoded cytochrome c oxidase II Homo sapiens 42-47 20662025-9 2010 CONCLUSIONS: The inhibition of PGE(2) production by LLL irradiation in compressed PDL cells may be due to the inhibition of COX-2 and cPLA(2)-alpha expression and is most pronounced immediately after the application of a compressive force. Prostaglandins E 31-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 124-129 20159031-3 2010 Elevated levels of COX-2 and concomitant overproduction of PGE(2) are often found in human cancers. Prostaglandins E 59-62 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24 21804201-2 2011 Nonsteroidal anti-inflammatory drugs (NSAIDs), inhibitors of COX-1 and/or COX-2, suppress inflammatory pain by reducing generation of prostanoids, mainly PGE(2), while they exhibit gastrointestinal, renal and cardiovascular toxicities. Prostaglandins E 154-157 mitochondrially encoded cytochrome c oxidase II Homo sapiens 74-79 20880055-14 2011 By contrast, COX-2 contributes substantially to the biosynthesis of PGE(2) . Prostaglandins E 68-71 mitochondrially encoded cytochrome c oxidase II Homo sapiens 13-18 21148739-5 2011 Use of pharmacological inhibitors suggested that the modulation in the expression of COX-2 and thereby the levels of PGE(2) and PGD(2) in endothelial cells by Ln is mediated through the alpha(6)beta(4) integrin-p38MAPK (mitogen-activated protein kinase)-NF-kappaB signaling pathway. Prostaglandins E 117-120 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-90 21760774-2 2011 Besides, PGE(2), a product of COX-2, was also under research as to whether it is involved in the upregulation of MMP-9 expression by COX-2. Prostaglandins E 9-12 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 21760774-2 2011 Besides, PGE(2), a product of COX-2, was also under research as to whether it is involved in the upregulation of MMP-9 expression by COX-2. Prostaglandins E 9-12 mitochondrially encoded cytochrome c oxidase II Homo sapiens 133-138 20830783-4 2010 The COX-2-specific inhibitor Celecoxib suppressed VEGF-C expression whereas the main COX-2 metabolite PGE(2) elevated VEGF-C expression in Anip973 and AGZY83-a cells in positive and negative experiments. Prostaglandins E 102-105 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-90 20830783-10 2010 The present data suggest that COX-2 regulates VEGF-C expression via the PGE(2) pathway, and that EP1/EP4 receptors are involved in PGE(2)-mediated VEGF-C production. Prostaglandins E 72-75 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 20718752-10 2010 Non-selective and selective COX-2 inhibitors, indomethacin and NS398, inhibited CIP-induced PGE(2) and cAMP production. Prostaglandins E 92-95 mitochondrially encoded cytochrome c oxidase II Homo sapiens 28-33 20689756-5 2010 EPA-FFA in cell culture medium was incorporated rapidly into phospholipid membranes of HCA-7 human CRC cells and acted as a substrate for COX-2, leading to reduced synthesis of PGE(2) and generation of PGE(3). Prostaglandins E 177-180 mitochondrially encoded cytochrome c oxidase II Homo sapiens 138-143 20689756-5 2010 EPA-FFA in cell culture medium was incorporated rapidly into phospholipid membranes of HCA-7 human CRC cells and acted as a substrate for COX-2, leading to reduced synthesis of PGE(2) and generation of PGE(3). Prostaglandins E 202-205 mitochondrially encoded cytochrome c oxidase II Homo sapiens 138-143 20689756-8 2010 We conclude that EPA-FFA drives a COX-2-dependent "PGE(2)-to-PGE(3) switch" in human CRC cells and that PGE(3) acts as a partial agonist at the PGE(2) EP4 receptor. Prostaglandins E 51-54 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 20689756-8 2010 We conclude that EPA-FFA drives a COX-2-dependent "PGE(2)-to-PGE(3) switch" in human CRC cells and that PGE(3) acts as a partial agonist at the PGE(2) EP4 receptor. Prostaglandins E 61-64 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 20689756-8 2010 We conclude that EPA-FFA drives a COX-2-dependent "PGE(2)-to-PGE(3) switch" in human CRC cells and that PGE(3) acts as a partial agonist at the PGE(2) EP4 receptor. Prostaglandins E 61-64 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 20689756-8 2010 We conclude that EPA-FFA drives a COX-2-dependent "PGE(2)-to-PGE(3) switch" in human CRC cells and that PGE(3) acts as a partial agonist at the PGE(2) EP4 receptor. Prostaglandins E 61-64 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 20733946-4 2010 TGF-beta stimulation of human CD4(+) T cells induced COX-2-dependent production of PGE(2). Prostaglandins E 83-86 mitochondrially encoded cytochrome c oxidase II Homo sapiens 53-58 20112284-6 2010 Moreover, COX-2-derived PGE(2) production appeared to involve in LPS-induced VCAM-1 expression which was attenuated by pretreatment with selective COX-2 inhibitors (NS-398 and celecoxib), transfection with COX-2 siRNA, or PGE(2) receptor antagonists. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 10-15 20112284-6 2010 Moreover, COX-2-derived PGE(2) production appeared to involve in LPS-induced VCAM-1 expression which was attenuated by pretreatment with selective COX-2 inhibitors (NS-398 and celecoxib), transfection with COX-2 siRNA, or PGE(2) receptor antagonists. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 147-152 20112284-6 2010 Moreover, COX-2-derived PGE(2) production appeared to involve in LPS-induced VCAM-1 expression which was attenuated by pretreatment with selective COX-2 inhibitors (NS-398 and celecoxib), transfection with COX-2 siRNA, or PGE(2) receptor antagonists. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 147-152 20180883-3 2010 In this study, we investigated the relationship between CXCL12, cyclooxygenase (COX)-2 and PGE(2) in human brain cells. Prostaglandins E 91-94 mitochondrially encoded cytochrome c oxidase II Homo sapiens 64-86 20004562-2 2010 Here, we investigated the role of different phospholipases (PL)A(2) in supplying arachidonic acid (AA) for COX-2-dependent PGE(2) generation and signaling pathways involved in activation of colon cancer cells by a physiologically relevant stimulus. Prostaglandins E 123-126 mitochondrially encoded cytochrome c oxidase II Homo sapiens 107-112 20074562-7 2010 These results suggest that inhibition of COX-1, despite causing intestinal hypermotility, bacterial invasion and iNOS expression, up-regulates the expression of COX-2, and the PGE(2) derived from COX-2 counteracts the deleterious events caused by COX-1 inhibition and maintains mucosal integrity. Prostaglandins E 176-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 196-201 20144869-3 2010 In addition, it displayed PGE(2) inhibition in a cell-based assay (0.42microM) and had over 238-fold selectivity for mPGES-1 over COX-2 and over 200-fold selectivity for mPGES-1 over 6-keto PGF(1alpha). Prostaglandins E 26-29 mitochondrially encoded cytochrome c oxidase II Homo sapiens 130-135 20004562-8 2010 Our results indicate that hypertonic stress activates PGE(2) generation by Caco-2 cells through a mechanism dependent on MAP kinase-regulated AA mobilization, increased cPLA(2)-alpha activity, and COX-2 induction. Prostaglandins E 54-57 mitochondrially encoded cytochrome c oxidase II Homo sapiens 197-202 20606295-10 2010 COX-2 and its derived PGE(2) are important factors for bFGF-induced in vivo angiogenesis. Prostaglandins E 22-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 19471853-6 2010 Also, we show that cyclooxygenase (COX)-1 and COX-2 play an important role in hypoxia-induced PGE(2) production, possibly via a mechanism involving changes in their respective activity levels under low oxygen conditions. Prostaglandins E 94-97 mitochondrially encoded cytochrome c oxidase II Homo sapiens 46-51 19843689-3 2009 In ever smokers, increased levels of urinary PGE-M reflect increased COX-2 activity. Prostaglandins E 45-48 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74 19846775-2 2009 In PGE(2) biosynthesis, cyclooxygenases (COX-1/COX-2) convert arachidonic acid to PGH(2), which can be isomerized to PGE(2) by microsomal PGE-synthase-1 (MPGES-1). Prostaglandins E 3-6 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-52 19846775-2 2009 In PGE(2) biosynthesis, cyclooxygenases (COX-1/COX-2) convert arachidonic acid to PGH(2), which can be isomerized to PGE(2) by microsomal PGE-synthase-1 (MPGES-1). Prostaglandins E 117-120 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-52 19846775-2 2009 In PGE(2) biosynthesis, cyclooxygenases (COX-1/COX-2) convert arachidonic acid to PGH(2), which can be isomerized to PGE(2) by microsomal PGE-synthase-1 (MPGES-1). Prostaglandins E 117-120 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-52 