ライフサイエンスコーパス: PGE2

1 aling molecules, including prostaglandin E2 (PGE2).

2 e concomitant increases in prostaglandin E2 (PGE2).

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

4 he COX-2 synthetic product prostaglandin E2 (PGE2).

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

6 denocarcinoma cells, as potential sources of PGE2.

7 the degradation of prostaglandins including PGE2.

8 elicits a gap junction-dependent release of PGE2.

9 pendence on the bronchoprotective actions of PGE2.

10 els of receptors for the antifibrotic factor PGE2.

11 king these cells resistant to any effects of PGE2.

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

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

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

15 ion of colon biopsy supernatants, histamine, PGE2, a small interfering RNA against EP2, or an agonist

16 anistically, tumor-derived prostaglandin E2 (PGE2) acted selectively on EP2 and EP4 receptors on NK c

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

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

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

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

21 , and these Mphis produced higher amounts of PGE2 after LPS stimulation compared with controls.

22 Of interest, PGE2 and cortisol, both well-demonstrated stimulants of

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

24 PGE2 and IL6 were identified as critical inflammatory me

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

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

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

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

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

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

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

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

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

34 ukemia burden, lower serum levels of IL1beta/PGE2, and lower tissue human ARC and beta-catenin levels

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

36 ed the secretion levels of cytokines VEGF-A, PGE2, and TGF-beta1 in hybrid spheroid system.

37 prostaglandin E receptor (EP)-2 and EP4 for PGE2 are coupled with activation of the cAMP and PKA pat

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

39 is receptor subtype and the pathways forming PGE2 are highly expressed in endometriotic lesions.

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

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

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

43 patients with IBS-D had increased levels of PGE2, based on enzyme-linked immunosorbent assay, and CO

44 to the development of AHR by reducing airway PGE2 biosynthesis in allergen- and aspirin-induced asthm

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

46 report that tumor-derived PGE2 blocks early activation of natural killer cells and

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

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

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

50 Abnormal synthesis of PGE2 by colonic mast cells appears to induce visceral hy

51 ncrease the synthesis of prostaglandin E(2) (PGE2) by mast cells, which activates the receptor PTGER2

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

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

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

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

56 033291, that binds with high affinity to the PGE2-degrading enzyme 15-hydroxyprostaglandin dehydrogen

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

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

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

60 mental factors, including IL-2, TGFbeta, and PGE2, direct the conversion from naive precursor to imma

61 Prostaglandin E2 (PGE2) disrupts TGFbeta signaling and suppresses myofibro

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

63 profibrotic cytokine TGF-beta, whereas many PGE2-downregulated genes were activated by TGF-beta.

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

65 are resistant to the antifibrotic effects of PGE2 due to suppression of a subset of PGE receptors.

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

67 however practical strategies to raise tissue PGE2 during IPF have been limited.

68 y a regulatory interaction between IL-10 and PGE2, dysregulation of which may drive aberrant Mphi act

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

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

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

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

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

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

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

76 During diuretic treatment, higher PGE2 excretion correlated with lower free water clearanc

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

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 was associated with significant increases in PGE2, histamine, and tryptase in the colonic mucosa.

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

101 22 production via PGE2 and regulation of the PGE2/IL-17A/IL-22 axis via IL-33 signaling during lung f

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

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

104 ation and cancer, the regulation and role of PGE2 in AML are largely unknown.

105 stability, is transcriptionally repressed by PGE2 in an EP4-dependent manner.

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

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

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

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

110 al hypersensitivity or increase the level of PGE2 in W/W(V) and Ptgs2(Y385F)mice.

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

112 PGE2 induced the expression of beta-catenin, which regul

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

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

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

116 e found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-kappaB in M

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

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

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

120 PGE2-initiated cAMP production in these cells was blocke

121 ls lose pericyte coverage substantially upon PGE2 injection into the skin.

122 P-mediated direct disruption of pericytes by PGE2 is a key process for vascular destabilization.

123 Although PGE2 is a recognized suppressor of neutrophil functions,

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

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

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

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

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

129 eed-forward induction of COX-2 expression by PGE2 is mediated via its receptors coupled with the cAMP

130 Prostaglandin E2 (PGE2) is a lipid mediator of inflammation, and its tissu

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

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

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

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

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

136 on of SW033291, a small molecule to increase PGE2 level locally, significantly boostes bone formation

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

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

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

140 tively, in association with increased airway PGE2 levels.

141 landin dehydrogenase (15-PGDH) and increases PGE2 levels.

142 , a finding associated with increased airway PGE2 levels.

