ライフサイエンスコーパス: PGE

1 PGE(2) combined with MSC-induced T(R)1-like cells repres

2 PGE(2) decreased cytokine production and inhibited signa

3 PGE(2) enhances its own production but suppresses acute

4 PGE(2) is therefore implicated in the development of ten

5 PGE(2) levels are significantly higher in the vitreous o

6 PGE(2) mimetic supplements can enhance the immunosuppres

7 PGE(2) modulates chemokine production, inhibiting the at

8 PGE(2) plays complex pro- or anti-inflammatory roles in

9 PGE(2) produces a two-fold greater density of dendritic

10 PGE(2) regulation of DC generation is specifically media

11 PGE(2) release was suppressed by means of preincubation

12 PGE(2) supports activation of dendritic cells but suppre

13 PGE(2) was found as the main prostanoid formed by the pa

14 PGE(2), an essential homeostatic factor, is also a key m

15 PGE(2), compared with nontreated controls, increased exp

16 PGE(2), compared with the untreated control, increased t

17 PGE(2)-deficient ptges(-/-) mice develop exaggerated pul

18 PGE(2)-dependent Axl phosphorylation led to AP-1 transac

19 e response to 3,7-dithia prostaglandin E(1) (PGE(1)).

20 erexpress iPLA(2)gamma and cyclooxygenase-1, PGE(2) production was induced by co-expression of consti

21 ngs depict a novel crosstalk between mPGES-1/PGE(2) and EGR1/beta-catenin signaling that is critical

22 osis: T(R)1-like cells + PGE(2): 11 +/- 10%; PGE(2) alone: 93 +/- 8.7%; T(R)1-like cells alone: 88 +/

23 , whereas treatment with prostaglandin E(2) (PGE(2) ) caused a marked increase in lamin A accumulatio

24 estigate the function of prostaglandin E(2) (PGE(2) ) signaling through its EP3 receptor in the neuro

25 Levels of prostaglandin E(2) (PGE(2)) and its processing enzyme, prostaglandin-endoper

26 ion can be suppressed by prostaglandin E(2) (PGE(2)) and the cyclic AMP-dependent protein kinase A (P

27 -knockout mice inhibited prostaglandin E(2) (PGE(2)) but not PGI(2) production in response to Ang II,

28 induces the synthesis of prostaglandin E(2) (PGE(2)) by infected macrophages to alter host immune res

29 ses (COX) and release of prostaglandin E(2) (PGE(2)) by lung cells, including alveolar macrophages.

30 n-coupled receptors, the prostaglandin E(2) (PGE(2)) E-prostanoid 3 (EP3) receptor binds agonist with

31 genase-2 (COX-2)-derived prostaglandin E(2) (PGE(2)) has been shown to be important in esophageal tum

32 bioactive lipid mediator prostaglandin E(2) (PGE(2)) has been shown to exert a myriad of effects on c

33 factor (TNF)-alpha, and prostaglandin E(2) (PGE(2)) in a dose-dependent manner both in normal and hi

34 Prostaglandin E(2) (PGE(2)) is an abundant lipid inflammatory mediator with

35 iments, we now show that prostaglandin E(2) (PGE(2)) is the trophic signal required for this expansio

36 Prostaglandin E(2) (PGE(2)) is thought to play a role in the pathogenesis of

37 one that is required for prostaglandin E(2) (PGE(2)) production and bronchiolar smooth muscle relaxat

38 It is noteworthy that prostaglandin E(2) (PGE(2)) production was significantly suppressed at an FO

39 monitored by quantifying prostaglandin E(2) (PGE(2)) production.

40 ced COX-2 and microsomal prostaglandin-E(2) (PGE(2)) synthase-1, mediated by the MyD88-dependent NFka

41 the role of visfatin in prostaglandin E(2) (PGE(2)) synthesis in chondrocytes.

42 roinflammatory molecule, prostaglandin E(2) (PGE(2)) to produce sex-specific brain development.