19843689-12 2009 Possibly, HNSCC patients with high COX-2 activity manifested by elevated urinary PGE-M will benefit from treatment with a COX-2 inhibitor. Prostaglandins E 81-84 mitochondrially encoded cytochrome c oxidase II Homo sapiens 35-40 19843689-12 2009 Possibly, HNSCC patients with high COX-2 activity manifested by elevated urinary PGE-M will benefit from treatment with a COX-2 inhibitor. Prostaglandins E 81-84 mitochondrially encoded cytochrome c oxidase II Homo sapiens 122-127 19428338-7 2009 IL-17A up-regulates cyclooxygenase (COX)-2 gene expression and thereby increases the level of prostaglandin (PG) E(2) in differentiated adipocyes. Prostaglandins E 94-114 mitochondrially encoded cytochrome c oxidase II Homo sapiens 20-42 19558494-7 2009 Further, 12-(R)-HETE, 12-(S)-HETE and PGE(2) upregulated the p-ERK and p-Akt levels, suggesting the involvement of ERK and Akt pathways in the 12-LOX- and COX-2-mediated regulation of growth in A431 cells. Prostaglandins E 38-41 mitochondrially encoded cytochrome c oxidase II Homo sapiens 155-160 19464432-2 2009 COX-1 is a constitutive enzyme while the expression of COX-2 is highly stimulated in the event of inflammatory processes, leading to the production of large amounts of prostaglandins (PGs), in particular PGE(2) and PGI(2), which are pro-inflammatory mediators. Prostaglandins E 204-207 mitochondrially encoded cytochrome c oxidase II Homo sapiens 55-60 19530988-1 2009 BACKGROUND: Most NSAIDs function by inhibiting biosynthesis of PGE(2) by inhibition of COX-1 and/or COX-2. Prostaglandins E 63-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 100-105 19818596-1 2009 BACKGROUND: Cyclooxygenase (COX)-2 is frequently overexpressed in non-small cell lung cancer (NSCLC) and results in increased levels of prostaglandin E2 (PGE(2)), an important signalling molecule implicated in tumourigenesis. Prostaglandins E 154-157 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-34 19638428-1 2009 Evidence points towards a pivotal role for cyclooxygenase (COX)-2 in promoting colorectal tumorigenesis through increasing prostaglandin E(2) (PGE(2)) levels. Prostaglandins E 143-146 mitochondrially encoded cytochrome c oxidase II Homo sapiens 43-65 18579232-1 2009 We demonstrate that serum IgG in chagasic patients interacting with the second extracellular loop of human cardiac M(2) muscarinic acetylcholine receptors (M(2) mAChR) trigger the production of PGE(2) and NO, that in turn induces COX-2/iNOS mRNA expression. Prostaglandins E 194-197 mitochondrially encoded cytochrome c oxidase II Homo sapiens 230-235 19601807-6 2009 Acetylating nonsteroidal anti-inflammatory drugs (NSAIDs), like aspirin, switches COX-2 from forming PGE(2) (promoting tumorigenesis) to 15-epi-LXA(4) (antitumorigenesis). Prostaglandins E 101-104 mitochondrially encoded cytochrome c oxidase II Homo sapiens 82-87 19416639-3 2009 The cloned stable transfectants with COX-1 or COX-2 exhibited higher expression levels of their corresponding mRNA and proteins, and greater production of PGE(2) upon stimulation with free arachidonic acid or A23187 than the parent cells and the transfectants with vector only. Prostaglandins E 155-158 mitochondrially encoded cytochrome c oxidase II Homo sapiens 46-51 19276291-13 2009 Urinary PGE-M is a promising biomarker for predicting response to COX-2 inhibition in NSCLC. Prostaglandins E 8-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 66-71 19126433-6 2009 In conclusion, colonic longitudinal muscle contraction is augmented by COX-2 activity, most likely via PGE(2) acting at EP(1) receptors. Prostaglandins E 103-106 mitochondrially encoded cytochrome c oxidase II Homo sapiens 71-76 19101538-6 2009 The intestinal level of PGE(2) dramatically decreased in response to administration of COX-1- and COX-2-selective inhibitors, and exogenously administered PGE(2) suppressed the exacerbation of colitis by NSAIDs. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 98-103 19439810-3 2009 Prostaglandin E(2) and thromboxan A(2) which are a products of two izoformes of cyclooxygenases (COX-1 and COX-2) in macrophages, play an important role in this process. Prostaglandins E 0-15 mitochondrially encoded cytochrome c oxidase II Homo sapiens 107-112 19439810-8 2009 Monocytes were differentiated to macrophages and cultured with 30 muM CLAs or linoleic acid for 48 h. The COX-1 and COX-2 products - PGE(2) and TXB(2), were measured by ELISA method. Prostaglandins E 133-136 mitochondrially encoded cytochrome c oxidase II Homo sapiens 116-121 19197941-4 2009 This inhibition was mediated by the COX-2-dependent production of prostaglandin E2 (PGE(2)) and by MSC through EP2 and EP4 inhibitory receptors expressed by Vgamma9Vdelta2 T lymphocytes. Prostaglandins E 84-87 mitochondrially encoded cytochrome c oxidase II Homo sapiens 36-41 19101538-9 2009 This study provides evidence that inhibition of both COX-1 and COX-2 and the resulting dramatic decrease in the intestinal level of PGE(2) is responsible for NSAID-dependent exacerbation of DSS-induced colitis. Prostaglandins E 132-135 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-68 19116880-5 2009 COX-2 promoter activity was determined by luciferase assays, protein expression by Western blotting, and secretion of prostaglandin E(2) (PGE(2)) by ELISA. Prostaglandins E 138-141 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 19754418-5 2009 mPGES-1 is functionally coupled to COX-2 being responsible for excessive PGE(2) generation connected to pathologies and current knowledge suggests key roles of mPGES-1 in inflammation, pain, fever, atherosclerosis, and tumorigenesis. Prostaglandins E 1-4 mitochondrially encoded cytochrome c oxidase II Homo sapiens 35-40 18790994-5 2008 The tryptase-stimulated PGE(2) production was inhibited by treating HSAEC with the cyclooxygenase (COX)-1-selective inhibitor SC-560 and the nonselective COX inhibitor aspirin but not by the COX-2-selective inhibitor CAY10404, indicating that the early release of arachidonic acid is metabolized by constitutive COX-1 to form PGE(2) in tryptase-stimulated HSAEC. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 191-196 19399184-2 2009 Current data suggest that resistance to treatment in HER2 cancers may be a consequence of NF-kappaB overexpression and increased COX2-derived prostaglandin E2 (PGE(2)). Prostaglandins E 160-163 mitochondrially encoded cytochrome c oxidase II Homo sapiens 129-133 19399184-12 2009 These data add to previous reports of an anti-tumor effect of t10c12 CLA and suggest an effect on the HER2 oncogene that may be through CLA mediated downregulation of COX2-derived PGE(2). Prostaglandins E 180-183 mitochondrially encoded cytochrome c oxidase II Homo sapiens 167-171 18842828-6 2008 COX-2 induction was associated with increased PGE(2) release. Prostaglandins E 46-49 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 18601905-6 2008 The abrogation of apoptosis is completely reversed by specific COX-2 inhibition, suggesting that HBx blocks p53-induced apoptosis via activation of COX-2/PGE(2) pathway. Prostaglandins E 154-157 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-68 18718465-4 2008 Exposure of ECs to PGE(2) increased ERK1/2 phosphorylation, COX-2 induction, 6-keto-PGF(1alpha) release and EC proliferation. Prostaglandins E 19-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 60-65 18725385-7 2008 Importantly, rendering normal and malignant MECs Cox-2 deficient inhibited their production of PGE(2) and acquisition of an EMT morphology as well as potentiated their nuclear accumulation of Smad2/3 and transcription of plasminogen activator inhibitor-1 and p15 messenger RNA. Prostaglandins E 95-98 mitochondrially encoded cytochrome c oxidase II Homo sapiens 49-54 18601905-6 2008 The abrogation of apoptosis is completely reversed by specific COX-2 inhibition, suggesting that HBx blocks p53-induced apoptosis via activation of COX-2/PGE(2) pathway. Prostaglandins E 154-157 mitochondrially encoded cytochrome c oxidase II Homo sapiens 148-153 18462443-6 2008 COX-2 expression was analysed by western immunoblotting, PGE(2) production by enzyme immunoassay and CTGF expression, and type I and III collagen expression by reverse transcriptase PCR and western immunoblotting. Prostaglandins E 57-60 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 18818458-1 2008 In the skeleton, prostaglandins, mainly PGE(2) produced by osteoblasts under COX-2 stimulation, play either a stimulatory or an inhibitory role in bone metabolism, depending on the physiological or pathological conditions. Prostaglandins E 40-43 