ライフサイエンスコーパス: PGE2

1 and n-6 PUFA derived 15-keto-PG E2 (15-keto-PGE2).

2 aling molecules, including prostaglandin E2 (PGE2).

3 e concomitant increases in prostaglandin E2 (PGE2).

4 denocarcinoma cells, as potential sources of PGE2.

5 the degradation of prostaglandins including PGE2.

6 elicits a gap junction-dependent release of PGE2.

7 rapid and increased production of COX-2 and PGE2.

8 gment formation and was rescued by exogenous PGE2.

9 last-like cells (HMOBs) were stimulated with PGE2.

10 T. suis secretes extremely high amounts of PGE2 (45-90 ng/mg protein) within their excretory/secret

11 onophore A23187 resulted in the formation of PGE2, 5-HETE, and LTB4 as the principal metabolites of C

12 PGE2, a major immunomodulatory prostanoid, acts as a pro

13 ing to increased production of prostaglandin PGE2, a secreted autacoid that maintains renal function.

14 ptor antagonists for EP2 and EP4, indicating PGE2 action.

15 In vitro, PGE2 activates platelets after binding to its receptor,

16 pathways are connected by prostaglandin E2 (PGE2) activation of the aromatase enzyme, as we reported

17 ed this severe phenotype because only 46% of PGE2-administered COX-2 knockout mice developed anastomo

18 rl1(-/-) mice, and normal mice produced less PGE2 after fungal exposure when administered IL-33, sugg

19 rotoporphyrin IX more efficiently attenuated PGE2 and IL-6 release in HG+IL-1beta-treated cells than

20 ptin(ob/ob) mice produced significantly less PGE2 and more PGE3 than controls, correlating with impro

21 ased on significant correlations among serum PGE2 and PD, CAL, and GCF TNF-alpha in PTB, periodontiti

22 ells with 15-epi-LXA4 or MaR1 down-regulated PGE2 and PGD2 production.

23 anisms of innate IL-17A/IL-22 production via PGE2 and regulation of the PGE2/IL-17A/IL-22 axis via IL

24 GCF levels of IL-1beta, IL-6, and PGE2 and serum levels of TNF-alpha and PGE2 were signifi

25 a mechanism by which WAE cells are formed by PGE2 and suggest a process of adaptive cellular reprogra

26 bmMFs) requires the generation of endogenous PGE2 and the intrinsic expression of EP2 receptors to am

27 are anticipated to elevate in vivo levels of PGE2 and to promote healing and tissue regeneration.

28 ine (6-OHDA), leading to the biosynthesis of PGE2 and upregulation of pro-inflammatory cytokine inter

29 ations suggested that activation of the COX2/PGE2 and YAP1 pathways also promoted acquired resistance

30 looxygenase-2, overproduce prostaglandin E2 (PGE2), and exhibit defective intracellular bacterial kil

31 egulatory factors, such as Prostaglandin E2 (PGE2), and their mechanisms of action on immune cells ha

32 sociated with a gradual decrease of LTB4 and PGE2, and a gradual increase in CXCL1 and CCL2.

33 rophil functions through its hydrolysis into PGE2, and by activating the EP2 receptor.

34 aseline and after stimulation with IL-1beta, PGE2, and specific EP receptor agonists.

35 n occur partially through prostaglandin E2- (PGE2-) and PKA-dependent phosphorylation of a specific s

36 biosynthesis of, and cellular responses to, PGE2 are critical for the precise orchestration of the i

37 ) and their final product, prostaglandin E2 (PGE2), are known to play important roles in the modulati

38 Therefore, the present study features PGE2 as a direct and robust mediator of anion/fluid secr

39 tunable form of cross-talk in which AECs use PGE2 as a signal to request SOCS3 from AMs to dampen the

40 from the cytosol was unaffected by PGE2, but PGE2 attenuated histamine-evoked IP3 accumulation.

41 idence of a negative feedback loop, in which PGE2 augments the expression of dual specificity phospha

42 There was no difference in mean tissue PGE2 between the two groups (difference = 5; 95%CI from

43 Genetic and pharmacological inhibition of PGE2 biosynthesis or signal transduction ameliorated los

44 one is sufficient to induce mature IL-1beta, PGE2 boosted LPS-induced IL-1beta production.