43 Prostaglandin E(2) (PGE(2)), produced by M. tuberculosis-infected macrophage

44 plasma concentrations of prostaglandin E(2) (PGE(2)), which induced M2 macrophage polarization in the

45 ese immune cells produce prostaglandin E(2) (PGE(2)), which influences adipocyte signaling.

46 amide (SNC80) to inhibit prostaglandin E(2) (PGE(2))-stimulated adenylyl cyclase activity.

47 flammatory cytokines and prostaglandin E(2) (PGE(2)).

48 its metabolite 13,14-dihydro-15-keto-PGE(2) (PGE-M) were abundant in wound fluid and induced OSM in w

49 ated from conception suggests that the COX-2/PGE(2) pathway might also be critical at the earliest st

50 itric oxide (20.5-69.3%), iNOS (22.8-93.6%), PGE(2) (64.0-88.3%), COX-2 (36.2-76.7%), and TNF-alpha (

51 EP2 was the most abundant PGE(2) receptor expressed by bone marrow cells, and its

52 Using the EP4 agonist PGE(1)OH in conjunction with TNFalpha, we found that PKA

53 The study reveals that, although PGE concentrations in rural airborne particulate matter

54 a combination of elevated IL-1ra, IL-10, and PGE(2), anti-inflammatory Th2 cytokines, and decreased I

55 Blocking IL-1ra, IL-10, and PGE(2), but not IL-6, heme oxygenase-1, and NO, attenuat

56 s accompanied by elevated IL-1ra, IL-10, and PGE(2).

57 subsequent induction of cyclooxygenase-2 and PGE(2) engagement of EP4 receptor.

58 from COX-1-dependent formation of PGD(2) and PGE(2) followed by COX-2-dependent production of PGE(2).

59 that ROS differentially regulate PGD(2) and PGE(2) production in BMDM.

60 consisting of IL-1beta, TNF-alpha, IL-6, and PGE(2) during viral uptake only stimulated HIV-1-specifi

61 phosphorylation (a marker of activation) and PGE(2) synthesis.

62 Both TLR agonists and PGE(2) promote the phosphorylation of the transcription

63 uential actions of cyclooxygenases (COX) and PGE synthases (PTGES).

64 orphological profile, and both estradiol and PGE(2) masculinized microglial number and morphology in

65 rable levels of EP(2) protein expression and PGE(2)-mediated cAMP accumulation, yet were resistant to

66 indings suggest impaired innate immunity and PGE(2) elevation post-BMT are due to hypomethylation of

67 ES1 expression, thymidine incorporation, and PGE(2) production.

68 lpha), IL-1beta, IL-6, nitric oxide (NO) and PGE(2) production in unstimulated macrophages, RAW264.7

69 argeted disruption of the genes for PTGS and PGE receptors (PTGERs).

70 Anthropogenic PGE signatures in airborne particles are thus not restri

71 ole aerosols indicate that the anthropogenic PGE fraction is primarily sourced from ore smelting proc

72 se findings were specific to fibroblasts, as PGE(2) decreased DNMT1 and DNMT3a expression in RAW macr

73 denylyl cyclase activity in vitro as well as PGE(2)-stimulated thermal allodynia in vivo.

74 py (EIS) and compared with those of the bare PGE.

75 IL)-1beta-induced PGE(2) production, because PGE(2) has been shown to mediate IL-1beta inhibition of

76 A significant correlation was seen between PGE(2) levels and IP-10 and VEGF (P = 0.04).

77 Both PGE(2) and its metabolite 13,14-dihydro-15-keto-PGE(2) (

78 se to Ang II, whereas celecoxib blocked both PGE(2) and PGI(2) production.