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

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

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

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

147 Tumor-derived PGE2-mediated induction of nuclear p50 NF-kappaB epigene

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

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

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

151 Thus, we show that PGE2 mediates sensory nerve to control bone homeostasis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 TAT3 phosphorylation and COX-2 expression by PGE2 or EP2 stimulation, which was attenuated by EP4 ove

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

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

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

172 Our results indicate that inhibition of the PGE2/p50/NO axis prevents MDSC-suppressive functions and

173 PGE2 partly rescued this severe phenotype because only 4

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

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

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

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

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

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

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

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

182 Although Cox-2 and its enzymatic product PGE2 play major roles in inflammation and cancer, the re

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

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

185 synthase-1 (mPGES-1), the enzyme generating PGE2, prevents blood-brain barrier P-gp up-regulation af

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

187 PGE2 production decreases 50% when fish oil consumption

188 greatly increase Cox-2 expression in MSC and PGE2 production in an ARC/IL1beta-dependent manner.

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

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

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

192 of antiapoptotic ARC by which ARC regulates PGE2 production in the tumor microenvironment and microe

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

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

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

196 Inhibition of PGE2 production through nonsteroidal anti-inflammatory d

197 While PGE2 production was suppressed by ibuprofen, PGD2 produc

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

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

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

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

202 as increased production of prostaglandin E2 (PGE2) promotes the differentiation of SEPs.

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

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

205 E2) secreted by osteoblastic cells activates PGE2 receptor 4 (EP4) in sensory nerves to regulate bone

206 We show that knockout of PGE2 receptor 4 in sensory nerves significantly reduces

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

208 macological inhibition of PGE2 synthesis and PGE2 receptor blockade enhanced bacterial killing in Mph

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

210 ll as pharmacologic inhibition of either the PGE2 receptor EP2 or NO production reprogrammed M-MDSCs

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

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

213 EP2 is the dominant PGE2 receptor mediating the induction of COX-2 at partur

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

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

216 The EP4 subtype of prostaglandin E2 (PGE2) receptors (EP4-R) is a particularly promising anti

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

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

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

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

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

222 2 and 0.34-fold HO-1), and prostaglandin E2 (PGE2) release was increased in samples with low HO-1 exp

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

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

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

226 PGE2 secreted by osteoblasts increases when bone density

227 Here we found prostaglandin E2 (PGE2) secreted by osteoblastic cells activates PGE2 rece

228 Later, PGE2, secreted from infected BMM s induces cAMP-PKA path

229 RGS4 modulated allergen-induced PGE2 secretion in human bronchial epithelial cells and p

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

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

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

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

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

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

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

237 pericyte-EC interaction using inhibitors of PGE2 signaling may offer a therapeutic strategy in cance

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

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

250 Here, we show that the exposure to PGE2 switches pericytes to a fast-migrating, loosely adh

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 Inhibition of human microsomal PGE2 synthase-1 reduces seizure-induced increases of P-g

256 at inhibiting microsomal prostaglandin E(2) (PGE2) synthase-1 (mPGES-1), the enzyme generating PGE2,

257 Furthermore, pharmacological inhibition of PGE2 synthesis and PGE2 receptor blockade enhanced bacte

258 Mice with reduced PGE2 synthesis develop systemic inflammation, associated

259 n reported to release IL1beta, which induces PGE2 synthesis in mesenchymal stromal cells (MSC), in tu

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

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

262 he expression of the rate-limiting enzyme in PGE2 synthesis-namely, cyclooxygenase-2 (COX-2).

263 ter inhibition of astrocytic glutathione and PgE2 synthesis.

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

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

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

267 Are PGE2 terminal synthases and receptors feasible therapeut

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

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

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

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

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

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

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

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

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

277 PGE2 treatment of fibroblasts activates the orphan nucle

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

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

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

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

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

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

284 In adult renal fibroblast cultures, PGE2 was able to upregulate many genes that are suppress

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

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

287 Tissue PGE2 was quantified by ELISA.

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

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

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

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

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

293 Induction of MITF and depletion of COX2 and PGE2 were also observed in NRF2-deleted melanoma cells i

294 or pathways for eicosanoid prostaglandin E2 (PGE2) were more highly induced in IL-10RB-/- Mphis, and

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

296 matory cytokines (i.e., VEGF, TGF-beta1, and PGE2) when stimulated with amyloid beta42 oligomers, lip

297 s, we show that there are elevated levels of PGE2 which activate sensory nerves, leading to sodium in

298 broblasts produce abundant prostaglandin E2 (PGE2), which plays a crucial role in parturition by stim

299 Among these is prostaglandin E2 (PGE2), which, in addition to its role as a bronchodilato

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