PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17920530-5 2007 Inhibition of phospholipase A2 (PLA2) and NOS prevented pSS IgG effects upon both PGE2 production and COX-1 mRNA levels. Dinoprostone 82-86 phospholipase A2 group IB Homo sapiens 14-30 18178864-8 2008 Immunofluorescence microscopy of phospholipase A2 (PLA2) and ELISA analysis of PGE2 revealed activation of PLA2 and production of PGE2 in response to CM but not S1P. Dinoprostone 79-83 phospholipase A2 group IB Homo sapiens 107-111 17920530-5 2007 Inhibition of phospholipase A2 (PLA2) and NOS prevented pSS IgG effects upon both PGE2 production and COX-1 mRNA levels. Dinoprostone 82-86 phospholipase A2 group IB Homo sapiens 32-36 16741924-6 2006 As indicated by pharmacological studies, the full PGE2-dependent potentiation of IL-1beta induced PLA2 secretion is associated with a change of regulation exerted by the subtypes 3 G(i)-coupled PGE2 receptors toward adenylyl cyclase(s) activated by the subtype 4 G(s)-linked PGE2 receptor. Dinoprostone 50-54 phospholipase A2 group IB Homo sapiens 98-102 17266940-0 2007 Histamine H3-receptor signaling in cardiac sympathetic nerves: Identification of a novel MAPK-PLA2-COX-PGE2-EP3R pathway. Dinoprostone 103-107 phospholipase A2 group IB Homo sapiens 94-98 16794572-10 2007 Quinacrine, [corrected] a PLA2 antagonist significantly blocked IL-1-induced [corrected] increase in PGE2 and corticosterone concentrations. Dinoprostone 101-105 phospholipase A2 group IB Homo sapiens 26-30 16794572-11 2007 These results demonstrated the hypotheses that IL-1 effects may be via PLA2-PGE2-corticosterone pathway and EPA attenuated IL-1 effects may be through the suppression of PLA2 expression, which then reduced PGE2 synthesis and corticosterone secretion. Dinoprostone 76-80 phospholipase A2 group IB Homo sapiens 71-75 16794572-11 2007 These results demonstrated the hypotheses that IL-1 effects may be via PLA2-PGE2-corticosterone pathway and EPA attenuated IL-1 effects may be through the suppression of PLA2 expression, which then reduced PGE2 synthesis and corticosterone secretion. Dinoprostone 206-210 phospholipase A2 group IB Homo sapiens 170-174 16766159-4 2006 Treatment of the cells with the PLA2 inhibitor 4-bromophenacyl bromide (BPB) decreased the cytokine-induced mPGES-1 expression accompanied by decreased PGE2 production whereas the addition of arachidonic acid (AA) upregulated mPGES-1 expression and PGE2 production. Dinoprostone 249-253 phospholipase A2 group IB Homo sapiens 32-36 16766159-4 2006 Treatment of the cells with the PLA2 inhibitor 4-bromophenacyl bromide (BPB) decreased the cytokine-induced mPGES-1 expression accompanied by decreased PGE2 production whereas the addition of arachidonic acid (AA) upregulated mPGES-1 expression and PGE2 production. Dinoprostone 152-156 phospholipase A2 group IB Homo sapiens 32-36 16807371-2 2006 PGE2 is produced from phospholipids by a cascade of enzymatic reactions involving phospholipase A2 (PLA2), cyclooxygenase (COX), and prostaglandin E synthase (PGES). Dinoprostone 0-4 phospholipase A2 group IB Homo sapiens 82-98 16807371-2 2006 PGE2 is produced from phospholipids by a cascade of enzymatic reactions involving phospholipase A2 (PLA2), cyclooxygenase (COX), and prostaglandin E synthase (PGES). Dinoprostone 0-4 phospholipase A2 group IB Homo sapiens 100-104 15187863-7 2004 Because cytosolic phospholipase-A2 and secretory phospholipase-A2 are involved in the production of prostaglandin-E2 and other inflammatory mediators, this study suggests that regulation of phospholipase-A2 expression level may be an alternative approach to control in vivo tendon inflammation. Dinoprostone 100-116 phospholipase A2 group IB Homo sapiens 18-34 16299051-3 2006 To explore other putative regulatory features we examined the role of phospholipase A2 (PLA2) and PGE synthase (PGES) enzymes in IL-1beta-induced PGE2 production. Dinoprostone 146-150 phospholipase A2 group IB Homo sapiens 70-86 16299051-3 2006 To explore other putative regulatory features we examined the role of phospholipase A2 (PLA2) and PGE synthase (PGES) enzymes in IL-1beta-induced PGE2 production. Dinoprostone 146-150 phospholipase A2 group IB Homo sapiens 88-92 16203828-0 2006 Systemic and intrathecal effects of a novel series of phospholipase A2 inhibitors on hyperalgesia and spinal prostaglandin E2 release. Dinoprostone 109-125 phospholipase A2 group IB Homo sapiens 54-70 15972573-12 2005 A cPLA2-selective inhibitor decreased both PLA2 activity in monkey granulosa cell lysates and PGE2 accumulation in cultures of human granulosa-lutein cells. Dinoprostone 94-98 phospholipase A2 group IB Homo sapiens 3-7 16569229-16 2006 IFN-gamma increased the levels of cytoplasmic phospholipase A2 in cultured neuronal cells and increased expression of cytoplasmic phospholipase A2 was associated with increased production of prostaglandin E2 in response to amyloid-beta1-42 or