45 nt, and at that time, levels were similar to PGE2, but less than 5-HETE and LTB4 The time course of H

46 ) removal from the cytosol was unaffected by PGE2, but PGE2 attenuated histamine-evoked IP3 accumulat

47 O regulatory mechanism was not responsive to PGE2/cAMP pathway modulation; however, treatment to redu

48 -induced IL-33 expression and that exogenous PGE2 can amplify IL-33 production via EP2 and EP4 recept

49 ever, recently it has been demonstrated that PGE2 can block the maturation of IL-1beta by inhibiting

50 meters, and increased GCF levels of IL-6 and PGE2 compared with the FTB group; there were no signific

51 gnificantly increased GCF levels of IL-6 and PGE2 compared with those with FTB.

52 In the placebo group, the mean tissue PGE2 concentration was 1005 +/- 129 pg/mL before treatme

53 In the rebamipide group, the mean tissue PGE2 concentration was 999 +/- 109 pg/mL before treatmen

54 Moreover, iNOS activity and PGE2 content, which were increased by LPS-induced period

55 ults show that Gas6, through upregulation of PGE2, contributes to cancer-induced venous thrombosis.

56 enzyme, including non-electrophilic PGE1 and PGE2, currently used in clinical practice.

57 In line with this observation, PGE2 decreased ILC2 proliferation.

58 COX2 inhibitors or genetic overexpression of PGE2-degrading enzyme 15-hydroxyprostaglandin dehydrogen

59 The effects of PGE2 depended on cAMP, were mimicked by an EPAC-selectiv

60 ts suggest that the balance between LTB4 and PGE2 determines the amount of IL-1beta inflammasome-depe

61 PGE2 did not inhibit ATP-induced mature IL-1beta product

62 Furthermore, PGE2 downregulated the expression of IL-2 receptor alpha

63 ed PGE2 signaling due to NSAIDs or increased PGE2 due to exogenous delivery dictates MuSC function, w

64 ia producing high level of prostaglandin E2 (PGE2) due to their thousands-fold higher cyclooxygenase-

65 looxygenase-derived endocannabinoids such as PGE2-EA or PGE2-G on neutrophils is unknown.

66 We show that PGE2-G, but not PGE2-EA, inhibits leukotriene B4 biosynthesis, superoxid

67 tively, our data demonstrate that endogenous PGE2, EP2 receptors, and EPAC are prerequisites for maxi

68 Our results suggest blockade of the PGE2-EP2 or EP4 signaling pathway restores NETosis after

69 Thus, the PGE2/Ep3 axis promotes cardiac healing after MI by activ

70 Mechanistically, the PGE2 EP4 interaction causes MuSC expansion by triggering

71 Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lympho

72 Dysregulation of the PGE2-estradiol pathway during the second week by treatme

73 bition of histamine-evoked Ca(2+) signals by PGE2 Exchange proteins activated by cAMP were not requir

74 PGE2 exerted an autocrine regulatory function in MSCs by

75 sence of various inflammatory cytokines with PGE2 failed to modulate the PGE2-mediated organoid swell

76 Inhibition of PGE2 formation, using pharmacologic mPGES1 and COX2 inhi

77 esponsible for the massive prostaglandin E2 (PGE2) formation during inflammation.

78 d expressed high levels of prostaglandin E2 (PGE2)-forming enzymes microsomal PGE2 synthase 1 (mPGES1

79 We show that PGE2-G and UDP are both agonists at P2Y6, but they activ

80 In conclusion, we show that PGE2-G inhibits human neutrophil functions through its h

81 ssion data, did not allow us to pinpoint one PGE2-G lipase, and rather support the involvement of an

82 -derived endocannabinoids such as PGE2-EA or PGE2-G on neutrophils is unknown.

83 The effects of PGE2-G required its hydrolysis into PGE2, were not obser

84 several GPCRs that are only expressed in the PGE2-G responder cell lines.