79 ulated control of 5-lipoxygenase activity by PGE(2), whereas adherent platelets lead to increased pro

80 esized that patients with disease defined by PGE-M suppression would benefit from the addition of apr

81 ncrease in DNMT3a expression was mediated by PGE(2) signaling via its E prostanoid 2 receptor and the

82 tion of E-type prostanoid (EP) 4 receptor by PGE(2) or an EP4-selective agonist (ONO AE1-329) enhance

83 of luminal area stenosis: T(R)1-like cells + PGE(2): 11 +/- 10%; PGE(2) alone: 93 +/- 8.7%; T(R)1-lik

84 crophage-dependent inflammation via the COX1/PGE(2)/EP4-dependent pathway.

85 roliferation, activated apoptosis, decreased PGE(2) formation, and decreased cell invasion; C16-C18 a

86 ing the APO866 inhibitor gradually decreased PGE(2) release, whereas the addition of exogenous nicoti

87 Deficient PGE(2) generation in the lung predisposes to airway hype

88 the final enzyme regulating COX-2-dependent PGE(2) synthesis.

89 s supports a model in which mPGES1-dependent PGE(2) produced by populations of cells native to the lu

90 recognized protective role of PTGS-2-derived PGE(2) in STZ-induced diabetes mediated by the receptor

91 Both cyclooxygenase-derived PGE(2) and IDO help to induce T(R)1-like cells by MSCs.

92 We show that mPGES1 determines PGE(2) levels in the naive lung and is required for incr

93 Mean +/- standard deviation PGE(2) levels were 25.11 +/- 11 pg/mL and 16.40 +/- 7 pg

94 Reduced DC development caused by diminished PGE(2) signaling is reversed by overexpression of Flt3 o

95 receptors (EP1-EP4), each mediating distinct PGE(2) functions.

96 3,7-dithia PGE(1) increased facility by 106% within 3 hours postmor

97 Microsomal prostaglandin E (PGE) synthase-1 (mPGES-1) is an inducible enzyme that co

98 We found that the prostaglandin E2 (PGE(2)) receptors EP2 and EP4 were upregulated on virus-

99 of interleukin (IL)-6 and prostaglandin E2 (PGE(2)), 2 inflammatory mediators known to skew differen

100 Nitric oxide (NO) and prostaglandin E2 (PGE(2)), downstream products, were also suppressed in do

101 rs including cytokines and prostaglandin E2 (PGE(2)), with limited side effects associated with tradi

102 tate high-efficiency precise genome editing (PGE) via homology-directed repair (HDR) pathways.

103 particle modified pencil graphite electrode (PGE) biosensor for detection of Bacillus cereus, causati

104 includes coating pencil graphite electrode (PGE) by means of electro-polymerization of 3-Thienyl bor

105 u) deposited onto pencil graphite electrode (PGE) has been utilized for covalent immobilization of ho

106 opy, a pretreated pencil graphite electrode (PGE) modified with multiwall carbon nanotubes (MWCNTs) a

107 tammetry (DPV) at pencil graphite electrode (PGE) showed that both molecules were electrochemically o

108 of GelMA modified Pencil Graphite Electrode (PGE) that serve as a functional platform was investigate

109 on the surface of pencil graphite electrode (PGE) via one-step electropolymerization of the imprinted

110 th the disposable pencil graphite electrode (PGE) was progressed for sensitive and selective detectio

111 omposite modified pencil graphite electrode (PGE).

112 ) on a disposable pencil graphite electrode (PGE).

113 on the surface of pencil graphite electrode (PGE).

114 on edge plane pyrolytic graphite electrodes (PGE/MWNT/Py) to which an anti-insulin antibody was coval

115 (PNPs) modified pencil graphite electrodes (PGEs) for construction of electrochemical cytosensor was

116 ified disposable pencil graphite electrodes (PGEs) were developed herein for electrochemical monitori

117 Platinum group elements (PGE) of anthropogenic origin have been reported in rainw

118 reased the input of platinum group elements (PGE) to the environment, and their coupled geochemical b

119 incorporating three platinum group elements (PGEs) for the first time.