HuPrP82-146. Dinoprostone 191-207 phospholipase A2 group IB Homo sapiens 130-146 15900018-2 2005 PLA(2) acts to generate arachidonic acid, which serves as the precursor substrate for COX-2 in the metabolic pathway leading to PGE(2) production. Dinoprostone 128-134 phospholipase A2 group IB Homo sapiens 0-6 15187863-7 2004 Because cytosolic phospholipase-A2 and secretory phospholipase-A2 are involved in the production of prostaglandin-E2 and other inflammatory mediators, this study suggests that regulation of phospholipase-A2 expression level may be an alternative approach to control in vivo tendon inflammation. Dinoprostone 100-116 phospholipase A2 group IB Homo sapiens 49-65 11506393-4 2001 PGE2 increase was biphasic with an early peak at 10 min (around 5 ng/mg protein) due to increased PLA2 activity. Dinoprostone 0-4 phospholipase A2 group IB Homo sapiens 98-102 14687699-3 2004 The following results indicate that the phospholipase A2 (PLA2)/COX/prostaglandin E (PGE2) pathway is implicated in this process: (1) The inhibitory effect of BK on Ang-(1-7)-stimulated enzyme is abolished in a dose-dependent manner by quinacrine (10(-9)-10(-6)M), a nonspecific PLA2 inhibitor, and by PACOCF3 (10(-7)M), an inhibitor of a Ca(2+)-independent PLA2. Dinoprostone 85-89 phospholipase A2 group IB Homo sapiens 40-56 12235959-2 2002 PGE2, one of the PGs, is produced by the action of the enzyme PGE synthase and cyclooxigenase (COX) on arachidonic acid liberated from the membrane phospholipid by phospholipase A2 (PLA2). Dinoprostone 0-4 phospholipase A2 group IB Homo sapiens 164-180 12235959-2 2002 PGE2, one of the PGs, is produced by the action of the enzyme PGE synthase and cyclooxigenase (COX) on arachidonic acid liberated from the membrane phospholipid by phospholipase A2 (PLA2). Dinoprostone 0-4 phospholipase A2 group IB Homo sapiens 182-186 11274966-3 2001 Our results demonstrate that the cytosolic PLA2 inhibitor, arachidonyl trifluoromethylketone and the cytosolic calcium-independent PLA2 (iPLA2) inhibitor, bromoenol lactone, decrease arachidonic acid release and prostaglandin E2 production in 3T6 fibroblast cultures stimulated by fetal calf serum. Dinoprostone 212-228 phospholipase A2 group IB Homo sapiens 43-47 11274966-3 2001 Our results demonstrate that the cytosolic PLA2 inhibitor, arachidonyl trifluoromethylketone and the cytosolic calcium-independent PLA2 (iPLA2) inhibitor, bromoenol lactone, decrease arachidonic acid release and prostaglandin E2 production in 3T6 fibroblast cultures stimulated by fetal calf serum. Dinoprostone 212-228 phospholipase A2 group IB Homo sapiens 131-135 10675243-3 2000 The purpose of this study was to determine the effect of selective cytoplasmic and secretory phospholipase A2 inhibitors on basal and stimulated arachidonic acid and prostaglandin E2 release in gallbladder cells. Dinoprostone 166-182 phospholipase A2 group IB Homo sapiens 93-109 11207202-5 2001 The fMLP-induced PGE2 output is inhibited by indomethacin, quinacrine, and U-73122, inhibitors of cyclooxygenase, phospholipase A2, and phospholipase C, respectively. Dinoprostone 17-21 phospholipase A2 group IB Homo sapiens 114-130 10614936-13 1999 The results indicate that surface roughness and 1,25-(OH)2 D3 mediate their effects through phospholipase A2, which catalyzes one of the rate-limiting steps in prostaglandin E2 production. Dinoprostone 160-176 phospholipase A2 group IB Homo sapiens 92-108 11729854-13 2000 CONCLUSIONS: The metabolic pathway of PGE2 formation is variable and the PLA2 enzyme involved in producing PGE2 is dependent on the stimulus and the cell line. Dinoprostone 38-42 phospholipase A2 group IB Homo sapiens 73-77 11132768-4 2000 PLA2 activity was measured using 3H-arachidonic acid release, PGE2 release and COX activity by ELISA, and COX2 content by flow cytometry. Dinoprostone 62-66 phospholipase A2 group IB Homo sapiens 0-4 11132768-12 2000 Uncoupling of inhibition of PLA2 and COX by annexin I and DEX support the hypothesis that COX is rate-limiting for PGE2 synthesis in FLS. Dinoprostone 115-119 phospholipase A2 group IB Homo sapiens 28-32 11729854-13 2000 CONCLUSIONS: The metabolic pathway of PGE2 formation is variable and the PLA2 enzyme involved in producing PGE2 is dependent on the stimulus and the cell line. Dinoprostone 107-111 phospholipase A2 group IB Homo sapiens 73-77 9826060-11 1998 Conversely, the phospholipase A2 inhibitor quinacrine (100 microM) blocked the release of arachidonic acid and PGE2 without affecting the NKA-stimulated formation of IP3. Dinoprostone 111-115 phospholipase A2 group IB Homo sapiens 16-32 10027847-7 1999 In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Dinoprostone 41-45 phospholipase A2 group IB Homo sapiens 128-144 10027847-8 1999 Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. Dinoprostone 33-37 phospholipase A2 group IB Homo sapiens 151-167 10065947-10 1999 The phospholipase A2 (PLA2) inhibitor, BPB, and