PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32882817-0 2020 IL-1beta and TNF-alpha Modulation of Proliferated and Committed Myoblasts: IL-6 and COX-2-Derived Prostaglandins as Key Actors in the Mechanisms Involved. Prostaglandins 98-112 tumor necrosis factor Mus musculus 13-22 33669841-9 2021 Importantly, in this work we also show that the COX-1-derived prostaglandins produced during the early steps of macrophage activation restrict tumor necrosis factor-alpha production. Prostaglandins 62-76 tumor necrosis factor Mus musculus 143-170 32882817-7 2020 Our data reveal a key role of IL-6 and COX-2-derived PGs in IL-1beta and TNF-alpha-induced myoblast proliferation and support the link between TNF-alpha and IL-6 and the activation of MRFs. Prostaglandins 53-56 tumor necrosis factor Mus musculus 73-82 29259703-10 2017 In this process, PGE2-EP2 signaling synergizes with TNF-alpha to amplify TNF-alpha-induced inflammatory responses, forms a positive feedback loop involving COX-2-PGE2-EP2 signaling to exacerbate PG-mediated inflammation once triggered, and alternates active cell populations participating in inflammation through forming self-amplification loop among neutrophils. Prostaglandins 17-19 tumor necrosis factor Mus musculus 52-61 32547156-6 2020 Moreover, IL-1, IL-6, and TNF-alpha knocked-out mice have delayed parturition and lower levels of PGs compared to the wild types. Prostaglandins 98-101 tumor necrosis factor Mus musculus 26-35 29259703-10 2017 In this process, PGE2-EP2 signaling synergizes with TNF-alpha to amplify TNF-alpha-induced inflammatory responses, forms a positive feedback loop involving COX-2-PGE2-EP2 signaling to exacerbate PG-mediated inflammation once triggered, and alternates active cell populations participating in inflammation through forming self-amplification loop among neutrophils. Prostaglandins 17-19 tumor necrosis factor Mus musculus 73-82 25978374-9 2015 Attenuation of hepatic TNF-alpha was mediated via the PGE2/E prostanoid 4 (EP4) pathway, and serum ALT levels were attenuated in an IL-10-dependent manner. Prostaglandins 61-71 tumor necrosis factor Mus musculus 23-32 17481558-2 2007 Using preadipogenic 3T3-L1 cells, we attempt to determine the response of adipocytes at different stages of the life cycle to TNFalpha with respect to the gene expression of the arachidonate cyclooxygenase (COX) pathway and the role of endogenous prostaglandins (PGs). Prostaglandins 247-261 tumor necrosis factor Mus musculus 126-134 17696964-6 2007 TNFalpha and LT are strong inducers of prostaglandins, but mice with disrupted prostaglandin or prostacyclin receptors exhibited running distances not significantly different from their wild-type littermates. Prostaglandins 39-53 tumor necrosis factor Mus musculus 0-8 17696964-6 2007 TNFalpha and LT are strong inducers of prostaglandins, but mice with disrupted prostaglandin or prostacyclin receptors exhibited running distances not significantly different from their wild-type littermates. Prostaglandins 39-52 tumor necrosis factor Mus musculus 0-8 20675368-4 2010 From a microarray, real-time polymerase chain reaction (PCR), and cytokine array studies, we showed down-regulation of the proinflammatory cytokines TNF-alpha, interleukin (IL)-1alpha, IL-1beta, IL-6, and the prostaglandin synthesis gene, cyclooxygenase (COX)-2, by TH2-3. Prostaglandins 209-222 tumor necrosis factor Mus musculus 149-158 17669394-12 2007 On the other hand, in LPS-primed mice, the B(1) kinin receptor mediates hypernociception by a mechanism dependent on TNF-alpha and IL-1beta, which could stimulate prostanoid and sympathetic amine production. Prostaglandins 163-173 tumor necrosis factor Mus musculus 117-126 17481558-2 2007 Using preadipogenic 3T3-L1 cells, we