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-82 18571826-5 2008 We analyzed COX-1, COX-2 and cPLA(2) steady state mRNA levels for 100-400 microM PPD after 2-24 h and found clear COX-2 induction for 400 microM PPD after 24 h, while cPLA(2) and COX-1 levels were increased dose-dependently between 8 and 24 h. Increased expression was accompanied by enhanced prostaglandin E(2) and F(2alpha) formation. Prostaglandins E 293-308 mitochondrially encoded cytochrome c oxidase II Homo sapiens 114-119 18414668-6 2008 Interestingly, we found that COX-2-associate PGE(2) production activated by influenza virus infection was significantly suppressed by over-expression of IL-32 but increased by IL-32-specific siRNA, suggesting there was a feedback mechanism between IL-32 and COX-2. Prostaglandins E 45-48 mitochondrially encoded cytochrome c oxidase II Homo sapiens 29-34 18358504-2 2008 RIAA inhibited LPS-stimulated PGE(2) formation with >200-fold selectivity of COX-2 (IC(50)=1.3 microg/ml) over COX-1 (IC(50)>289 microg/ml). Prostaglandins E 30-33 mitochondrially encoded cytochrome c oxidase II Homo sapiens 80-85 18493301-8 2008 Co-incubation of Nuc with COX-2-expressing neutrophil lysates also increased their capacity to produce PGE(2). Prostaglandins E 103-106 mitochondrially encoded cytochrome c oxidase II Homo sapiens 26-31 18414668-6 2008 Interestingly, we found that COX-2-associate PGE(2) production activated by influenza virus infection was significantly suppressed by over-expression of IL-32 but increased by IL-32-specific siRNA, suggesting there was a feedback mechanism between IL-32 and COX-2. Prostaglandins E 45-48 mitochondrially encoded cytochrome c oxidase II Homo sapiens 258-263 20852730-10 2008 The number of responsive peaks also decreased slightly yet significantly when either the COX-2/PGE(2) or the NOS/nitric oxide pathway was disrupted. Prostaglandins E 95-98 mitochondrially encoded cytochrome c oxidase II Homo sapiens 89-94 18285354-7 2008 Pre-treatment with the MAPK inhibitors SP600125 (JNK inhibitor), SB202190 (p38 inhibitor) or PD98059 (ERK inhibitor) significantly inhibited AGE-BSA induction of COX-2 expression and production of PGE(2). Prostaglandins E 197-200 mitochondrially encoded cytochrome c oxidase II Homo sapiens 162-167 18261978-5 2008 Furthermore, NSA9 reduced the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 mRNA and protein, which control the production of NO and PGE(2), respectively. Prostaglandins E 157-160 mitochondrially encoded cytochrome c oxidase II Homo sapiens 77-99 18029351-10 2008 Furthermore, COX-2 induction or expression markedly enhanced iNOS-induced cPLA(2)alpha S-nitrosylation and activation, leading to 9-, 23-, and 20-fold increase of AA release and 100-, 38-, and 88-fold of PGE(2) production in A549, SG231, and HEK293 cells, respectively, whereas COX-2 alone leads to less than 2-fold change. Prostaglandins E 204-207 mitochondrially encoded cytochrome c oxidase II Homo sapiens 13-18 18209033-9 2008 Furthermore, the up-regulation of PGE(2) and PGI(2) production was markedly down-regulated by indomethacin and a selective COX-2 inhibitor. Prostaglandins E 34-37 mitochondrially encoded cytochrome c oxidase II Homo sapiens 123-128 17918156-1 2008 Recent studies have shown that inhibition of cyclooxygenases (e.g. COX-2) exerts antitumorigenic effects on hepatocellular carcinomas (HCCs), which are to a significant extent due to the abrogation of PGE(2) synthesis. Prostaglandins E 201-204 mitochondrially encoded cytochrome c oxidase II Homo sapiens 67-72 23392784-4 2007 Following peripheral trauma or injury, inflammatory mediators such as phospholipase A(2) are upregulated, inducing the release of arachidonic acid, which is then converted to prostanoids such as prostaglandin E(2) (PGE(2)) via the action of the enzyme cyclo-oxygenase (COX)-2. Prostaglandins E 215-218 mitochondrially encoded cytochrome c oxidase II Homo sapiens 252-275 17673564-7 2007 The biosynthesis of PGE(2) was reduced between 50 and 80% (P < 0.05 vs. vehicle) in the presence of either COX-1- or COX-2-selective blockers, demonstrating that both isoforms are enzymatically active. Prostaglandins E 20-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 120-125 17825288-8 2007 Upregulation of iNOS and COX-2 resulted in increased production of NO and PGE(2). Prostaglandins E 74-77 mitochondrially encoded cytochrome c oxidase II Homo sapiens 25-30 18030357-3 2007 Cyclooxygenase (Cox-2), a pro-inflammatory mediator, is a CREB target that induces prostaglandin E(2) (PGE(2)) and suppresses apoptosis. Prostaglandins E 103-106 mitochondrially encoded cytochrome c oxidase II Homo sapiens 16-21 17878511-3 2007 PGE(2) is formed from arachidonic acid by cyclooxygenase (COX-1 and COX-2)-catalyzed formation of prostaglandin H(2) (PGH(2)) and further transformation by PGE synthases. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 68-73 17254563-9 2007 The inhibitors of cyclooxygenase (COX)-2 and protein kinase A (PKA) at 100 microM inhibited the actions of nicotine, suggesting that the endogenous prostaglandin E(2) might be, at least, partially involved the actions of nicotine. Prostaglandins E 148-163 mitochondrially encoded cytochrome c oxidase II Homo sapiens 18-40 17546626-3 2007 On the other hand, 15-hydroxy-prostaglandin dehydrogenase (15-PGDH), which is involved in the degradation pathway of PG including PGE(2,) thus counteracting the activities of COX-2 and PGES, was found to be downregulated in human epithelial tumors, indicating a tumor suppressor activity of this enzyme. Prostaglandins E 130-133 mitochondrially encoded cytochrome c oxidase II Homo sapiens 175-180 17403097-9 2007 VSMC ability to synthesize PGE(2) and PGI(2) fitted mPGES-1 and COX-2 expression, respectively. Prostaglandins E 27-30 mitochondrially encoded cytochrome c oxidase II Homo sapiens 64-69 17403097-11 2007 Results from COX-1 and COX-2 silencing and selective inhibition showed that both COX-1 and COX-2 were involved in the biosynthesis of PGE(2) and their relative contribution depended on the time of incubation with IL-1beta. Prostaglandins E 134-137 mitochondrially encoded cytochrome c oxidase II Homo sapiens 23-28 17403097-11 2007 Results from COX-1 and COX-2 silencing and selective inhibition showed that both COX-1 and COX-2 were involved in the biosynthesis of PGE(2) and their relative contribution depended on the time of incubation with IL-1beta. Prostaglandins E 134-137 mitochondrially encoded cytochrome c oxidase II Homo sapiens 91-96 17629358-9 2007 We found that these cells produce PGE(2) by synthesizing COX-2 and microsomal prostaglandin E synthase-1 (mPGES-1) in response to excitotoxicity and neuroinflammation. Prostaglandins E 34-37 mitochondrially encoded cytochrome c oxidase II Homo sapiens 57-62 17131340-8 2007 The molecular modeling of FPA-306 in the COX-2 active site showed that FPA-306 is potentially able to inhibit the activity of enzyme by blocking the active site, thereby resulting in decreased PGE(2) production. Prostaglandins E 193-196 mitochondrially encoded cytochrome c oxidase II Homo sapiens 41-46 17342254-8 2007 These results suggest that LPS enhances the production of nicotine-induced PGE(2) by an increase in COX-2 expression in osteoblasts, that nicotine-LPS-induced PGE2 interacts with the osteoblast Ep4 receptor primarily in autocrine or paracrine mode, and that the nicotine-LPS-induced PGE(2) then decreases ALPase activity and increases M-CSF expression. Prostaglandins E 75-78 mitochondrially encoded cytochrome c oxidase II Homo sapiens 100-105 17131340-2 2007 Expression of COX-2 is detectable in 75% of PCs among which 50% showed overexpression, suggesting the importance of COX-2 enzyme and its metabolic product prostaglandin E2 (PGE(2)) in PC. Prostaglandins E 173-176 mitochondrially encoded cytochrome c oxidase II Homo sapiens 14-19 17131340-2 2007 Expression of COX-2 is detectable in 75% of PCs among which 50% showed overexpression, suggesting the importance of COX-2 enzyme and its metabolic product prostaglandin E2 (PGE(2)) in PC. Prostaglandins E 173-176 mitochondrially encoded cytochrome c oxidase II Homo sapiens 116-121 17308114-5 2007 Moreover, COX-1/COX-2 inhibitors block ET-induced PGE(2) and VEGF secretion, matrix metalloproteinase (MMP) activation, and cell invasion, indicating that both enzymes function as downstream mediators of ET-induced invasive properties. Prostaglandins E 50-53 mitochondrially encoded cytochrome c oxidase II Homo sapiens 16-21 17046175-10 2007 These results suggest that IL-1beta-induced catabolic action on tendon fibroblasts occurs via the upregulation of two key