120 Elevated PGE(2) is a hallmark of most inflammatory lesions.

121 group exhibits paternal genome elimination (PGE), an unusual mode of sex determination that involves

122 These effects of exogenous PGE(2) on lamin A expression were mediated via the EP(2)

123 Promiscuous gene expression (PGE) by thymic epithelial cells (TEC) is essential for g

124 h diminished levels of proangiogenic factors PGE(2) and VEGF in cutaneous wounds of diabetic mice.

125 Bronchoalveolar lavage fluid PGE(2) concentrations were comparable in all groups.

126 ol lipase were required for providing AA for PGE(2) biosynthesis.

127 ne conversion and establishes guidelines for PGE in human cells.

128 The mobilized fractions measured for PGE in PM(10), PM(2.5), and PM(1) were highly variable,

129 s uncover a previously unrecognized role for PGE(2) in the promotion of tumor progression.

130 Our findings reveal a novel role for PGE(2)/EP2/protein kinase A signaling in the suppression

131 The [(3)H]PGE(2) binding of W203A in broken cell membrane fraction

132 resent; however, high affinity binding [(3)H]PGE(2) was observed in broken cell preparations washed f

133 However, T(R)1-like cells were deficient in PGE(2) and 4-fold less potent than were MSCs in suppress

134 Deficits in PGE(2) expression, HDMEC migration, and tube formation c

135 hat mPGES1 mediates acid-induced increase in PGE(2) production and cell proliferation.

136 naive lung and is required for increases in PGE(2) after OVA-induced allergy.

137 process that leads to sustained increases in PGE(2).

138 olved because insulin was unable to increase PGE(2) release.

139 eceptor expression with concurrent increased PGE(2) levels in injury.

140 dent fashion, and COX-1 deficiency increased PGE(2) production after LPS.

141 The results showed increased PGE(2) release in the lungs and NE-associated COX-2 in t

142 OX-2, not mPGES-1, mediates IL-1beta-induced PGE(2) production and subsequent inhibition of insulin s

143 ts to examine interleukin (IL)-1beta-induced PGE(2) production, because PGE(2) has been shown to medi

144 sus, suggesting a key role for COX-2-induced PGE(2) production in immune response to S. mucilaginosus

145 have shown that COX-2 mediates acid-induced PGE(2) production.

146 endothelial cells decreased cytokine-induced PGE(2) production primarily through inhibition of micros

147 indicating that mPGES-1 mediates LPS-induced PGE(2) production in BMDM.

148 Metalloproteinase-induced PGE(2) levels and MMP-9 expression were markedly attenua

149 Interestingly, single-nick-induced PGE using ODN donors produced conversion tracts biased e

150 PAF induced PGE(2) release from HVSMCs in a concentration- and time-

151 was essential for the control of PAF-induced PGE(2) release.

152 M)(3)) inhibitor diminished visfatin-induced PGE(2) release in chondrocytes.

153 During inducible PGE(2) synthesis, cPLA(2) hydrolyzes arachidonic acid (A

154 fy both an alternative pathway for inducible PGE(2) synthesis and a role for lipid-modifying enzymes

155 and decreased the effect of SNC80 to inhibit PGE(2)-stimulated thermal allodynia.

156 or the liberation of AA to be converted into PGE(2) by F. tularensis-infected macrophages.

157 re synthesized by the prostanoid isomerases, PGE synthases (PGES) and PGD synthases (PGDS), respectiv

158 (2) and its metabolite 13,14-dihydro-15-keto-PGE(2) (PGE-M) were abundant in wound fluid and induced

159 dvancing methods to quantify the trace level PGE emissions as a technique to more accurately estimate

160 Like PGE(2), leukotrienes (LTs) are potent mediators of DC mi

161 ctions of LTB(4) and the cAMP-inducing lipid PGE(2), suggesting that interplay between pro- and anti-

162 nes, chemokines, and lipid mediators, mainly PGE(2) with induction of cyclooxygenase-2 (COX-2) in the

163 In contrast, PAR(2)-mediated PGE(2) production, smooth muscle relaxation, and decreas

164 asal BCG vaccination enhances COX-2-mediated PGE(2) release by alveolar macrophages and further sugge

165 ophages in vitro had elevated COX-2-mediated PGE(2) release, but macrophages in vivo exhibited less a

166 verexpress iPLA(2)gamma, complement-mediated PGE(2) production was reduced by inhibitors of MAP/ERK k

167 acterize oligodeoxynucleotide (ODN)-mediated PGE using Cas9 and its nickase variants in human cells.