the PKC inhibitor, BIS, reduced PGE2 production, whereas dexamethasone, indomethacin, and NS-398 completely abolished PGE2 production induced by IL-1beta, TNFalpha, and the combination. Dinoprostone 80-84 phospholipase A2 group IB Homo sapiens 4-20 10065947-10 1999 The phospholipase A2 (PLA2) inhibitor, BPB, and the PKC inhibitor, BIS, reduced PGE2 production, whereas dexamethasone, indomethacin, and NS-398 completely abolished PGE2 production induced by IL-1beta, TNFalpha, and the combination. Dinoprostone 80-84 phospholipase A2 group IB Homo sapiens 22-26 9873232-6 1999 Nicotine (2 microg/ml) prevented the effect of PGE2; (2) both cotinine (EC50 470-500 fmol/l) and nicotine (EC50 18-32 pmol/l) activated PLA2 in human placental tissues. Dinoprostone 47-51 phospholipase A2 group IB Homo sapiens 136-140 9629250-20 1998 Phospholipase A2 converts membrane phospholipids into arachidonic acid, the substrate for conversion by the activated cyclooxygenase and lipoxygenase to PGE2 and leukotrienes that activate the release of LHRH. Dinoprostone 153-157 phospholipase A2 group IB Homo sapiens 0-16 9144546-5 1997 PLA2, AC, COX, NOS, and sGC inhibitors counteracted SP and PGE2 effects, except for PLA2, which did not affect PGE2. Dinoprostone 59-63 phospholipase A2 group IB Homo sapiens 0-4 9556056-7 1998 Arachidonic acid and prostaglandin E2, two downstream products of phospholipase A2 action, also increased PKC activity. Dinoprostone 21-37 phospholipase A2 group IB Homo sapiens 66-82 9219677-2 1997 Calcium-containing crystals including HA, are known to have a number of biologic effects on culture cells such induction of mitogenesis, stimulation of Prostaglandin E2 (PGE2) production via the phospholipase A2/cyclo-oxygenase pathway, activation of phospholipase C and inositol phospholipid hydrolysis, induction of metalloproteinase synthesis and induction of proto-oncogenes (c-fos and c-myc). Dinoprostone 152-168 phospholipase A2 group IB Homo sapiens 195-211 9219677-2 1997 Calcium-containing crystals including HA, are known to have a number of biologic effects on culture cells such induction of mitogenesis, stimulation of Prostaglandin E2 (PGE2) production via the phospholipase A2/cyclo-oxygenase pathway, activation of phospholipase C and inositol phospholipid hydrolysis, induction of metalloproteinase synthesis and induction of proto-oncogenes (c-fos and c-myc). Dinoprostone 170-174 phospholipase A2 group IB Homo sapiens 195-211 9351889-5 1997 Inhibition of endogenous PGE2 production by blockers of phospholipase A2 activity (quinacrine or 3[4-octadecyl]-benzoylacrylic acid; OBBA), or inhibition of cyclooxygenase activity by indomethacin reduced the stimulation of Isc and Gt by hyposmotic solutions. Dinoprostone 25-29 phospholipase A2 group IB Homo sapiens 56-72 9353419-1 1997 Exposure of human rheumatoid synovial fibroblasts (RSF) to interleukin 1beta (IL-1beta) results in the coordinate up-regulation of 85-kDa phospholipase A2 (PLA2) and mitogen-inducible cyclooxygenase (COX II) and subsequent biosynthesis of prostaglandin E2 (PGE2). Dinoprostone 239-255 phospholipase A2 group IB Homo sapiens 138-154 9353419-1 1997 Exposure of human rheumatoid synovial fibroblasts (RSF) to interleukin 1beta (IL-1beta) results in the coordinate up-regulation of 85-kDa phospholipase A2 (PLA2) and mitogen-inducible cyclooxygenase (COX II) and subsequent biosynthesis of prostaglandin E2 (PGE2). Dinoprostone 239-255 phospholipase A2 group IB Homo sapiens 156-160 9353419-1 1997 Exposure of human rheumatoid synovial fibroblasts (RSF) to interleukin 1beta (IL-1beta) results in the coordinate up-regulation of 85-kDa phospholipase A2 (PLA2) and mitogen-inducible cyclooxygenase (COX II) and subsequent biosynthesis of prostaglandin E2 (PGE2). Dinoprostone 257-261 phospholipase A2 group IB Homo sapiens 138-154 9353419-1 1997 Exposure of human rheumatoid synovial fibroblasts (RSF) to interleukin 1beta (IL-1beta) results in the coordinate up-regulation of 85-kDa phospholipase A2 (PLA2) and mitogen-inducible cyclooxygenase (COX II) and subsequent biosynthesis of prostaglandin E2 (PGE2). Dinoprostone 257-261 phospholipase A2 group IB Homo sapiens 156-160 9322222-19 1997 Phospholipase A2 converts membrane phospholipids into arachidonic acid, the substrate for conversion by the activated cyclooxygenase to PGE2 which then activates the release of LHRH. Dinoprostone 136-140 phospholipase A2 group IB Homo sapiens 0-16 9247974-2 1997 The production of PGE2 was increased by stimulating the cells with EGF for 2 h and reached a maximum for 10 h. EGF was also found to augment the release of arachidonic acid (AA) following the increase in phospholipase A2 (PLA2) activity (1.7-fold). Dinoprostone 18-22 phospholipase A2 group IB Homo sapiens 204-220 9247974-2 1997 The production of PGE2 was increased by stimulating the cells with EGF for 2 h and reached a maximum for 10 h. EGF was also found to