inflammatory mediators, cPLA(2) and COX-2, which are responsible for the synthesis of PGE(2). Prostaglandins E 208-211 mitochondrially encoded cytochrome c oxidase II Homo sapiens 158-163 17197641-11 2007 COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans. Prostaglandins E 158-161 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 17130490-2 2006 Activated monocytes express cyclooxygenase (COX)-2, promoting prostaglandin-E(2) (PGE(2)) secretion, whereas COX-1 expression is constitutive. Prostaglandins E 82-85 mitochondrially encoded cytochrome c oxidase II Homo sapiens 28-50 17178883-8 2006 Thus, PPARdelta induces COX-2 expression and the COX-2-derived PGE(2) further activates PPARdelta via cPLA(2)alpha. Prostaglandins E 63-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 49-54 16957004-5 2006 Experimental studies demonstrate that prostaglandin E(2) (PGE(2)), mainly derived from the COX-2 reaction, is an important mediator, acting as a retrograde messenger via a presynaptic PGE(2) subtype 2 receptor (EP(2)) in modulation of synaptic events. Prostaglandins E 58-61 mitochondrially encoded cytochrome c oxidase II Homo sapiens 91-96 17085321-6 2006 These results argue against redundancy in pathways for PGE(2) synthesis, and suggest that at various stages of inflammation different stimuli may influence ERK activation and COX-2 expression, so as to tightly regulate the kinetics and amount of PGE(2) produced by airway epithelial cells in response to lung inflammation. Prostaglandins E 246-249 mitochondrially encoded cytochrome c oxidase II Homo sapiens 175-180 16966384-8 2006 Consistent with this, we found that COX-2 and PKA inhibitors prevented the effects of nicotine on adhesion molecule expression and cytokine production, indicating that the mechanism of action of nicotine may be via endogenous PGE(2) production. Prostaglandins E 226-229 mitochondrially encoded cytochrome c oxidase II Homo sapiens 36-41 17097894-12 2006 Leptin suppresses hCG-induced PGE(2) formation through the inhibition of COX-2 and mPGES expression. Prostaglandins E 30-33 mitochondrially encoded cytochrome c oxidase II Homo sapiens 73-78 16957004-5 2006 Experimental studies demonstrate that prostaglandin E(2) (PGE(2)), mainly derived from the COX-2 reaction, is an important mediator, acting as a retrograde messenger via a presynaptic PGE(2) subtype 2 receptor (EP(2)) in modulation of synaptic events. Prostaglandins E 184-187 mitochondrially encoded cytochrome c oxidase II Homo sapiens 91-96 16357062-11 2006 IL-1beta-stimulated HRG expression and release were also inhibited by celecoxib, and exogenous PGE(2) restored this inhibitory effect, suggesting the activation of an IL-1beta-COX-2-PGE(2) pathway that culminates in the release of HRG from fibroblasts. Prostaglandins E 95-98 mitochondrially encoded cytochrome c oxidase II Homo sapiens 176-181 16818638-8 2006 These data indicate that PGDH may serve a tumor suppressor function in colorectal cancer and provide a possible COX-2-independent way to target PGE(2) to inhibit cancer progression. Prostaglandins E 144-147 mitochondrially encoded cytochrome c oxidase II Homo sapiens 112-117 16818642-8 2006 In addition, elevated levels of PGE(2) in hypoxic colorectal tumor cells enhance vascular endothelial growth factor expression and HIF-1 transcriptional activity by activating the mitogen-activated protein kinase pathway, showing a potential positive feedback loop that contributes to COX-2 up-regulation during hypoxia. Prostaglandins E 32-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 285-290 16574793-5 2006 Seminal plasma and PGE(2) signaling via the EP4 receptor induced the activation of cyclooxygenase (COX)-2 and vascular endothelial growth factor (VEGF) promoters, expression of COX-2 and VEGF mRNA and protein, and secretion of VEGF protein into the culture medium. Prostaglandins E 19-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 83-105 16574793-5 2006 Seminal plasma and PGE(2) signaling via the EP4 receptor induced the activation of cyclooxygenase (COX)-2 and vascular endothelial growth factor (VEGF) promoters, expression of COX-2 and VEGF mRNA and protein, and secretion of VEGF protein into the culture medium. Prostaglandins E 19-22 mitochondrially encoded cytochrome c oxidase II Homo sapiens 177-182 16476713-11 2006 These data suggest that PGE(2) blocking agents may decrease PGE(2) production not only by direct COX-2 inhibition but also by down regulating COX-2 expression and synthesis. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-102 16476713-11 2006 These data suggest that PGE(2) blocking agents may decrease PGE(2) production not only by direct COX-2 inhibition but also by down regulating COX-2 expression and synthesis. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 142-147 16861295-8 2006 These results suggest that the inhibitory effects of clodronate on tooth movement and osteoclasts may be due, at least in part, to the inhibition of COX-2-dependent PGE(2) production and RANKL expression in PDL cells. Prostaglandins E 165-168 mitochondrially encoded cytochrome c oxidase II Homo sapiens 149-154 16357062-11 2006 IL-1beta-stimulated HRG expression and release were also inhibited by celecoxib, and exogenous PGE(2) restored this inhibitory effect, suggesting the activation of an IL-1beta-COX-2-PGE(2) pathway that culminates in the release of HRG from fibroblasts. Prostaglandins E 182-185 mitochondrially encoded cytochrome c oxidase II Homo sapiens 176-181 16341840-1 2006 AIMS/HYPOTHESIS: The cyclooxygenase-2 (PTGS2, previously known as COX2) enzyme and its products, such as prostaglandin E(2) (PGE(2)), have been implicated in the pathogenesis of several inflammatory diseases including islet dysfunction under diabetic conditions. Prostaglandins E 125-128 mitochondrially encoded cytochrome c oxidase II Homo sapiens 66-70 16423868-5 2006 PGE(2) and PGF(2alpha) reverse COX-2-mediated inhibition of IL-1beta induction of cytokine expression and PG production. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 31-36 16353170-4 2006 Microsomal PGES (mPGES-1) is an enzyme downstream to COX-2 and affects PGE(2) production only. Prostaglandins E 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 53-58 16712450-7 2006 Studies have shown higher levels of COX-2 isoform in breast cancer tissue when compared to normal breast tissue, and this is accompanied by high concentrations of prostaglandin E(2) (PGE(2)). Prostaglandins E 163-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 36-41 16712450-7 2006 Studies have shown higher levels of COX-2 isoform in breast cancer tissue when compared to normal breast tissue, and this is accompanied by high concentrations of prostaglandin E(2) (PGE(2)). Prostaglandins E 183-186 mitochondrially encoded cytochrome c oxidase II Homo sapiens 36-41 16712450-12 2006 High levels of COX-2 expression result in higher levels of prostaglandin E(2) (PGE(2)), which in turn increases CYP19 expression through increases in intracellular cyclic AMP levels and activation of promoter II. Prostaglandins E 79-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 16423868-11 2006 Together, the data indicate an autocrine-amplifying loop involving IL-1beta-regulated Sertoli function mediated by COX-2-induced PGE(2) and PGF(2alpha) production. Prostaglandins E 129-132 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-120 16184416-4 2005 Recently, three different PGE synthases have been identified, that convert COX-2 metabolites into PGE2. Prostaglandins E 26-29 mitochondrially encoded cytochrome c oxidase II Homo sapiens 75-80 16247187-3 2005 Dexamethasone, that decreases the expression of COX-2 and mucosal generation of PGE(2), delays ulcer healing that can be reversed by the addition of small dose of exogenous PGE(2). Prostaglandins E 173-176 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53 16247187-4 2005 Proton pump inhibitors (PPI) such as omeprazole and PGE analogs, accelerate ulcer healing mainly due to potent inhibition of gastric acid secretion, but they also augment the COX-2 expression and enzyme activity in the ulcerated mucosa. Prostaglandins E 52-55 mitochondrially encoded cytochrome c oxidase II Homo sapiens 175-180 16247187-6 2005 The ulcer healing activity of growth factors (e.g. EGF, TGF alpha, HGF) and certain gut hormones (gastrin, CCK) as well as melatonin, can be attenuated by treatment with COX-1 or COX-2 inhibitors which suppress the release of PGE(2) but enhance the expression of COX-2. Prostaglandins E 226-229 mitochondrially encoded cytochrome c oxidase II Homo sapiens 179-184 15950941-3 2005 Flow cytometry analysis suggests that IL-20-dependent inhibition of COX-2/PGE(2) occurs through the IL-22R1/IL-20R2 dimers. Prostaglandins E 74-77 mitochondrially encoded cytochrome c oxidase II Homo sapiens 68-73 15950941-6 2005 Altogether our findings revealed that IL-20 is a negative modulator of COX-2/PGE(2) and inhibits angiogenesis. Prostaglandins E 77-80 mitochondrially encoded cytochrome c oxidase II Homo sapiens 71-76 16210874-4 2005 COX-2-derived bioactive lipids, including the primary prostaglandin (PG) generated in colorectal tumors, PGE(2), are known to stimulate cell migration, proliferation and tumor-associated neovascularization while inhibiting cell death. Prostaglandins E 105-108 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15358613-1 2005 The proinflammatory mediator cyclooxygenase (COX)-2 and its product PGE(2) are induced in the ischemic heart, contributing to inflammatory cell infiltration, fibroblast proliferation, and cardiac hypertrophy. Prostaglandins E 68-71 mitochondrially encoded cytochrome c oxidase II Homo sapiens 29-51 15358613-2 2005 PGE(2) synthesis coupled to COX-2 involves two membrane-localized PGE synthases, mPGES-1 and mPGES-2; however, it is not clear how these synthases are regulated in cardiac myocytes and fibroblasts. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 28-33 16210874-5 2005 Here we briefly review the role of NSAIDs in preventing CRC, as well as the proposed mechanism by which a COX-2-derived PG, PGE(2), promotes colon cancer. Prostaglandins E 124-127 mitochondrially encoded cytochrome c oxidase II Homo sapiens 106-111 15544595-1 2004 BACKGROUND: Cyclooxygenase (COX)-2 is a key inducible enzyme that regulates the production of anti-inflammatory prostaglandin E(2). Prostaglandins E 112-127 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-34 15494133-6 2004 Levels of PGE-M in healthy humans are suppressed significantly not only by the nonselective COX inhibitor ibuprofen but also by the COX-2 selective inhibitor rofecoxib, suggesting that the majority of PGE2 formed in vivo is derived from COX-2. Prostaglandins E 10-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 132-137 15494133-6 2004 Levels of PGE-M in healthy humans are suppressed significantly not only by the nonselective COX inhibitor ibuprofen but also by the COX-2 selective inhibitor rofecoxib, suggesting that the majority of PGE2 formed in vivo is derived from COX-2. Prostaglandins E 10-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 237-242 15494133-8 2004 Levels of PGE-M were found to be greatly increased in humans with unresectable non-small cell cancer of the lung, and this increase is dramatically reduced by administration of the COX-2 inhibitor celecoxib, implying that COX-2 contributes significantly to the overproduction of PGE2. Prostaglandins E 10-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 181-186 15494133-8 2004 Levels of PGE-M were found to be greatly increased in humans with unresectable non-small cell cancer of the lung, and this increase is dramatically reduced by administration of the COX-2 inhibitor celecoxib, implying that COX-2 contributes significantly to the overproduction of PGE2. Prostaglandins E 10-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 222-227 15471850-5 2004 Co-incubation of rat and human islets with selective COX-2 inhibitors SC-58236 and Celecoxib, respectively, attenuated cytokine-induced PGE(2) formation. Prostaglandins E 136-139 mitochondrially encoded cytochrome c oxidase II Homo sapiens 53-58 15383564-10 2004 The effect of a COX-2 inhibition in LN-18-COX2 is reversible after administration of PGE(2). Prostaglandins E 85-88 mitochondrially encoded cytochrome c oxidase II Homo sapiens 42-46 14762100-2 2004 Acetylation of COX-2 by aspirin activates a transcellular biosynthetic pathway that switches eicosanoid biosynthesis from prostaglandin E(2) to 15-epi-lipoxin (LX)A(4) or aspirin-triggered lipoxin (ATL). Prostaglandins E 122-137 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 15269139-7 2004 COX-2 inhibitors and, in part, COX-1 inhibitor blocked ET-1-induced PGE(2) and vascular endothelial growth factor release, indicating that both enzymes participate in PGE(2) production to a different extent. Prostaglandins E 167-170 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 15113997-1 2004 OBJECTIVE: To investigate the effects of the cyclooxygenase-2 (cox-2)-dependent prostaglandins D(2) (PGD(2)), E(2) (PGE(2)) and F(2)alpha (PGF(2)alpha) on the redifferentiation and cartilage matrix production of dedifferentiated articular chondrocytes. Prostaglandins E 116-119 mitochondrially encoded cytochrome c oxidase II Homo sapiens 63-68 15067222-9 2004 These findings suggest that the expression of COX-2 is correlated with the release of PGE(2) from IL-1beta-challenged HTSMCs, which is mediated, at least in part, through p42/p44 and p38 MAPKs and NF-kappaB signaling pathways in HTSMCs. Prostaglandins E 86-89 mitochondrially encoded cytochrome c oxidase II Homo sapiens 46-51 15024003-8 2004 Moreover, ECM-induced PGE(2) and MMP-9 expression by elicited COX-2(-/-) macrophages is markedly reduced when compared with the response of either COX-2(+/-) or COX-2(+/+) macrophages. Prostaglandins E 22-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 62-67 15078741-10 2004 COX-1 and COX-2 activity was determined by measuring serum thromboxane (TX) B(2) and endotoxin-induced PGE(2) generation in whole blood. Prostaglandins E 103-106 mitochondrially encoded cytochrome c oxidase II Homo sapiens 10-15 14742435-9 2004 Our results suggest that COX-2/PGE(2) may exert pro-oncogenic effects through synergistic induction of receptor tyrosine kinase-dependent signaling pathway, thus, provide a novel mechanism for the combinatorial treatment of colonic neoplasms targeting both COX-2/PGE(2) and the EGFR system that has demonstrated remarkable advantages. Prostaglandins E 31-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 25-30 14742435-9 2004 Our results suggest that COX-2/PGE(2) may exert pro-oncogenic effects through synergistic induction of receptor tyrosine kinase-dependent signaling pathway, thus, provide a novel mechanism for the combinatorial treatment of colonic neoplasms targeting both COX-2/PGE(2) and the EGFR system that has demonstrated remarkable advantages. Prostaglandins E 31-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 257-262 14742435-9 2004 Our results suggest that COX-2/PGE(2) may exert pro-oncogenic effects through synergistic induction of receptor tyrosine kinase-dependent signaling pathway, thus, provide a novel mechanism for the combinatorial treatment of colonic neoplasms targeting both COX-2/PGE(2) and the EGFR system that has demonstrated remarkable advantages. Prostaglandins E 263-266 mitochondrially encoded cytochrome c oxidase II Homo sapiens 25-30 14751245-1 2004 Prostaglandin E(2) (PGE(2)), a major cyclooxygenase (COX-2) metabolite, plays important roles in tumor biology and its functions are mediated through one or more of its receptors EP1, EP2, EP3, and EP4. Prostaglandins E 20-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 53-58 14762933-6 2004 Exposure of human macrophages to mechanical stretch with particles upregulated the expression of cyclooxygenase (COX)-2 mRNA but not COX-1 mRNA, this expression resulting in a 97-fold increase in PGE(2) production compared to the nonstimulated cells. Prostaglandins E 196-199 mitochondrially encoded cytochrome c oxidase II Homo sapiens 97-119 14694045-7 2003 Moreover, increased levels of PGE(2) and PGF(2alpha) were measurable in sera from patients with GBS, CIDP, or VN and in cell culture supernatants from in vitro stimulated macrophages, indicative of COX-2 activity. Prostaglandins E 30-33 mitochondrially encoded cytochrome c oxidase II Homo sapiens 198-203 14696113-7 2004 This suggests that COX-2/PGE(2) activation involves in EGF-induced proliferation and locates at the downstream of ERK1/2 activation. Prostaglandins E 25-28 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24 14764680-4 2004 CD40 ligation of monocytes induced the synthesis of a significant amount of PGE(2) via inducible expression of the cyclooxygenase (COX)-2 gene. Prostaglandins E 76-79 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-137 14634122-5 2003 Addition of exogenous PGE(1) or PGE(2) inhibited MMP-1, reversed the effects of COX inhibitors, and inhibited ERK activation, suggesting that COX-2 activity tonically inhibits MMP-1 production via ERK inhibition by E PGs. Prostaglandins E 22-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 142-147 14634122-5 2003 