168 ively, our results suggest that ODN-mediated PGE utilizes synthesis-dependent strand annealing and si

169 nase (COX)-2, was coincident with membranous PGE(2) synthase, and was not significantly altered by a

170 aluated prostaglandin E2 urinary metabolite (PGE-M) in an independent population for association with

171 Microsomal PGE synthase-1 (mPGES-1) is an inducible enzyme that spe

172 Microglial cyclooxygenase-2, microsomal PGE synthase, and PGE2 expression were increased 2- to 2

173 ghts the role of cyclooxygenase-2/microsomal PGE synthase 1/PGE2 signaling in hypertension and diabet

174 cence, we detected both COX-2 and microsomal PGE synthase-1 (mPGES-1) but not COX-1 in the Golgi appa

175 ave increased levels of COX-2 and microsomal PGE synthase-1 (mPGES-1).

176 IL-6 coinduced Cox-2 and microsomal PGE synthase-1, and inhibited the expression of 15-hydro

177 PS exposure induced expression of microsomal PGE synthase-1 (mPGES-1), a key enzyme in PGE2 biosynthe

178 n primarily through inhibition of microsomal PGE synthase-1 (mPGES-1), not COX-2.

179 limit of 0.34 mug mL(-1) at ds-DNA modified PGE.

180 lized with thiol linker on the GNPs modified PGE.

181 Moreover, PGE(2) differentially affects T cell activation, cytokin

182 a DNA functionalized biosensor (DNA/CA@MWCNT/PGE) was prepared and characterized for the detection an

183 ro; in contrast, intranasal BCG activated no PGE(2) release in the lungs, because COX-1 and COX-2 in

184 in significantly inhibited the levels of NO, PGE(2), IL-6, TNF-alpha, iNOS and COX-2.

185 also attenuated LPS-induced PGD(2), but not PGE(2) production, suggesting the critical role of NOX-g

186 -PGDS-mediated production of PGD(2), but not PGE(2), in mouse BMDM.

187 Conversely LPS-induced PGD(2), but not PGE(2), production, was potentiated with the cotreatment

188 o attenuated the LPS-induced PGD(2), but not PGE(2), production.

189 Silencing of DNMT3a negated the ability of PGE(2) to increase DNMT activity.

190 ous CREB gene did not prevent the ability of PGE(2) to promote IL-10 transcription.

191 y 60% enhancement by blocking or ablating of PGE(2) receptor subtype 1 (EP1), approximately 30% enhan

192 We show that addition of PGE(2) strongly downregulates CD46 expression in activat

193 Administration of PGE(2) to TLR2(-/-) mice resulted in impaired clearance

194 matory mediator TNFalpha 24 or 48 h ahead of PGE(2) do not show the enhanced and prolonged hyperalges

195 -2, enzymes essential in the biosynthesis of PGE(2) from arachidonic acid.

196 We show that the combined blockade of PGE(2) and PD-1 signaling was therapeutic in terms of im

197 se, mediates LPS-induced late-phase burst of PGE(2) generation, and regulates LPS-induced iNOS expres

198 GES or PU.1, attenuated LPS-induced burst of PGE(2) production indicating that mPGES-1 mediates LPS-i

199 the absolute change in mean concentration of PGE(2) (the primary end point).