augment the release of arachidonic acid (AA) following the increase in phospholipase A2 (PLA2) activity (1.7-fold). Dinoprostone 18-22 phospholipase A2 group IB Homo sapiens 222-226 8832976-0 1996 Suppression of human synovial fibroblast 85 kDa phospholipase A2 by antisense reduces interleukin-1 beta induced prostaglandin E2. Dinoprostone 113-129 phospholipase A2 group IB Homo sapiens 48-64 8832976-1 1996 OBJECTIVE: To evaluate the relative roles of rheumatoid synovial fibroblast phospholipases A2 (PLA2) in interleukin- 1beta (IL-1 beta) stimulated prostaglandin E2 (PGE2) production. Dinoprostone 146-162 phospholipase A2 group IB Homo sapiens 95-99 8832976-2 1996 METHODS: The role of the cytosolic 85 kDa PLA2 in IL-1beta induced human rheumatoid synovial fibroblast PGE2 formation was directly evaluated using an antisense phosphorothioate oligonucleotide to the initiation site of the 85 kDa PLA2 mRNA. Dinoprostone 104-108 phospholipase A2 group IB Homo sapiens 42-46 8832976-8 1996 CONCLUSION: These data directly support a role for the 85 kDa PLA2, but not the 14 kDa PLA2, in IL- 1beta stimulated PGE2 production from human rheumatoid synovial fibroblast. Dinoprostone 117-121 phospholipase A2 group IB Homo sapiens 62-66 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 283-299 phospholipase A2 group IB Homo sapiens 214-230 8633180-4 1995 The mechanism by which Con A mobilized f(Ca2+)i is not clear, but we found that the level of prostaglandin E2, a metabolite from arachidonic acid, increased after stimulation with Con A, indicating the possibility of arachidonic acid released by phospholipase A2. Dinoprostone 93-109 phospholipase A2 group IB Homo sapiens 246-262 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 283-299 phospholipase A2 group IB Homo sapiens 232-236 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 301-305 phospholipase A2 group IB Homo sapiens 214-230 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 301-305 phospholipase A2 group IB Homo sapiens 232-236 7957239-1 1994 Treatment of human synovial cells with interleukin-1 (IL-1) results in a large increase in the production of prostaglandin E2 (PGE2), a function in which the activation of phospholipase A2 (PLA2) is a key step. Dinoprostone 109-125 phospholipase A2 group IB Homo sapiens 172-188 8567845-7 1995 The effect of PGE2 on PGF2 alpha production is inhibited by staurosporin and this inhibition was reversed by addition of arachidonic acid indicating that protein kinase C is involved in phospholipase A2 activation. Dinoprostone 14-18 phospholipase A2 group IB Homo sapiens 186-202 8567845-11 1995 Stimulation of cyclo-oxygenase to synthesize PGE2 activates phospholipase A2 to release arachidonic acid which is the substrate for lipoxygenase activity. Dinoprostone 45-49 phospholipase A2 group IB Homo sapiens 60-76 8567845-3 1995 To understand better the role of PGE2 in the induction of PGF2 alpha synthesis through modulation of phospholipase A2, inhibitors of this enzyme were used. Dinoprostone 33-37 phospholipase A2 group IB Homo sapiens 101-117 8567845-4 1995 The effects of PGE2 were blocked by phospholipase A2 inhibitors and this inhibition was reversed by addition of arachidonic acid. Dinoprostone 15-19 phospholipase A2 group IB Homo sapiens 36-52 8567845-5 1995 These data indicate that PGE2 activates phospholipase A2 to produce arachidonic acid. Dinoprostone 25-29 phospholipase A2 group IB Homo sapiens 40-56 7724577-18 1995 The increase in cGMP increases intracellular free calcium, activating phospholipase A2 to provide arachidonic acid, the substrate for conversion by the activated cyclooxygenase to PGE2, which then activates the release of LHRH. Dinoprostone 180-184 phospholipase A2 group IB Homo sapiens 70-86 7724577-19 1995 Since alcohol inhibits the conversion of labeled arachidonic acid to PGE2, it must act either directly to inhibit cyclooxygenase or perhaps it may act by blocking the increase in intracellular free calcium induced by cGMP, which is crucial for activation of of both phospholipase A2 and cyclooxygenase. Dinoprostone 69-73 phospholipase A2 group IB Homo sapiens 266-301 7957239-1 1994 Treatment of human synovial cells with interleukin-1 (IL-1) results in a large increase in the production of prostaglandin E2 (PGE2), a function in which the activation of phospholipase A2 (PLA2) is a key step. Dinoprostone 109-125 phospholipase A2 group IB Homo sapiens 190-194 7957239-1 1994 Treatment of human synovial cells with interleukin-1 (IL-1) results in a large increase in the production of prostaglandin E2 (PGE2), a function in which the activation of phospholipase A2 (PLA2) is a key step. Dinoprostone 127-131 phospholipase A2 group IB Homo sapiens 172-188 7957239-1 1994 Treatment of human synovial cells with interleukin-1 (IL-1) results in a large increase in the production of prostaglandin E2 (PGE2), a function in which the activation of phospholipase A2 (PLA2) is a key step. Dinoprostone 127-131 phospholipase A2 group IB Homo sapiens 190-194 7957239-2 1994 In order to identify the enzymes that are linked to IL-1-mediated arachidonate availability and subsequent PGE2 production, we have investigated the changes in gene expression of the 85-kDa cytosolic PLA2 (cPLA2), the 14-kDa secretory PLA2 (sPLA2) and the two forms of cyclooxygenase in human synoviocytes after stimulation with recombinant IL-1 beta. Dinoprostone 107-111 phospholipase A2 group IB Homo sapiens 200-204 7929310-2 1994 The presence of an immunologically related 85-kDa PLA2 and type II 14-kDa PLA2 was demonstrated in human monocytes and their roles examined in lipopolysaccharide (LPS)-induced monocyte prostaglandin E2 (PGE2) formation. Dinoprostone 185-201 phospholipase A2 group IB Homo sapiens 50-54 7929310-2 1994 The presence of an immunologically related 85-kDa PLA2 and type II 14-kDa PLA2 was demonstrated in human monocytes and their roles examined in lipopolysaccharide (LPS)-induced monocyte prostaglandin E2 (PGE2) formation. Dinoprostone 203-207 phospholipase A2 group IB Homo sapiens 74-78 7929310-2 1994 The presence of an immunologically related 85-kDa PLA2 and type II 14-kDa PLA2 was demonstrated in human monocytes and their roles examined in lipopolysaccharide (LPS)-induced monocyte prostaglandin E2 (PGE2) formation. Dinoprostone 185-201 phospholipase A2 group IB Homo sapiens 74-78 7929310-9 1994 Taken together, these data support a role for the cytosolic 85-kDa PLA2 in LPS-induced monocyte PGE2 formation. Dinoprostone 96-100 phospholipase A2 group IB Homo sapiens 67-71 7929310-2 1994 The presence of an immunologically related 85-kDa PLA2 and type II 14-kDa PLA2 was demonstrated in human monocytes and their roles examined in lipopolysaccharide (LPS)-induced monocyte prostaglandin E2 (PGE2) formation. Dinoprostone 203-207 phospholipase A2 group IB Homo sapiens 50-54 8033515-6 1994 Blockade of cyclo-oxygenase with indomethacin or of lipoxygenase with ICI 207968 or of phospholipase A2 with mepacrine inhibited release of prostaglandin E2 or leukotriene C4 or both of these plus platelet-activating factor, respectively. Dinoprostone 140-156 phospholipase A2 group IB Homo sapiens 87-103 8055950-1 1994 Stimulation of peripheral blood leukocytes with lipopolysaccharide results in the synthesis of inflammatory cytokines including interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha and prostaglandin E2 correlating with an increase in phospholipase A2 activity. Dinoprostone 195-211 phospholipase A2 group IB Homo sapiens 244-260 8167224-2 1994 More particularly, the objective was to ascertain whether an increase in type II PLA2 tissue content and PLA2 enzymatic activity is associated with the previously documented stimulatory effect of LPS on prostaglandin E2 (PGE2) release from choriodecidua. Dinoprostone 203-219 phospholipase A2 group IB Homo sapiens 81-85 8005507-6 1994 The significant increase of phospholipase A2 activity in term amniotic fluids and with PRM, in comparison with what is seen in young fluids suggests the active participation of the soluble form of this enzyme as mediator in the increase of Prostaglandin E2 seen in the amniotic fluid of the two first groups. Dinoprostone 240-256 phospholipase A2 group IB Homo sapiens 28-44 8167224-2 1994 More particularly, the objective was to ascertain whether an increase in type II PLA2 tissue content and PLA2 enzymatic activity is associated with the previously documented stimulatory effect of LPS on prostaglandin E2 (PGE2) release from choriodecidua. Dinoprostone 203-219 phospholipase A2 group IB Homo sapiens 105-109 8167224-2 1994 More particularly, the objective was to ascertain whether an increase in type II PLA2 tissue content and PLA2 enzymatic activity is associated with the previously documented stimulatory effect of LPS on prostaglandin E2 (PGE2) release from choriodecidua. Dinoprostone 221-225 phospholipase A2 group IB Homo sapiens 81-85 8167224-2 1994 More particularly, the objective was to ascertain whether an increase in type II PLA2 tissue content and PLA2 enzymatic activity is associated with the previously documented stimulatory effect of LPS on prostaglandin E2 (PGE2) release from choriodecidua. Dinoprostone 221-225 phospholipase A2 group IB Homo sapiens 105-109 8126383-7 1994 In conclusion, the evidence suggests that dihydropyridines inhibit PGE2 production in amnion cells by directly inhibiting PLA2 rather than its actions on calcium channels. Dinoprostone 67-71 phospholipase A2 group IB Homo sapiens 122-126 8026724-10 1994 The stimulatory effect of sucralfate on LPC synthesis and PGE2 generation was inhibited by phospholipase A2 inhibitors, mepacrine and BPB. Dinoprostone 58-62 phospholipase A2 group IB Homo sapiens 91-107 1836009-10 1991 A potential mechanism by which sphingosine could increase TNF alpha-induced PGE2 production involves enhancement of