85 btractive screening approach where mRNA from PGE2-G response-positive and -negative cell lines was su

86 The effects of PGE2-G were prevented by EP1/EP2 receptor antagonist AH-

87 We show that PGE2-G, but not PGE2-EA, inhibits leukotriene B4 biosynt

88 hus, the glyceryl ester of prostaglandin E2, PGE2-G, mobilizes Ca(2+) and activates protein kinase C

89 To identify the endogenous receptor for PGE2-G, we performed a subtractive screening approach wh

90 UDP receptor P2Y6 as the specific target of PGE2-G.

91 The identification of the PGE2-G/P2Y6 pair uncovers the signalling mode of PG-Gs a

92 were necessary for both IL-33 production and PGE2 generation, and exogenous PGE2 partly reversed the

93 PGE2 had no effect on the Ca(2+) signals evoked by prote

94 ious endogenous secretagogues, we found that PGE2 had the lowest EC50 value with regard to the induct

95 PGE2 has been shown to increase the transcription of pro

96 PGE2 has key roles in many early inflammatory events, su

97 ypothalamus, but the origin of the pyrogenic PGE2 has not been clearly determined.

98 Prostaglandin E2 (PGE2) has emerged as a principal mediator for COX-2 casc

99 human lymphoid organs manifest similar COX-2/PGE2 hyperactivity and T cell suppression.

100 22 production via PGE2 and regulation of the PGE2/IL-17A/IL-22 axis via IL-33 signaling during lung f

101 eductions in HO-1 expression and increase in PGE2/IL-6 production were observed in HG+IL-1beta-stimul

102 anti-inflammatory mediators IDO, IL-10, and PGE2 in a COX-2-dependent manner.

103 PGE2 synthesis in AECs and neutralization of PGE2 in AEC-CM implicated this prostanoid as the major A

104 enic DC following administration of dimethyl PGE2 in conjunction with LPS.

105 tube formation and wound-healing activity of PGE2 in human vascular endothelial cells (HUVECs) althou

106 This review summarizes the role of PGE2 in kidney disease outcomes that accelerate cardiova

107 roperties compared with TsSPs and commercial PGE2 in modulating LPS-induced expression of many cytoki

108 have begun to elucidate the contribution of PGE2 in these events.

109 d its prostanoid products, prostaglandin E2 (PGE2 ) in particular, are key contributors in in vitro m

110 Here we identified prostaglandin E2 (PGE2) in the tumor as a key mediator of resistance to im

111 TNBC cell lines in which NO induced COX2 and PGE2 induced NOS2 proteins.

112 generation of Tr1 cells, we propose that the PGE2-induced inhibition of IL-27 in activated cDC repres

113 apies, including Tol-DC, Rapa-DC, DC-10, and PGE2-induced myeloid-derived suppressor cells.

114 This hyperactive COX-2/PGE2-induced suppression is evident during antigen-speci

115 PGE2 inhibited GATA-3 expression, as well as production

116 hat, in addition to bone marrow-derived DCs, PGE2 inhibits IL-27 production in macrophages and in spl

117 y function of PGE2 We showed previously that PGE2 inhibits IL-27 production in murine bone marrow-der

118 PGE2-initiated cAMP production in these cells was blocke

119 Our results unravel a unique LTD4-PGE2 interaction affecting mast cells through CysLT1R an

120 four major labor triggers, prostaglandin E2 (PGE2), interleukin (IL)-1beta, IL-6, and tumor necrosis

121 As PGE2 is a multifunctional prostanoid with diverse roles

122 Although PGE2 is a recognized suppressor of neutrophil functions,

123 These findings show for the first time that PGE2 is a regulator of nephron formation in the zebrafis

124 calcium-evoked production of the vasodilator PgE2 is critically dependent on brain levels of the anti

125 reduced, astrocyte calcium-evoked release of PgE2 is decreased and vasodilation triggered by increase

126 , we made a striking finding that endogenous PGE2 is essential for LPS-induced pro-IL-1beta productio

127 gagement of the DUSP1-TTP regulatory axis by PGE2 is likely to contribute to the switch between initi