attempt to determine the response of adipocytes at different stages of the life cycle to TNFalpha with respect to the gene expression of the arachidonate cyclooxygenase (COX) pathway and the role of endogenous prostaglandins (PGs). Prostaglandins 263-266 tumor necrosis factor Mus musculus 126-134 17481558-4 2007 Moreover, the cells at different cycle stages exhibited the specific gene expression of isoformic enzymes of prostaglandin (PG) synthases for PGs of the D(2), E(2), and F(2alpha) series upon exposure to TNFalpha. Prostaglandins 109-122 tumor necrosis factor Mus musculus 203-211 17481558-7 2007 The cells during the differentiation phase were the most sensitive to TNFalpha in terms of the decrease in adipogenesis without the mediation of endogenous PGs. Prostaglandins 156-159 tumor necrosis factor Mus musculus 70-78 17481558-10 2007 The action of TNFalpha on preadipocytes can be modulated by the production of endogenous PGs through the induction of COX-2. Prostaglandins 89-92 tumor necrosis factor Mus musculus 14-22 16253995-1 2005 The cytokine tumor necrosis factor-alpha (TNFalpha) induces Ca2+-dependent glutamate release from astrocytes via the downstream action of prostaglandin (PG) E2. Prostaglandins 138-153 tumor necrosis factor Mus musculus 13-40 16253995-1 2005 The cytokine tumor necrosis factor-alpha (TNFalpha) induces Ca2+-dependent glutamate release from astrocytes via the downstream action of prostaglandin (PG) E2. Prostaglandins 138-153 tumor necrosis factor Mus musculus 42-50 15181007-0 2004 Cyclooxygenase-1-dependent prostaglandin synthesis modulates tumor necrosis factor-alpha secretion in lipopolysaccharide-challenged murine resident peritoneal macrophages. Prostaglandins 27-40 tumor necrosis factor Mus musculus 61-88 15722559-0 2005 RAW264.7 cells lack prostaglandin-dependent autoregulation of tumor necrosis factor-alpha secretion. Prostaglandins 20-33 tumor necrosis factor Mus musculus 62-89 15291404-10 2004 Repletion of prostaglandin (PGE2) in the Mphi model significantly decreased TNF-alpha in all groups. Prostaglandins 13-26 tumor necrosis factor Mus musculus 76-85 15060681-3 2004 Prostaglandins and leukotrienes are thought to play opposing roles in regulating TNF production by monocytes and macrophages. Prostaglandins 0-14 tumor necrosis factor Mus musculus 81-84 12890694-3 2003 GC-MS analysis revealed that only COX-2-generated prostanoids were produced in response to TNF, thus providing further evidence of COX-2 selectivity. Prostaglandins 50-61 tumor necrosis factor Mus musculus 91-94 15142275-10 2004 Attenuation of lipopolysaccharide- and TNF-induced release of prostaglandin E2 from cultured macrophage cells by P-NT.II suggests that the peptide may influence the prostaglandin-mediated inflammatory response in rheumatoid arthritis by limiting the bioavailability of arachidonic acid through sPLA2 inhibition. Prostaglandins 62-75 tumor necrosis factor Mus musculus 39-42 12468616-6 2002 Furthermore, although inhibiting prostaglandin production enhanced TNF secretion by macrophages from mice fed the corn oil diet, it did not affect IL-10 secretion by macrophages in this group. Prostaglandins 33-46 tumor necrosis factor Mus musculus 67-70 12781703-2 2003 We have examined the potential for exogenous prostanoids, acting in a paracrine fashion, and endogenous prostanoids, acting in an autocrine fashion, to regulate secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-10, and IL-12 in DC. Prostaglandins 104-115 tumor necrosis factor Mus musculus 174-201 12047755-8 2002 In comparison with control animals, the suppression of PG synthesis produced higher inflammation and expression of TNF-alpha, interleukin-1alpha and interferon-gamma (IFN-gamma), but almost complete disappearance of