Addition of exogenous PGE(1) or PGE(2) inhibited MMP-1, reversed the effects of COX inhibitors, and inhibited ERK activation, suggesting that COX-2 activity tonically inhibits MMP-1 production via ERK inhibition by E PGs. Prostaglandins E 32-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 142-147 14634122-8 2003 Our data indicate that: 1) ERK activation mediates MMP-1 but not MMP-13 release from FLSCs, 2) COX-2-derived E PGs inhibit MMP-1 release from FLSCs via inhibition of ERK, and 3) COX inhibitors, by attenuating PGE inhibition of ERK, enhance the release of MMP-1 by FLSC. Prostaglandins E 209-212 mitochondrially encoded cytochrome c oxidase II Homo sapiens 95-100 15075458-7 2003 These results suggest that inhibition of COX-1, despite causing intestinal hypermotility, bacterial invasion and iNOS expression, up-regulates the expression of COX-2, and the PGE(2) derived from COX-2 counteracts deleterious events caused by COX-1 inhibition and maintains the mucosal integrity. Prostaglandins E 176-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 196-201 12517972-4 2003 Indeed, PGE(2) also induced and enhanced IL-1beta-induced COX-2 expression. Prostaglandins E 8-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 58-63 12821125-5 2003 In COX-2 expressing cells, exogenous AA and PGE(2) increased VEGF synthesis via the EP(2) receptor. Prostaglandins E 44-47 mitochondrially encoded cytochrome c oxidase II Homo sapiens 3-8 12821125-9 2003 PGE(2) generated by specific COX-2 activity increases VEGF secretion in human PaCa cells through an autocrine mechanism. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 29-34 15017670-11 2003 CONCLUSIONS: In hepatolithiasis, an enhanced synthesis of sPLA(2)-/COX-2-derived PGE(2) and its actions mediated via the EP(4) receptor in the bile ducts may be of pathobiological significance for chronic proliferative cholangitis. Prostaglandins E 81-84 mitochondrially encoded cytochrome c oxidase II Homo sapiens 67-72 12773508-5 2003 NS-398, a cyclooxygenase (COX)-2-selective inhibitor, suppressed LPS-enhanced EP(2)R/EP(4)R expression, suggesting that COX-2-issued prostaglandin E(2) (PGE(2)) modulates DC function through stimulation of specific EPR subtypes. Prostaglandins E 153-156 mitochondrially encoded cytochrome c oxidase II Homo sapiens 120-125 12578976-5 2003 In this study, we compared the effects of PGE(2) and PGE(3) on (i) cell proliferation in NIH 3T3 fibroblasts, (ii) expression and transcriptional regulation of the COX-2 gene in NIH 3T3 fibroblasts, and (iii) the production of an inflammatory cytokine, IL-6, in RAW 264.7 macrophages. Prostaglandins E 42-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 164-169 12578976-5 2003 In this study, we compared the effects of PGE(2) and PGE(3) on (i) cell proliferation in NIH 3T3 fibroblasts, (ii) expression and transcriptional regulation of the COX-2 gene in NIH 3T3 fibroblasts, and (iii) the production of an inflammatory cytokine, IL-6, in RAW 264.7 macrophages. Prostaglandins E 53-56 mitochondrially encoded cytochrome c oxidase II Homo sapiens 164-169 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 30-35 12578976-7 2003 PGE(2) and PGE(3) both induce COX-2 mRNA via similar signaling mechanisms; however, compared with PGE(2), PGE(3) is significantly less efficient in inducing COX-2 gene expression. Prostaglandins E 11-14 mitochondrially encoded cytochrome c oxidase II Homo sapiens 157-162 14647459-7 2003 This suggests that COX-2 is the major source of PGE(2) in this cell line. Prostaglandins E 48-51 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24 12890715-1 2003 (1) Unlike other nonsteroidal anti-inflammatory drugs that inhibit formation of cyclooxygenase (COX)-dependent eicosanoids, acetylation of COX-2 by aspirin switches eicosanoid biosynthesis from prostaglandin E(2) (PGE(2)) to 15-epi-lipoxin A(4) (15-epi-LXA(4) or aspirin-triggered lipoxin, ATL). Prostaglandins E 194-209 mitochondrially encoded cytochrome c oxidase II Homo sapiens 139-144 12890715-1 2003 (1) Unlike other nonsteroidal anti-inflammatory drugs that inhibit formation of cyclooxygenase (COX)-dependent eicosanoids, acetylation of COX-2 by aspirin switches eicosanoid biosynthesis from prostaglandin E(2) (PGE(2)) to 15-epi-lipoxin A(4) (15-epi-LXA(4) or aspirin-triggered lipoxin, ATL). Prostaglandins E 214-217 mitochondrially encoded cytochrome c oxidase II Homo sapiens 139-144 12591723-2 2003 Tumor COX-2-dependent production of PGE(2) triggers the synthesis of lymphocyte and macrophage interleukin (IL)-10 that, in turn, is known to potently suppress COX-2 in normal cells. Prostaglandins E 36-39 mitochondrially encoded cytochrome c oxidase II Homo sapiens 6-11 12591723-2 2003 Tumor COX-2-dependent production of PGE(2) triggers the synthesis of lymphocyte and macrophage interleukin (IL)-10 that, in turn, is known to potently suppress COX-2 in normal cells. Prostaglandins E 36-39 mitochondrially encoded cytochrome c oxidase II Homo sapiens 160-165 12576462-5 2003 RESULTS: In contrast to C6 glioma cells, microglia isolated from intracranial C6 tumors produced high levels of PGE(2) through a COX-2-dependent pathway. Prostaglandins E 112-115 mitochondrially encoded cytochrome c oxidase II Homo sapiens 129-134 12162776-8 2002 Meloxicam (a specific COX-2 inhibitor) suppressed the induction of cytokines on IL-6 mRNA levels, and these effects could be reversed by exogenous prostaglandin E(2). Prostaglandins E 147-162 mitochondrially encoded cytochrome c oxidase II Homo sapiens 22-27 12401798-11 2002 Of several prostaglandins tested, only PGE(2) reversed the effects of a COX-2 inhibitor in hypoxic cells. Prostaglandins E 39-42 mitochondrially encoded cytochrome c oxidase II Homo sapiens 72-77 12460774-9 2002 The results show that purified mPGES-1 has a specific activity similar to Cox-2, consistent with its postulated role in Cox-2 mediated PGE(2) formation. Prostaglandins E 32-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 120-125 12237321-4 2002 Here we investigated the role of the COX-2 metabolites PGE(2) and TXA2 in regulating human umbilical vein endothelial cell (HUVEC) adhesion and spreading. Prostaglandins E 55-58 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 12237321-11 2002 In conclusion, these results demonstrate that PGE(2) accelerates alpha(V)beta(3)-mediated endothelial cell adhesion through cAMP-dependent PKA activation and induces alpha(V)beta(3)-dependent spreading via cAMP- and PKA-dependent Rac activation and may contribute to the further understanding of the regulation of vascular integrins alpha(V)beta(3) by COX-2/PGE(2) during tumor angiogenesis and inflammation. Prostaglandins E 46-49 mitochondrially encoded cytochrome c oxidase II Homo sapiens 352-357 12417326-5 2002 DNA fragmentation was also increasd in COX-2 non-expressing cell lines (SW-480 and HCT-116) by exposure to celecoxib for 6-24 h. All six COX-2 inhibitors suppressed the production of prostaglandin E(2) by HT-29 cells, suggesting that the pro-apoptotic effect of celecoxib was unrelated to inhibition of COX-2. Prostaglandins E 183-198 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 12417326-5 2002 DNA fragmentation was also increasd in COX-2 non-expressing cell lines (SW-480 and HCT-116) by exposure to celecoxib for 6-24 h. All six COX-2 inhibitors suppressed the production of prostaglandin E(2) by HT-29 cells, suggesting that the pro-apoptotic effect of celecoxib was unrelated to inhibition of COX-2. Prostaglandins E 183-198 mitochondrially encoded cytochrome c oxidase II Homo sapiens 137-142 12417326-5 2002 DNA fragmentation was also increasd in COX-2 non-expressing cell lines (SW-480 and HCT-116) by exposure to celecoxib for 6-24 h. All six COX-2 inhibitors suppressed the production of prostaglandin E(2) by HT-29 cells, suggesting that the pro-apoptotic effect of celecoxib was unrelated to inhibition of COX-2. Prostaglandins E 183-198 mitochondrially encoded cytochrome c oxidase II Homo sapiens 137-142 12107070-6 2002 In contrast, COX-2, generally considered an inducible isoform, is constitutively expressed in the Thy-1(-) subset, which only minimally produces PGE(2). Prostaglandins E 145-148 mitochondrially encoded cytochrome c oxidase II Homo sapiens 13-18 12468269-4 2002 An increase in COX-2 immunoreactive protein was also seen after incubation of isolated human adipocytes for 48 h. The release of PGE(2) by adipocytes incubated for 48 h was about 4% that by intact adipose tissue explants while the release of prostacyclin was about 1.5% that by tissue. Prostaglandins E 129-132 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 