128 Here we show that Prostaglandin E2 (PGE2) is an inflammatory cytokine that directly targets

129 to adhesion formation, and Prostaglandin E2 (PGE2) is associated with both adhesion formation and ten

130 Prostaglandin E2 (PGE2) is associated with proliferation and angiogenesis

131 Prostaglandin E2 (PGE2) is derived from arachidonic acid, whereas PGE3 is

132 duction in other brain areas and the overall PGE2 level in the brain do not influence the febrile res

133 Further, changes in Cox activity or PGE2 levels affected expression of the transcription fac

134 ucible CreER(T2) under the Slco1c1 promoter, PGE2 levels in the CSF were only weakly related to the m

135 s 15-PGDH with Ki = 0.1 nM in vitro, doubles PGE2 levels in vivo, and shows efficacy in mouse models

136 lated cells may underlie the reduced urinary PGE2 levels with acetazolamide, thereby contributing to

137 ubjected to restraint stress showed elevated PGE2 levels.

138 inflammation by increasing prostaglandin E2 (PGE2) levels in ovarian cancer cells.

139 Our findings reveal that PGE2 limits ILC2 activation and propose that selective E

140 protein; P <0.05); and 3) prostaglandin E2 (PGE2) (LPS: 159.20 +/- 38.70 pg/mg wet weight versus LPS

141 he ubiquitous induction of mPGES-1-dependent PGE2 may be crucial for innate immune system activation

142 EP1 siRNA blocked PGE2-mediated beta1-integrin expression.

143 H inhibitors to initiate or amplify low-dose PGE2-mediated cervical ripening or (ii) EP2 receptor ant

144 Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic inflammation.

145 ollectively, these findings demonstrate that PGE2-mediated modulation of the dopaminergic motivationa

146 r, which EP receptor is the culprit of COX-2/PGE2-mediated neuronal inflammation and degeneration rem

147 y cytokines with PGE2 failed to modulate the PGE2-mediated organoid swelling response.

148 The same feedback mechanism contributes to PGE2-mediated suppression of TNF release.

149 This PGE2-mediated swelling response was dependent on environ

150 Because PGE2 mediates the pyrogenic effect of IL-1beta, these ef

151 eloid cells and, therefore, reprogramming of PGE2 metabolism in tumor microenvironment provides an op

152 enzyme downstream of COX-1 that synthesizes PgE2 (microsomal prostaglandin E synthase-1) depends cri

153 after colonic surgery, and administration of PGE2 might be favorable for a selection of patients.

154 bition of histamine-evoked Ca(2+) signals by PGE2 occurs through "hyperactive signaling junctions," w

155 ore, we investigated the autocrine effect of PGE2 on human adult stem cells from cord blood or adipos

156 The effects of PGE2 on human ILC2 proliferation and intracellular cytok

157 examined the effect of endogenously produced PGE2 on IL-1beta production.

158 sults have led us to reexamine the effect of PGE2 on IL-1beta production.

159 The inhibitory effect of PGE2 on p28 and irf1 expression does not involve endogen

160 response because of the inhibiting effect of PGE2 on TNF-alpha production.

161 le response is dependent on local release of PGE2 onto its target neurons and not on the overall PGE2

162 esponse is dependent on the local release of PGE2 onto its target neurons, possibly by a paracrine me

163 Although PGE2 or 15-PGDH inhibitor alone did not alter gestationa

164 on-dependent inhibition of Ca(2+) signals by PGE2 or butaprost (to activate EP2 receptors selectively

165 Treatment with PGE2 or EP2 selective agonist butaprost, but not EP4 ago

166 way during the second week by treatment with PGE2 or lipopolysaccharides produces enduring consequenc

167 l length, treatment with 15-PGDH inhibitor + PGE2 or metabolism-resistant dimethyl-PGE2 resulted in p

168 Incubation with either exogenous PGE2 or selective EP2 agonist significantly increased ex

169 Modulating levels of prostaglandin E2 (PGE2) or PGB2 restricted distal segment formation and ex

170 PGE2 partly rescued this severe phenotype because only 4

171 roduction and PGE2 generation, and exogenous PGE2 partly reversed the suppression of IL-33 production

172 ere, we report that the proinflammatory COX2/PGE2 pathway and the YAP1 growth-regulatory pathway coop

173 study identified a pivotal role for the COX/PGE2 pathway in the regulation of NO production during t

174 our study demonstrates that the COX2/mPGES1/PGE2 pathway involved in the regulation of PD-L1 express

175 r, the precise mechanism(s) by which the COX/PGE2 pathway regulates sapovirus replication remains lar

176 first time that IL-17A impacts on the COX-2/PGE2 pathway, molecules known to contribute to disease e

177 ol was associated with activation of the COX/PGE2 pathway.