iNOS expression, which coexisted with a significant increment of bacterial load. Prostaglandins 55-57 tumor necrosis factor Mus musculus 115-124 12047755-11 2002 When PG production was suppressed in animals suffering advanced phase infection, a significant reduction of pneumonia and bacillus load with striking increment of granuloma size was seen, and the expression of IFN-gamma, TNF-alpha and iNOS was also improved. Prostaglandins 5-7 tumor necrosis factor Mus musculus 221-230 11853703-8 2002 These results indicate that, under certain conditions, cyclooxygenase-2-dependent prostaglandin synthesis is critical for the bone resorption induced by IL-1beta, TNF-alpha, and LPS, and for the osteoclastogenesis induced by these pro-inflammatory molecules and calciotropic hormones. Prostaglandins 82-95 tumor necrosis factor Mus musculus 163-172 9002955-7 1997 The actions of TNF-alpha and IL-6 were inhibited by indomethacin, an inhibitor for prostaglandin synthesis, and by neutralizing anti-IFN-gamma and anti-IL-3 antibodies. Prostaglandins 83-96 tumor necrosis factor Mus musculus 15-24 11201877-10 2000 For example, the down-regulatory effects of local prostaglandin production can be controlled with essential fatty acid deficient diets or indomethacin, RNI can be blocked in CGD and GKO mice by treatment with aminoguanidine, NG monomethyl arginine or N6-(1-iminoethyl)-L-lysine, and local elaboration of TNF alpha can be neutralized by anti-TNF alpha antibody or excess TNF alpha receptor. Prostaglandins 50-63 tumor necrosis factor Mus musculus 304-313 11201877-10 2000 For example, the down-regulatory effects of local prostaglandin production can be controlled with essential fatty acid deficient diets or indomethacin, RNI can be blocked in CGD and GKO mice by treatment with aminoguanidine, NG monomethyl arginine or N6-(1-iminoethyl)-L-lysine, and local elaboration of TNF alpha can be neutralized by anti-TNF alpha antibody or excess TNF alpha receptor. Prostaglandins 50-63 tumor necrosis factor Mus musculus 341-350 11201877-10 2000 For example, the down-regulatory effects of local prostaglandin production can be controlled with essential fatty acid deficient diets or indomethacin, RNI can be blocked in CGD and GKO mice by treatment with aminoguanidine, NG monomethyl arginine or N6-(1-iminoethyl)-L-lysine, and local elaboration of TNF alpha can be neutralized by anti-TNF alpha antibody or excess TNF alpha receptor. Prostaglandins 50-63 tumor necrosis factor Mus musculus 341-350 10497256-3 1999 We report here that prostaglandin E(2) (PGE(2)), one of the major prostaglandins produced in the brain, acts as a potent and selective inhibitor of tumor necrosis factor alpha (TNF-alpha) production in lipopolysaccharide-stimulated primary microglia and the microglial cell line BV-2. Prostaglandins 66-80 tumor necrosis factor Mus musculus 148-175 10497256-3 1999 We report here that prostaglandin E(2) (PGE(2)), one of the major prostaglandins produced in the brain, acts as a potent and selective inhibitor of tumor necrosis factor alpha (TNF-alpha) production in lipopolysaccharide-stimulated primary microglia and the microglial cell line BV-2. Prostaglandins 66-80 tumor necrosis factor Mus musculus 177-186 11301049-1 2001 To know which receptors of prostaglandins are involved in the regulation of TNFalpha and interleukin 10 (IL-10) production, we examined the production of these cytokines in murine peritoneal macrophages stimulated with zymosan. Prostaglandins 27-41 tumor necrosis factor Mus musculus 76-84 11301049-6 2001 These functional effects of prostaglandins well accorded with the mRNA expression of TNFalpha and IL-10 when such expression was examined by the RT-PCR method. Prostaglandins 28-42 tumor necrosis factor Mus musculus 