phospholipase A2 (PLA2) and/or cyclooxygenase (Cox) activity, the rate-limiting enzymes in PGE2 production. Dinoprostone 76-80 phospholipase A2 group IB Homo sapiens 116-132 7548116-6 1993 Furthermore, A549 cell PLA2 stimulated prostaglandin E2 release (approx. Dinoprostone 39-55 phospholipase A2 group IB Homo sapiens 23-27 8431204-11 1993 CONCLUSION: Our findings strongly suggest that AA and PGE2 production by IL-1-triggered synoviocytes are largely dependent upon PLA2-mediated hydrolysis of PC and PE and to a lesser extent upon the earlier degradation of PI. Dinoprostone 54-58 phospholipase A2 group IB Homo sapiens 128-132 8171073-4 1994 Furthermore, phospholipase A2 stimulated PGE2 production in cells cultured with M199 + HS but had no influence on PGE2 output by cells cultured with F12:DME + FCS. Dinoprostone 41-45 phospholipase A2 group IB Homo sapiens 13-29 7686736-5 1993 The activation of phospholipase A2 (PLA2), and the subsequent release of arachidonic acid and the primary metabolite prostaglandin E2, also was found to be time- and concentration-dependent. Dinoprostone 117-133 phospholipase A2 group IB Homo sapiens 18-34 7686736-5 1993 The activation of phospholipase A2 (PLA2), and the subsequent release of arachidonic acid and the primary metabolite prostaglandin E2, also was found to be time- and concentration-dependent. Dinoprostone 117-133 phospholipase A2 group IB Homo sapiens 36-40 1581109-4 1992 1,25-(OH)2D3-dependent alkaline phosphatase and phospholipase A2 activity were correlated with production of PGE2 and PGE1 in the MC-3T3-E1 cells. Dinoprostone 109-113 phospholipase A2 group IB Homo sapiens 48-64 1761509-0 1991 Augmentation of prostaglandin E2 production by mammalian phospholipase A2 added exogenously. Dinoprostone 16-32 phospholipase A2 group IB Homo sapiens 57-73 1761509-1 1991 Rat group II phospholipase A2 added exogenously to A23187-activated HL-60 granulocytes augmented their production of prostaglandin E2. Dinoprostone 117-133 phospholipase A2 group IB Homo sapiens 13-29 1761509-2 1991 Human group II phospholipase A2 and porcine group I phospholipase A2 augmented the prostaglandin E2 production in a similar manner. Dinoprostone 83-99 phospholipase A2 group IB Homo sapiens 15-31 1761509-2 1991 Human group II phospholipase A2 and porcine group I phospholipase A2 augmented the prostaglandin E2 production in a similar manner. Dinoprostone 83-99 phospholipase A2 group IB Homo sapiens 52-68 2230125-11 1990 Both phospholipase A2 and PLAP induced production by human monocytes of PGE2 and leukotriene B4 by neutrophils. Dinoprostone 72-76 phospholipase A2 group IB Homo sapiens 5-21 2019723-12 1991 In women, there is an increase of phospholipase A2 activity in amnios and uterus with an increase of PGE2 in the first tissue and of PGF2 alpha in the second one. Dinoprostone 101-105 phospholipase A2 group IB Homo sapiens 34-50 2158512-8 1990 Moreover, the inhibition by rIFN-gamma of PGE2 and collagenase was reversed by the addition of phospholipase A2. Dinoprostone 42-46 phospholipase A2 group IB Homo sapiens 95-111 2111570-5 1990 The phospholipase A2 inhibitor quinacrine was able to prevent the TPA-induced increase in PGE2 synthesis even in the presence of exogenous arachidonic acid suggesting that phospholipase A2 may be a target for PKC action. Dinoprostone 90-94 phospholipase A2 group IB Homo sapiens 4-20 2111570-5 1990 The phospholipase A2 inhibitor quinacrine was able to prevent the TPA-induced increase in PGE2 synthesis even in the presence of exogenous arachidonic acid suggesting that phospholipase A2 may be a target for PKC action. Dinoprostone 90-94 phospholipase A2 group IB Homo sapiens 172-188 2775481-3 1989 Also the zymosan-induced formation of thromboxane and prostaglandin E2 from endogenous sources which is thought to involve phospholipase A2 remains unaffected in the presence of this compound. Dinoprostone 54-70 phospholipase A2 group IB Homo sapiens 123-139 2621392-11 1989 In addition, the enhancement of PGE2 production in osteoblasts was due to activation of both phospholipase A2 and PGE2-synthesizing enzymes. Dinoprostone 32-36 phospholipase A2 group IB Homo sapiens 93-109 2507329-7 1989 It seems likely, therefore, that activation of phospholipase A2 which occurs during a short incubation with IL-1, TNF alpha or bradykinin releases substrate, AA, which is more rapidly converted to PGE2 by cells in which CO has been induced. Dinoprostone 197-201 phospholipase A2 group IB Homo sapiens 47-63 2566335-8 1989 Physiological regulators of PLA2 activity; calcium, cortisol, estrogen, progesterone, and PGE2 are documented abnormalities in some patients with affective disorders and consistent with excessive PLA2 activity. Dinoprostone 90-94 phospholipase A2 group IB Homo sapiens 28-32 2566335-8 1989 Physiological regulators of PLA2 activity; calcium, cortisol, estrogen, progesterone, and PGE2 are documented abnormalities in some