178 e cyclooxygenase (COX) and prostaglandin E2 (PGE2) pathway.

179 t involve the modulation of IL-23 but rather PGE2; PGE2 was significantly increased in fungal-exposed

180 The inflammatory mediators, COX-2 and PGE2, played a key role in this effect, as indicated by

181 hypothesis that astrocytic prostaglandin E2 (PgE2) plays a key role for cerebrovascular CO2 reactivit

182 LTD4 plus PGE2 potentiated vascular permeability and edema, gearin

183 LTD4 plus PGE2-potentiated effects are partially sensitive to CysL

184 In conclusion, PGE2 produced by MSCs contributes to maintenance of self

185 of the autocrine loop components regulating PGE2 production and signaling, namely IL-1 type I recept

186 PGE2 production decreases 50% when fish oil consumption

187 The level of PGE2 production from an equivalent number of MSCs was do

188 In contrast, PGE2 production in other brain areas and the overall PGE

189 xamined the role of local versus generalized PGE2 production in the brain for the febrile response.

190 to its target neurons and not on the overall PGE2 production in the brain.SIGNIFICANCE STATEMENT By u

191 n of cyclooxygenase-2 (COX-2) expression and PGE2 production in the UVB-exposed skin.

192 E synthase-1 suppressed the 6-OHDA-triggered PGE2 production in these cells.

193 COX-2-induced PGE2 production is essential for intestinal wound healin

194 Inhibition of PGE2 production through nonsteroidal anti-inflammatory d

195 While PGE2 production was suppressed by ibuprofen, PGD2 produc

196 By blocking PGE2 production with indomethacin, we made a striking fi

197 ainst COX-1 and COX-2, significantly reduced PGE2 production, as well as PSaV replication.

198 ) exhibited decreased Ptges mRNA expression, PGE2 production, lower CCR7-dependent DC migration, and

199 ates COX-1 activity and generates downstream PgE2 production.

200 we demonstrate that local prostaglandin E2 (PGE2) production in deep brain areas, such as the hypoth

201 se 2 (COX-2) and resultant prostaglandin E2 (PGE2) production.

202 e further demonstrate that the production of PGE2 provides a protective effect against the antiviral

203 Creation of WAE cells via the PGE2-Ptger4 pathway was required in vivo, as mice with l

204 psies were collected at both endoscopies for PGE2 quantification and histopathological analysis (seco

205 We also show that a PGE2 receptor agonist increased, whereas a PGE2 synthase

206 Our results suggest that PGE2 receptor EP2 is a key mediator of COX-2 activity-in

207 e tested the hypothesis that deletion of the PGE2 receptor EP4 in S100a4-lineage cells would decrease

208 ime quantitative PCR was performed to detect PGE2 receptor expression.

209 Triggering of PGE2 receptors increases HSC survival in part via the PK

210 Disruption of the PGE2 receptors Ptger2a and Ptger4a similarly affected th

211 This sequence allows digital signaling from PGE2 receptors, through cAMP and PKA, to histamine-evoke

212 tive intestinal peptide or prostaglandin E2 (PGE2), regulate intestinal anion/fluid secretion, but th

213 TRPV1, a PGE2-regulated channel in nociceptive neurons was also i

214 We set out to investigate how PGE2 regulates human ILC2 function.

215 ocyte activation in pFRG/RTN triggered local PGE2 release and blunted the hypercapnic response.

216 cells showed that both cell types increased PGE2 release in response to IH.

217 difying respiratory-related behavior through PGE2 release in the pFRG/RTN.