12391247-5 2002 Production of PGE(2) in response to exogenous arachidonic acid was also increased by adenosine and correlated with COX-2 protein levels. Prostaglandins E 14-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-120 12487927-9 2002 (3) COX-2 expression was correlated with PGE(2), 6-keto-PGF(1 alpha) and TXB(2) (P < 0.01). Prostaglandins E 41-44 mitochondrially encoded cytochrome c oxidase II Homo sapiens 4-9 12487927-10 2002 CONCLUSIONS: (1) Our data suggest that COX-2 overexpression leads to increased PGE(2), 6-keto-PGF(1 alpha) and TXB(2) biosynthesis, which may be mechanisms underlying the contribution of COX-2 to the development of ovarian serous carcinoma. Prostaglandins E 79-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 39-44 12487927-10 2002 CONCLUSIONS: (1) Our data suggest that COX-2 overexpression leads to increased PGE(2), 6-keto-PGF(1 alpha) and TXB(2) biosynthesis, which may be mechanisms underlying the contribution of COX-2 to the development of ovarian serous carcinoma. Prostaglandins E 79-82 mitochondrially encoded cytochrome c oxidase II Homo sapiens 187-192 11950805-8 2002 Injured tissues treated with the selective COX-1 inhibitor SC-560 (5x10(-6) M) or the COX-2 inhibitor NS-398 (5x10(-6) M) recovered to control levels of resistance within three hours, associated with significant elevations of PGE and 6-keto-PGF1alpha compared with untreated tissues. Prostaglandins E 226-229 mitochondrially encoded cytochrome c oxidase II Homo sapiens 86-91 12006564-9 2002 Intriguingly, we found that PGE(2) was one of the major factors in MECM, which was responsible for up-regulating COX-2 expression in ESC. Prostaglandins E 28-31 mitochondrially encoded cytochrome c oxidase II Homo sapiens 113-118 12006564-11 2002 In conclusion, malignant endometrial epithelial cells secrete PGE(2) that induces COX-2 expression in normal endometrial stromal cells in a paracrine fashion through activation of transcription and stabilization of COX-2 mRNA. Prostaglandins E 62-65 mitochondrially encoded cytochrome c oxidase II Homo sapiens 82-87 12006564-11 2002 In conclusion, malignant endometrial epithelial cells secrete PGE(2) that induces COX-2 expression in normal endometrial stromal cells in a paracrine fashion through activation of transcription and stabilization of COX-2 mRNA. Prostaglandins E 62-65 mitochondrially encoded cytochrome c oxidase II Homo sapiens 215-220 12032335-8 2002 A selective COX-2 inhibitor reduced platelet production of both PGE(2) and TXB(2) to a significantly greater extent in patients than in healthy subjects. Prostaglandins E 64-67 mitochondrially encoded cytochrome c oxidase II Homo sapiens 12-17 12032335-10 2002 We conclude that both COX-isoforms contribute to prostanoid formation during human megakaryocytopoiesis and that COX-2-derived PGE(2) and TXA(2) may play an unrecognized role in inflammatory and hemostatic responses in clinical syndromes associated with high platelet turnover. Prostaglandins E 127-130 mitochondrially encoded cytochrome c oxidase II Homo sapiens 113-118 12050227-6 2002 In conclusion, PLA(2), COX-1, and COX-2 are expressed during early human embryonic development and may contribute to the production of PGs such as PGE(2) in human embryogenesis. Prostaglandins E 147-150 mitochondrially encoded cytochrome c oxidase II Homo sapiens 34-39 11950805-10 2002 CONCLUSIONS: The results suggest that recovery of resistance is triggered by PGE and PGI2, which may be elaborated by either COX-1 or COX-2. Prostaglandins E 77-80 mitochondrially encoded cytochrome c oxidase II Homo sapiens 134-139 11859113-4 2002 Constitutively present in BM-DC, cyclooxygenase (COX)-1 did not contribute significantly to the total pool of PGE(2) compared with the LPS-induced COX-2-produced PGE(2). Prostaglandins E 162-165 mitochondrially encoded cytochrome c oxidase II Homo sapiens 147-152 11859113-6 2002 In addition, selective inhibition of COX-2, but not COX-1, was followed by significant decrements in PGE(2) and IL-10, a concomitant restoration of IL-12 production, and an enhancement of DC stimulatory potential. Prostaglandins E 101-104 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 11859113-10 2002 We conclude that COX-2-mediated PGE(2) up-regulates IL-10, which down-regulates IL-12 production and the APC function of BM-DC. Prostaglandins E 32-35 mitochondrially encoded cytochrome c oxidase II Homo sapiens 17-22 11882577-1 2002 Interleukin-1beta (IL-1beta), a proinflammatory cytokine, induces cyclooxygenase-2 (COX-2) in cultured neonatal ventricular myocytes (NVMs), resulting in the preferential production of prostaglandin E(2) (PGE(2)). Prostaglandins E 205-208 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 11882577-11 2002 We concluded that (1) PGE(2) production requires the induction of its specific synthase; (2) in myocytes, the inducible enzymes COX-2 and PGES are perinuclear; and (3) PGE(2) and sulprostone induce cardiac myocyte growth but seem to activate a different subset of EP receptors. Prostaglandins E 22-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 128-133 11300882-3 2001 These pyrido[1,2-c]pyrimidines inhibited the generation of PGE(2) by COX-2 in RAW 264.7 macrophages stimulated with lipopolysaccharide. Prostaglandins E 59-62 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74 11926591-2 2002 Vascular endothelial growth factor (VEGF) has been shown to play important roles in inflammation and is upregulated by the prostaglandin E series through COX-2 in several cell types. Prostaglandins E 123-138 mitochondrially encoded cytochrome c oxidase II Homo sapiens 154-159 11779161-4 2002 We hypothesized that increased expression of COX-2, with resultant increased levels of PGE(2) in human PIN cells, activates the IL-6 signaling pathway. Prostaglandins E 87-90 mitochondrially encoded cytochrome c oxidase II Homo sapiens 45-50 11779161-10 2002 These data provide mechanistic evidence that increased expression of COX-2/PGE(2) contributes to prostate cancer development and progression via activation of the IL-6 signaling pathway. Prostaglandins E 75-78 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74 11532880-2 2001 Activity of one of the COX isoforms, COX-2, results in production of prostaglandin E(2) (PGE(2)) via the endoperoxide PGH(2). Prostaglandins E 89-92 mitochondrially encoded cytochrome c oxidase II Homo sapiens 37-42 11532880-11 2001 Selective inhibition of COX-2 activity in HCA-7 cells by NS-398 significantly inhibited PGE(2) production, but altered neither MDA nor M(1)G levels. Prostaglandins E 88-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 24-29 11509629-1 2001 The two cyclooxygenase (COX) isoforms, COX-1 and COX-2, both metabolize arachidonic acid to PGH(2), the common substrate for thromboxane A(2) (TXA(2)), prostacyclin (PGI(2)), and PGE(2) synthesis. Prostaglandins E 179-182 mitochondrially encoded cytochrome c oxidase II Homo sapiens 49-54 11509629-5 2001 By contrast, COX-2 up-regulation was associated with large increases in the synthesis of PGI(2) and PGE(2) (54- and 84-fold increases, respectively). Prostaglandins E 100-103 mitochondrially encoded cytochrome c oxidase II Homo sapiens 13-18 11509629-6 2001 Addition of the selective COX-2 inhibitor, NS-398, almost completely abolished PGI(2) and PGE(2) synthesis, but had little effect on TXA(2) synthesis. Prostaglandins E 90-93 mitochondrially encoded cytochrome c oxidase II Homo sapiens 26-31 11509629-10 2001 The apparent PGI(2) and PGE(2) linkage with COX-2 activity may be explained by a temporal increase in total COX activity, together with selective up-regulation of PGI synthase and PGE synthase, and different kinetic characteristics of the terminal synthases. Prostaglandins E 24-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-49 11290559-10 2001 We conclude that a decreased capacity to up-regulate COX-2 expression and COX-2-derived PGE(2) synthesis in the presence of increasing levels of profibrotic mediators such as TGF-beta(1) may lead to unopposed fibroblast proliferation and collagen synthesis and contribute to the pathogenesis of pulmonary fibrosis. Prostaglandins E 88-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 74-79 11751489-12 2001 Taken together, our results suggest that overexpression of mPGES in addition to COX-2 contributes to increased amounts of PGE(2) in colorectal adenomas and cancer. Prostaglandins E 122-126 mitochondrially encoded cytochrome c oxidase II Homo sapiens 80-85 11418589-3 2001 As did the membrane-bound PGE(2) synthase, the perinuclear enzymes thromboxane synthase and PGI(2) synthase generated their respective