patients with affective disorders and consistent with excessive PLA2 activity. Dinoprostone 90-94 phospholipase A2 group IB Homo sapiens 196-200 3001128-5 1985 The ability of cells to produce PGE2 in response to a calcium ionophore (A23187), an activator of phospholipase A2 (melittin), arachidonic acid, or serum was maximal during the period of early exponential growth. Dinoprostone 32-36 phospholipase A2 group IB Homo sapiens 98-114 3118014-2 1987 PLC had a more pronounced effect than PLA-2, particularly on the output of PGE-2. Dinoprostone 75-80 phospholipase A2 group IB Homo sapiens 38-43 3118014-3 1987 The ratios of the outputs of PGF-2 alpha and PGE-2 were similar after stimulation by A23187 and PLA-2, but this ratio was lower after stimulation by PLC. Dinoprostone 45-50 phospholipase A2 group IB Homo sapiens 96-101 3477611-7 1987 Treatment of cotyledonary microsomes with porcine phospholipase A2 (PLA2; 0.125 units/ml) also stimulated PG synthesis, PGE2 increasing to 216 +/- 27% and PGF2 alpha to 172 +/- 14% of control (P less than 0.05, n = 5) respectively. Dinoprostone 120-124 phospholipase A2 group IB Homo sapiens 50-66 3477611-7 1987 Treatment of cotyledonary microsomes with porcine phospholipase A2 (PLA2; 0.125 units/ml) also stimulated PG synthesis, PGE2 increasing to 216 +/- 27% and PGF2 alpha to 172 +/- 14% of control (P less than 0.05, n = 5) respectively. Dinoprostone 120-124 phospholipase A2 group IB Homo sapiens 68-72 2901097-10 1988 Thus, IL-1 enhanced receptor-mediated release of prostaglandin E2 in response to bradykinin, bombesin, and thrombin by increasing the cellular levels of phospholipase A2, cyclooxygenase, and GTP-binding regulatory protein(s). Dinoprostone 49-65 phospholipase A2 group IB Homo sapiens 153-169 3017321-5 1986 Since PLA2-inhibition by dexamethasone is claimed to be mediated via lipocortin, these results suggest that a lipocortin-like protein is present in pituitary cells and could be involved in the TPA-induced secretions of PGE2 and ACTH. Dinoprostone 219-223 phospholipase A2 group IB Homo sapiens 6-10 6315876-0 1983 Characterization of brain synaptic vesicle phospholipase A2 activity and its modulation by calmodulin, prostaglandin E2, prostaglandin F2 alpha, cyclic AMP, and ATP. Dinoprostone 103-119 phospholipase A2 group IB Homo sapiens 43-59 25263660-2 2015 1alpha,25(OH)2D3 binding to Pdia3 leads to phospholipase-A2 (PLA2)-activating protein (PLAA) activation, stimulating cytosolic PLA2 and resulting in prostaglandin E2 (PGE2) release and PKCalpha activation, subsequently stimulating differentiation. Dinoprostone 167-171 phospholipase A2 group IB Homo sapiens 61-65 6311214-2 1983 Prostaglandin E2, cyclic-AMP and cyclic-GMP inhibited phospholipase A2 in the presence or absence of calmodulin. Dinoprostone 0-16 phospholipase A2 group IB Homo sapiens 54-70 32842948-8 2022 The data from animal and human studies elucidated that PGI2, PGF2alpha, PGD2, isoprostanes, PGE2, PLA2, LTs are increased in MS. PLA2 inhibition modulates the progression of the disease. Dinoprostone 92-96 phospholipase A2 group IB Homo sapiens 129-133 26316080-3 2015 Phospholipase A2 is in part effective by fostering formation of prostaglandin E2, which triggers Ca(2+) entry. Dinoprostone 64-80 phospholipase A2 group IB Homo sapiens 0-16 29483877-10 2018 There is a decrease in the percentage of AA, associated with an increase of PLA2, COX2/TXA2R, CYP450 4A, and 5-LOX which leads to a greater synthesis of PGE2 than of 6-keto-PGF1alpha, thus contributing to the formation of the aortic aneurysm. Dinoprostone 153-157 phospholipase A2 group IB Homo sapiens 76-80 26056075-6 2015 High glucose induced also activation of PLA2/COX-2 pathway, as revealed by increased phosphorylation of cPLA2, COX-2 expression and PGE2 release. Dinoprostone 132-136 phospholipase A2 group IB Homo sapiens 40-44 25263660-2 2015 1alpha,25(OH)2D3 binding to Pdia3 leads to phospholipase-A2 (PLA2)-activating protein (PLAA) activation, stimulating cytosolic PLA2 and resulting in prostaglandin E2 (PGE2) release and PKCalpha activation, subsequently stimulating differentiation. Dinoprostone 149-165 phospholipase A2 group IB Homo sapiens 43-59 25263660-2 2015 1alpha,25(OH)2D3 binding to Pdia3 leads to phospholipase-A2 (PLA2)-activating protein (PLAA) activation, stimulating cytosolic PLA2 and resulting in prostaglandin E2 (PGE2) release and PKCalpha activation, subsequently stimulating differentiation. Dinoprostone 149-165 phospholipase A2 group IB Homo sapiens 61-65 24808633-0 2014 An Asp49 phospholipase A2 from snake venom induces cyclooxygenase-2 expression and prostaglandin E2 production via activation of NF-kappaB, p38MAPK, and PKC in macrophages. Dinoprostone 83-99 phospholipase A2 group IB Homo sapiens 9-25 25263660-2 2015 1alpha,25(OH)2D3 binding to Pdia3 leads to phospholipase-A2 (PLA2)-activating protein (PLAA) activation, stimulating cytosolic PLA2 and resulting in