218 2 and 0.34-fold HO-1), and prostaglandin E2 (PGE2) release was increased in samples with low HO-1 exp

219 eviously, we revealed that prostaglandin E2 (PGE2), released during hypercapnic challenge, increases

220 s of NOS2 and COX2, NO and prostaglandin E2 (PGE2), respectively, promote feed-forward NOS2/COX2 cros

221 itor + PGE2 or metabolism-resistant dimethyl-PGE2 resulted in preterm cervical ripening and delivery

222 lesion size and bacterial load and decreased PGE2 secretion and Th17 cells compared with nondiabetic

223 This cell contact-mediated decrease in PGE2 secretion down-regulated the suppressive effect of

224 ed effects of TNF-alpha and greatly enhances PGE2 secretion from ASM cells.

225 city through EP2 in an autocrine manner, and PGE2 secretion is down-regulated by cell-to-cell contact

226 wever, TNF-induced COX-2 mRNA expression and PGE2 secretion is repressed by FTY720 and FTY720-P.

227 treated with specific inhibitors to suppress PGE2 secretion, and proliferation was assessed.

228 cted the worm's motility but did not inhibit PGE2 secretion, suggesting that the worms can synthesize

229 optotic cells (IACs) drive prostaglandin E2 (PGE2) secretion to generate Th17 cells.

230 were not observed with the non-hydrolyzable PGE2-serinol amide, and were completely prevented by met

231 -induced the production of prostaglandin E2 (PGE2) show that, esculetin, curcumin and hesperetin were

232 loss-of-function experiments, we found that PGE2 signaling acts as a rheostat for muscle stem-cell f

233 Loss of PGE2 signaling by specific genetic ablation of the EP4 r

234 Decreased PGE2 signaling due to NSAIDs or increased PGE2 due to ex

235 f cyclooxygenase-2/microsomal PGE synthase 1/PGE2 signaling in hypertension and diabetes, and outline

236 Mechanistically, COX2/PGE2 signaling induced promoter methylation of let-7, re

237 arious stimuli in the presence or absence of PGE2 signaling modifiers.

238 ctor, Nurr1 Our findings reveal that loss of PGE2 signaling to MuSCs during recovery from injury impe

239 ture system, we found that prostaglandin E2 (PGE2) signaling through one of its receptors, Ptger4, wa

240 riosis we demonstrated overexpression of the PGE2-signaling pathway (including COX-2, EP2, EP4) in en

241 PGE2 significantly increased RANKL messenger RNA (mRNA)

242 demonstrate that pFRG/RTN astrocytes are the PGE2 source.

243 hen cocultured with THP-1, RANKL released by PGE2-stimulated HMOBs is adequate to drive THP-1 differe

244 ortic smooth muscle cells, prostaglandin E2 (PGE2) stimulates adenylyl cyclase (AC) and attenuates th

245 Prostaglandin E2 (PGE2) stimulates HSC renewal and engraftment through, fo

246 or recombinant IFN-gamma, concurrently with PGE2 stimulation, reduced RANKL, but not OPG, expression

247 eated with an anti-IFN-gamma antibody before PGE2 stimulation.

248 This impairment in the generation of PGE2 subsequently reduces its ability to induce IL-1RI.

249 An acute treatment with PGE2 suffices to robustly augment muscle regeneration by

250 muscles following intramuscular delivery of PGE2 suggests a previously unrecognized indication for t

251 PGE2) through inducible COX-2 and microsomal PGE2 synthase 1 (mPGES-1) (1).

252 glandin E2 (PGE2)-forming enzymes microsomal PGE2 synthase 1 (mPGES1) and COX2.

253 a PGE2 receptor agonist increased, whereas a PGE2 synthase inhibitor decreased, the levels of IL-17A

254 e of PGE2 synthesis or genetic deletion of a PGE2 synthase similarly attenuated the increase in bronc

255 Mice with reduced PGE2 synthesis develop systemic inflammation, associated

256 llenge, and both pharmacologic inhibition of PGE2 synthesis in AECs and neutralization of PGE2 in AEC

257 eninges, were left unaffected, hence leaving PGE2 synthesis largely intact in major parts of the brai

258 Moreover, pharmacologic blockade of PGE2 synthesis or genetic deletion of a PGE2 synthase si

259 ter inhibition of astrocytic glutathione and PgE2 synthesis.