85-93 7827287-5 1994 These results indicate that TNF-alpha production is modulated by endogenous prostaglandins in vivo and that enhanced production of TNF-alpha by cyclooxygenase inhibitors may lead to exacerbation of some inflammatory processes. Prostaglandins 76-90 tumor necrosis factor Mus musculus 28-37 8852946-11 1996 We conclude that (1) IL-1, TNF-alpha, and PTH, but not IL-6 nor IL-11, can increase the expression of PGHS-2, cPLA2, and PGE2 production in cultured mouse calvariae; (2) IL-4 inhibits PGE2 production in both control and stimulated calvarial cultures by inhibiting PGHS-2 and cPLA2; and (3) IL-4 has an inhibitory effect on bone resorption which is independent of PG production. Prostaglandins 102-104 tumor necrosis factor Mus musculus 27-36 1335420-2 1992 Tumor necrosis factor-alpha is known to induce inflammatory mediators such as leukotrienes and prostanoids. Prostaglandins 95-106 tumor necrosis factor Mus musculus 0-27 1527636-4 1992 With increasing dietary (n-3): (n-6) ratio there was a decrease in the prostaglandin production by resident peritoneal macrophages, which may partly explain the increased TNF production. Prostaglandins 71-84 tumor necrosis factor Mus musculus 171-174 1475281-6 1992 In contrast, TNF-alpha suppressed PG synthesis and inhibited Ia surface expression. Prostaglandins 34-36 tumor necrosis factor Mus musculus 13-16 1475281-8 1992 Pretreatment with MAb to TNF had no effect on Con A-induced Ia levels, but significantly inhibited suppressed PG synthesis. Prostaglandins 110-112 tumor necrosis factor Mus musculus 25-28 1428359-8 1992 These data indicate that IL-6 and TNF production are differently susceptible to glucocorticoids, and that prostaglandins can physiologically provide a negative feedback regulation of IL-6 and TNF synthesis. Prostaglandins 106-120 tumor necrosis factor Mus musculus 192-195 1398747-8 1992 PG secretion increased following appearance of cell-associated TNF but when PG had accumulated in the medium there was no further increase in TNF production. Prostaglandins 0-2 tumor necrosis factor Mus musculus 63-66 1782670-0 1991 Involvement of prostaglandin-producing pathway in the cytotoxic action of tumor necrosis factor. Prostaglandins 15-28 tumor necrosis factor Mus musculus 74-95 1782670-4 1991 The cytotoxic action of TNF on L929 cells was inhibited by indomethacin, suggesting that prostaglandin may be involved in the action. Prostaglandins 89-102 tumor necrosis factor Mus musculus 24-27 1782670-5 1991 Therefore, TNF-stimulated prostaglandin production was examined in L929 and TNF-resistant sublines. Prostaglandins 26-39 tumor necrosis factor Mus musculus 11-14 1782670-5 1991 Therefore, TNF-stimulated prostaglandin production was examined in L929 and TNF-resistant sublines. Prostaglandins 26-39 tumor necrosis factor Mus musculus 76-79 1782670-8 1991 These results suggest that arachidonate release and subsequent prostaglandin production are important for the cytotoxic action of TNF and that these processes are mediated by GTP-binding protein (G protein) that is coupled to the TNF-receptor. Prostaglandins 63-76 tumor necrosis factor Mus musculus 130-133 1782670-8 1991 These results suggest that arachidonate release and subsequent prostaglandin production are important for the cytotoxic action of TNF and that these processes are mediated by GTP-binding protein (G protein) that is coupled to the TNF-receptor. Prostaglandins 63-76 tumor necrosis factor Mus musculus 230-233 3197264-5 1988 A regulatory mechanism of E-series prostaglandins (PGE) might be involved in the induction of hyporesponsiveness in macrophages of tolerant mice, as the LPS-stimulated TNF release could be inhibited in a dose dependent manner by preincubation with PGE1. Prostaglandins 