prostaglandin E2 (PGE2) release and PKCalpha activation, subsequently stimulating differentiation. Dinoprostone 167-171 phospholipase A2 group IB Homo sapiens 43-59 23881867-10 2013 This suggests that IL-13-enhanced PLA2 activity regulates COX-2/PGE2 expression through C/EBP-alpha activation. Dinoprostone 64-68 phospholipase A2 group IB Homo sapiens 34-38 22449386-8 2012 Also, phospholipase A2 (PLA2)/cyclooxygenase (COX) pathway is up-regulated in carbachol-induced SCA-9 cell proliferation, because prostaglandin E2 liberation (P<0.001) is increased and COX-1 expression is turned up (P<0.001). Dinoprostone 130-146 phospholipase A2 group IB Homo sapiens 6-22 23850486-2 2013 Here, we showed that liposomes consisting of phosphatidylserine and lysophosphatidylcholine, a lipolysis product of phosphatidylcholine by PLA2, were phagocytosed by microglia, but failed to induce secretion of PGE2. Dinoprostone 211-215 phospholipase A2 group IB Homo sapiens 139-143 22449386-8 2012 Also, phospholipase A2 (PLA2)/cyclooxygenase (COX) pathway is up-regulated in carbachol-induced SCA-9 cell proliferation, because prostaglandin E2 liberation (P<0.001) is increased and COX-1 expression is turned up (P<0.001). Dinoprostone 130-146 phospholipase A2 group IB Homo sapiens 24-28 21417548-2 2011 METHODS: PLA2 involvement in OA chondrocytes was analysed by (a) arachidonic acid (AA) and oleic acid release, (b) PLA2 mRNA analysis, and (c) prostaglandin E2 (PGE2) production in cultured OA chondrocytes in response to various cytokines and platelet activating factor (PAF). Dinoprostone 143-159 phospholipase A2 group IB Homo sapiens 9-13 21964881-2 2011 We provide evidence that the phospholipase A(2)/cyclooxygenase-2/prostaglandin E synthase/prostaglandin E(2) (PCPP) axis is positioned at the core of a natural regulatory circuit controlling the initiation, magnitude, duration, and resolution of the inflammatory response. Dinoprostone 90-108 phospholipase A2 group IB Homo sapiens 29-47 20167933-8 2011 Inhibition of phospholipase A2 and cyclooxygenase prevented ADO-dependent increases in GJIC, suggesting the involvement of PGE2. Dinoprostone 123-127 phospholipase A2 group IB Homo sapiens 14-30 21417548-2 2011 METHODS: PLA2 involvement in OA chondrocytes was analysed by (a) arachidonic acid (AA) and oleic acid release, (b) PLA2 mRNA analysis, and (c) prostaglandin E2 (PGE2) production in cultured OA chondrocytes in response to various cytokines and platelet activating factor (PAF). Dinoprostone 161-165 phospholipase A2 group IB Homo sapiens 9-13 19947915-7 2010 The inhibition of PLA2 (phospholipase A2) and COX-1 (cyclo-oxygenase-1) but not COX-2 impaired beta-AR increase of PGE2, an effect that was restored by the addition of low concentrations of PGE2, suggesting that PGE2 generation is implicated in the mechanism underlying beta-AR-agonist-mediated CD40 overexpression. Dinoprostone 115-119 phospholipase A2 group IB Homo sapiens 18-22 19947915-7 2010 The inhibition of PLA2 (phospholipase A2) and COX-1 (cyclo-oxygenase-1) but not COX-2 impaired beta-AR increase of PGE2, an effect that was restored by the addition of low concentrations of PGE2, suggesting that PGE2 generation is implicated in the mechanism underlying beta-AR-agonist-mediated CD40 overexpression. Dinoprostone 115-119 phospholipase A2 group IB Homo sapiens 24-40 19947915-7 2010 The inhibition of PLA2 (phospholipase A2) and COX-1 (cyclo-oxygenase-1) but not COX-2 impaired beta-AR increase of PGE2, an effect that was restored by the addition of low concentrations of PGE2, suggesting that PGE2 generation is implicated in the mechanism underlying beta-AR-agonist-mediated CD40 overexpression. Dinoprostone 190-194 phospholipase A2 group IB Homo sapiens 18-22 19947915-7 2010 The inhibition of PLA2 (phospholipase A2) and COX-1 (cyclo-oxygenase-1) but not COX-2 impaired beta-AR increase of PGE2, an effect that was restored by the addition of low concentrations of PGE2, suggesting that PGE2 generation is implicated in the mechanism underlying beta-AR-agonist-mediated CD40 overexpression. Dinoprostone 190-194 phospholipase A2 group IB Homo sapiens 24-40 19947915-7 2010 The inhibition of PLA2 (phospholipase A2) and COX-1 (cyclo-oxygenase-1) but not COX-2 impaired beta-AR increase of PGE2, an effect that was restored by the addition of low concentrations of PGE2, suggesting that PGE2 generation is implicated in the mechanism underlying beta-AR-agonist-mediated CD40 overexpression. Dinoprostone 190-194 phospholipase A2 group IB Homo sapiens 18-22 19947915-7 2010 The inhibition of PLA2 (phospholipase A2) and COX-1 (cyclo-oxygenase-1) but not COX-2 impaired beta-AR increase of PGE2, an effect that was restored by the addition of low concentrations of PGE2, suggesting that PGE2 generation is implicated in the mechanism underlying beta-AR-agonist-mediated CD40 overexpression. Dinoprostone 190-194 phospholipase A2 group IB Homo sapiens 24-40