260 by COX1-mediated cerebral prostaglandin E2 (PGE2) synthesis.

261 Furthermore, partly restoring the PGE2 synthesizing capacity in the anterior hypothalamus

262 gnitude of the febrile response, whereas the PGE2 synthesizing capacity in the hypothalamus, as refle

263 Further, we showed that inflammation-induced PGE2 targeted EP1 receptors on striatal dopamine D1 rece

264 Are PGE2 terminal synthases and receptors feasible therapeut

265 ions, mainly via producing prostaglandin E2 (PGE2) that activates four membrane receptors, EP1-EP4.

266 increases the secretion of prostaglandin E2 (PGE2), the enzymatic product of Ptges, in WT but not in

267 th vehicle, diclofenac, or prostaglandin E2 (PGE2), the most important COX-2 product in the intestine

268 of IL-17A and IL-22 occurred at the level of PGE2 This was confirmed by in vivo cyclooxygenase 2 inhi

269 es macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and microsomal PGE2 syntha

270 Furthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R)

271 We further show that PGE2, through PI3K/AKT activation, promoted Forkhead box

272 Changes in gastric PGE2 tissue concentration were also evaluated.

273 ould partly be reversed by administration of PGE2 to COX-2 mice.

274 d diabetes, and outlines the contribution of PGE2 to other aspects of the metabolic syndrome, particu

275 The ability of PGE2 to selectively autoamplify its own synthesis in str

276 We conclude that T. suis secretes PGE2 to suppress proinflammatory responses in human DCs,

277 ) or prostaglandin E2 analog (16,16-dimethyl PGE2) to adipose tissue vasculature.

278 ver occurs upon binding of prostaglandin E2 (PGE2) to EP3 receptors in the median preoptic nucleus of

279 Exogenous PGE2 treatment limited NETosis of neutrophils collected

280 ment with EP1 agonist mimicked the effect of PGE2 treatment.

281 COX-2 overexpression or Prostaglandin E2 (PGE2) treatment increased beta1-integrin expression in N

282 ressing T cell sensitivity to activation via PGE2, underscoring the importance of FRCs in shaping the

283 ATP2A1 is likely to promote tumorogenesis by PGE2 uptake into the endothelial cells, suggesting that

284 Here, we show that PGE2 uses cell-specific EP2 receptor-mediated increases

285 on, suggesting that the worms can synthesize PGE2 via a COX-independent pathway.

286 ivation triggers LTB4 production and further PGE2 via IL-1beta/IL-1R signalling.

287 t in murine bone marrow-derived macrophages, PGE2 via the cAMP/protein kinase A pathway is potently i

288 The effect of endogenous PGE2 was mediated by EP2 receptor.

289 HUVECs) although the amount of extracellular PGE2 was not affected by an OATP2A1 inhibitor.

290 Tissue PGE2 was quantified by ELISA.

291 lve the modulation of IL-23 but rather PGE2; PGE2 was significantly increased in fungal-exposed Il1rl

292 reased, while the level of prostaglandin E2 (PGE2) was decreased.

293 increases via the release of the vasodilator PgE2 We demonstrate that hypercapnia (increased CO2) evo

294 hat promotes the proinflammatory function of PGE2 We showed previously that PGE2 inhibits IL-27 produ

295 on through the EP3 receptor as compared with PGE2 We tested the hypothesis that enriching pancreatic

296 Serum levels of PGE2 were positively correlated with probing depth (PD)

297 Increased amounts of PGE2 were present in AEC-CM after LPS challenge, and bot

298 , and PGE2 and serum levels of TNF-alpha and PGE2 were significantly higher in women with periodontit

299 fects of PGE2-G required its hydrolysis into PGE2, were not observed with the non-hydrolyzable PGE2-s

300 tive feedback loop from IL-1beta and back to PGE2, which itself is induced by IL-1beta, is likely to