35-49 tumor necrosis factor Mus musculus 168-171 1998408-0 1991 Blockade of prostaglandin production increases cachectin synthesis and prevents depression of macrophage functions after hemorrhagic shock. Prostaglandins 12-25 tumor necrosis factor Mus musculus 47-56 1908334-0 1991 In vitro cytokine release by activated murine peritoneal macrophages: role of prostaglandins in the differential regulation of tumor necrosis factor alpha, interleukin 1, and interleukin 6. Prostaglandins 78-92 tumor necrosis factor Mus musculus 127-154 1908334-7 1991 The release of TNF-alpha is inhibited by prostaglandins, whereas increased levels of PGE2 and PGI2 correlate with higher levels of IL-6. Prostaglandins 41-55 tumor necrosis factor Mus musculus 15-24 2001418-0 1991 Tumor necrosis factor-alpha stimulates phosphatidylinositol breakdown by phospholipase C to coordinately increase the levels of diacylglycerol, free arachidonic acid and prostaglandins in an osteoblast (MC3T3-E1) cell line. Prostaglandins 170-184 tumor necrosis factor Mus musculus 0-27 2001418-6 1991 Therefore, we conclude that, in the MC3T3-E1 cell line, tumor necrosis factor-alpha activates a phosphatidylinositol-specific phospholipase C (phosphatidylinositol inositolphosphohydrolase; EC 3.1.4.3) to release diacylglycerol, and increases the metabolism of diacylglycerol to liberate arachidonate for prostaglandin synthesis. Prostaglandins 305-318 tumor necrosis factor Mus musculus 56-83 35203267-6 2022 However, the co-stimulation with prostaglandin (PG) E2 resulted in a marked increase in the secretion of various cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-6, and IL-13, accompanied by an increase in their mRNA levels. Prostaglandins 33-46 tumor necrosis factor Mus musculus 132-159 2803915-2 1989 A single injection of TNF-alpha caused an enhanced production of PGE2 by spleen cells from treated animals, that was significant within 1 h of treatment, and persisted until at least 6 h. These results suggest that the anorectic effect of TNF-alpha may be mediated by a prostaglandin intermediate. Prostaglandins 270-283 tumor necrosis factor Mus musculus 22-31 2803915-2 1989 A single injection of TNF-alpha caused an enhanced production of PGE2 by spleen cells from treated animals, that was significant within 1 h of treatment, and persisted until at least 6 h. These results suggest that the anorectic effect of TNF-alpha may be mediated by a prostaglandin intermediate. Prostaglandins 270-283 tumor necrosis factor Mus musculus 239-248 3106013-0 1987 Tumor necrosis factor-alpha (cachectin) stimulates bone resorption in mouse calvaria via a prostaglandin-mediated mechanism. Prostaglandins 91-104 tumor necrosis factor Mus musculus 0-27 3366472-5 1988 Since indomethacin inhibits production by spleen cells of the NC/TNF inhibitory factor, it is suggested that prostaglandins are involved in the regulation of its production. Prostaglandins 109-123 tumor necrosis factor Mus musculus 65-68 3106013-0 1987 Tumor necrosis factor-alpha (cachectin) stimulates bone resorption in mouse calvaria via a prostaglandin-mediated mechanism. Prostaglandins 91-104 tumor necrosis factor Mus musculus 29-38 3131072-11 1987 A possible mechanism of action of TNF is the release and metabolism of polyunsaturated fatty acids, which would explain the synthesis of prostaglandins and leukotrienes by many cell types after TNF treatment. Prostaglandins 137-151 tumor necrosis factor Mus musculus 34-37 3131072-11 1987 A possible mechanism of action of TNF is the release and metabolism of polyunsaturated fatty acids, which would explain the synthesis of prostaglandins and leukotrienes by many cell types after TNF treatment. Prostaglandins 137-151 tumor necrosis factor Mus musculus 194-197