products via COX-2 in preference to COX-1 in both the -induced immediate and interleukin-1-induced delayed responses. Prostaglandins E 26-29 mitochondrially encoded cytochrome c oxidase II Homo sapiens 148-153 11323387-7 2001 Three hours after exposure to AA, the synthesis of PGE(2) via COX-2 was also increased. Prostaglandins E 51-54 mitochondrially encoded cytochrome c oxidase II Homo sapiens 62-67 10899936-5 2000 The AdCAT:-induced increase in PGE(2) formation was inhibited by NS-398, a selective inhibitor of COX-2 enzymatic activity. Prostaglandins E 31-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 98-103 11112151-2 2000 Treatment with exogenous PGE(2) resulted in enhanced expression of IL-1 beta-induced COX-2 protein and messenger RNA (mRNA) as compared with the effect of the cytokine per se. Prostaglandins E 25-28 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-90 11112151-5 2000 Treatment with cycloheximide to inhibit translation, and with dexamethasone or actinomycin D to inhibit transcription, linked the effect of PGE(2) to the transcriptional level of COX-2 mRNA rather than to a potential effect on protein and/or mRNA stabilization. Prostaglandins E 140-143 mitochondrially encoded cytochrome c oxidase II Homo sapiens 179-184 11112151-6 2000 PGE(2) increased adenylate cyclase activity in a concentration dependent manner, and forskolin, a direct activator of adenylate cyclase, caused a marked increase in IL-1 beta-dependent COX-2, suggesting the existence of a causal relationship between the two events. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 185-190 11112151-8 2000 The effect of PGE(2) on COX-2 expression may contribute to the hypothesized antiinflammatory role of PGE(2) in human airways, providing a self-amplifying loop leading to increased biosynthesis of PGE(2) during an inflammatory event. Prostaglandins E 14-17 mitochondrially encoded cytochrome c oxidase II Homo sapiens 24-29 11112151-8 2000 The effect of PGE(2) on COX-2 expression may contribute to the hypothesized antiinflammatory role of PGE(2) in human airways, providing a self-amplifying loop leading to increased biosynthesis of PGE(2) during an inflammatory event. Prostaglandins E 101-104 mitochondrially encoded cytochrome c oxidase II Homo sapiens 24-29 11112151-8 2000 The effect of PGE(2) on COX-2 expression may contribute to the hypothesized antiinflammatory role of PGE(2) in human airways, providing a self-amplifying loop leading to increased biosynthesis of PGE(2) during an inflammatory event. Prostaglandins E 101-104 mitochondrially encoded cytochrome c oxidase II Homo sapiens 24-29 10942778-12 2000 We conclude that S1P inhibits proliferation of hMF, probably via an intracellular mechanism, through early COX-2-dependent release of prostaglandin E(2) and cAMP, and delayed COX-2 induction. Prostaglandins E 134-149 mitochondrially encoded cytochrome c oxidase II Homo sapiens 107-112 10869354-4 2000 mPGES expression was markedly induced by proinflammatory stimuli in various tissues and cells and was down-regulated by dexamethasone, accompanied by changes in COX-2 expression and delayed PGE(2) generation. Prostaglandins E 1-4 mitochondrially encoded cytochrome c oxidase II Homo sapiens 161-166 11040187-9 2000 RESULTS: LTD(4) and LTB(4), but not LTC(4), caused a time- and dose-dependent increase in expression and/or membrane accumulation of COX-2, beta-catenin, and Bcl-2, as well as PGE(2) production. Prostaglandins E 176-179 mitochondrially encoded cytochrome c oxidase II Homo sapiens 133-138 10484519-2 1999 In the present study, we demonstrated that the COX-2-selective inhibitor, NS-398, prevented tumor necrosis factor-alpha (TNF)- and phorbol myristate acetate (PMA)-mediated increases in PGE(2) production by cultured MTAL cells. Prostaglandins E 185-189 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-52 10848516-5 2000 Both selective COX-2 inhibitors decreased PGE(2) and 6ketoPGF(1alpha) production in vitro; both inhibitors constricted the isolated ductus in vitro. Prostaglandins E 42-45 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 10843735-5 2000 A COX-2 inhibitor and cPLA(2)inhibitor markedly suppressed the IL-1beta-induced delayed PGE(2)generation, while a type IIA sPLA(2)inhibitor failed to affect it. Prostaglandins E 88-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 2-7 10843735-7 2000 These results indicate that IL-1beta-induced delayed PGE(2)generation in these human fibroblasts mainly depends on de novo induction of COX-2 and cPLA(2), irrespective of the constitutive presence of COX-1, and that IFN-gamma and IL-4 inhibit IL-1beta-induced delayed PGE(2)generation by suppressing, predominantly, COX-2 expression. Prostaglandins E 53-56 mitochondrially encoded cytochrome c oxidase II Homo sapiens 136-141 10828079-6 2000 In primary keratinocytes transiently transfected with a full-length COX-2 promoter linked to a luciferase reporter gene, we observed enhanced transcription by AA, PGE(2), and the other prostaglandins. Prostaglandins E 163-166 mitochondrially encoded cytochrome c oxidase II Homo sapiens 68-73 10828079-8 2000 SQ 22536, an adenylate cyclase inhibitor, inhibited COX-2 mRNA induction by PGE(2) in a dose-dependent manner suggesting that PGE(2)-induced expression may be through one of the cAMP-linked PGE(2) receptors. Prostaglandins E 76-79 mitochondrially encoded cytochrome c oxidase II Homo sapiens 52-57 10828079-8 2000 SQ 22536, an adenylate cyclase inhibitor, inhibited COX-2 mRNA induction by PGE(2) in a dose-dependent manner suggesting that PGE(2)-induced expression may be through one of the cAMP-linked PGE(2) receptors. Prostaglandins E 126-129 mitochondrially encoded cytochrome c oxidase II Homo sapiens 52-57 10828079-8 2000 SQ 22536, an adenylate cyclase inhibitor, inhibited COX-2 mRNA induction by PGE(2) in a dose-dependent manner suggesting that PGE(2)-induced expression may be through one of the cAMP-linked PGE(2) receptors. Prostaglandins E 126-129 mitochondrially encoded cytochrome c oxidase II Homo sapiens 52-57 10852985-9 2000 Assays performed with blood from RA/MTX patients showed preferential inhibition of COX-2 activity (PGE(2) = 10.11 +/- 2.42 ng/ml) when compared with blood of normal donors (PGE(2) = 37.7 +/- 4.36 ng/ml; P = 0.001). Prostaglandins E 99-102 mitochondrially encoded cytochrome c oxidase II Homo sapiens 83-88 10666314-5 2000 Under these conditions, mRNA and protein levels of the inducible form of cyclooxygenase (COX-2) were upregulated together with its product, PGE(2), a proinflammatory prostaglandin. Prostaglandins E 140-143 mitochondrially encoded cytochrome c oxidase II Homo sapiens 89-94 10531345-5 1999 Both types IIA and V sPLA(2), the AA released by which was efficiently converted to prostaglandin E(2), markedly augmented IL-1-induced expression of cyclooxygenase (COX)-2 in a heparin-sensitive fashion, whereas type X sPLA(2) lacked the ability to augment COX-2 expression, thereby exhibiting the poor prostaglandin E(2)-biosynthetic response unless either of the COX isozymes was forcibly introduced into type X sPLA(2)-expressing cells. Prostaglandins E 84-99 mitochondrially encoded cytochrome c oxidase II Homo sapiens 150-172 10229670-4 1999 PGE generation by goldfish macrophages was similarly inhibited by the glucocorticoid, dexamethasone, and an inhibitor of protein synthesis, cycloheximide, suggesting that this stimulation may be due to an inducible enzyme equivalent to mammalian COX-2. Prostaglandins E 0-3 mitochondrially encoded cytochrome c oxidase II Homo sapiens 246-251 10411562-6 1999 In an in vitro human whole blood assay, rofecoxib selectively inhibited lipopolysaccharide-induced, COX-2-derived PGE(2) synthesis with an IC(50) value of 0.53 +/- 0.02 microM compared with an IC(50) value of 18.8 +/- 0.9 microM for the inhibition of COX-1-derived thromboxane B(2) synthesis after blood coagulation. Prostaglandins E 114-117 mitochondrially encoded cytochrome c oxidase II Homo sapiens 100-105 12512030-1 2003 BACKGROUND & AIMS: The effects of leukotriene (LT) D(4) on intestinal epithelial cells govern events that are involved in cell survival and colon cancer, notably increased expression of cyclooxygenase (COX)-2 and enhanced production of prostaglandin E(2). Prostaglandins E 240-255 mitochondrially encoded cytochrome c oxidase II Homo sapiens 190-212 8595066-12 1995 With the in vitro assay, nimesulide (0.01 to 100 mumol/l) did not inhibit PGE formation by COX-1 but caused a concentration-related inhibition of PGE formation by COX-2 (4-60%). Prostaglandins E 146-149 mitochondrially encoded cytochrome c oxidase II Homo sapiens 163-168