200 The absolute mean tissue concentration of PGE(2) was reduced by 67.6 +/- 229.68 pg/mL in arm A, 12

201 Concentrations of PGE(2) in bronchoalveolar lavage fluid were measured by

202 One neonatal dose of PGE(2) masculinizes the POA and behavior, and simultaneo

203 salt-inducible kinases mimics the effect of PGE(2) on IL-10 production.

204 The effects of PGE(2) and EP receptor agonists on CD3/CD28-stimulated c

205 1 expression is essential for the effects of PGE(2) deficiency.

206 degradation and the pattern of expression of PGE(2) receptors.

207 ealth risks at chronic levels, the extent of PGE pollution is of global concern.

208 DR (sub)pathways leading to the formation of PGE products remain elusive.

209 The function of PGE(2) signaling through its EP3 receptor was examined i

210 a novel ASC-RIPK2 axis in the generation of PGE(2) that is repressed in patients diagnosed with chro

211 The impact of PGE(2) reflects the balance between its cyclooxygenase 2

212 revious studies identified the importance of PGE(2) in regulating macrophage functions, but little is

213 ements, especially through the inhalation of PGE-associated airborne particulate matter (PM), have be

214 Inhibition of PGE synthase reduced TF in vivo and in vitro and prevent

215 -146a in BMSCs correlated with inhibition of PGE synthase-2 and inhibition of PGE2 release.

216 directly associated with increased levels of PGE metabolites.

217 threefold, accompanied by reduced levels of PGE(2).

218 he mPGES1(-/-) mice, suggesting that loss of PGE(2) does not impair induction of a Th2 response.

219 Overall, the mobility of PGE in airborne PM samples was notable, with a mean of 5

220 r of the MAPK-mediated regulatory network of PGE(2) production.

221 imize and measure analytical performances of PGE/P(TBA0.5Th0.5) based electrode.

222 d that COX-2 mediated the high production of PGE(2) and, to a lesser extent, other prostanoids after

223 nting the subsequent increased production of PGE(2) and/or IL-6 by the tumor cell lines.

224 munity is related to increased production of PGE(2) by AMs.

225 ary for induction of COX-2 and production of PGE(2) by S. mucilaginosus.

226 orrelation existed between the production of PGE(2) or IL-6 by cancer cells and their resistance to c

227 Complement-mediated production of PGE(2) was amplified in GECs that overexpress iPLA(2)gam

228 2) followed by COX-2-dependent production of PGE(2).

229 he expression of COX-2 and the production of PGE(2).

230 C subpopulations, we discovered a program of PGE that is common between medullary (m) and cortical TE

231 tioning the use of Os isotopes as proxies of PGE sources to the environment.

232 sis vaccine, stimulated increased release of PGE(2) by macrophages activated in vitro; in contrast, i

233 In this study we investigated the role of PGE(2) and its receptors in the barrier function of huma

234 We have investigated the role of PGE(2), which binds to the E-prostanoid family of G prot

235 Conflicting roles of PGE(2) in T cell functions have been reported, and the r

236 at least partly explain the diverse roles of PGE(2) in T cell functions.

237 tanoic acid [KH064]) attenuated secretion of PGE(2) from human immune cells stimulated with the fatty

238 ia and vascular remodeling in the setting of PGE(2) deficiency depend on thromboxane A(2) and signali

239 -2(+) macrophages were the primary source of PGE(2) release in the lungs, since there was only slight

240 Suppression of PGE(2) synthesis by the cyclooxygenase inhibitors aspiri

241 antity of rGO assembling onto the surface of PGE by passive adsorption was optimized.

242 ilized the capture probe onto the surface of PGE, hybridization was achieved with a biotinylated (fro

243 steinyl-leukotrienes was reduced and that of PGE(2) enhanced in AMs in vitro and the lungs of l/l mic

244 vented the estradiol-induced upregulation of PGE(2), indicating that microglia are essential to the f

245 conjugate to the surface insulin-antibody on PGE/MWNT/Py electrodes.

246 hrough a positive feedback loop dependent on PGE(2) binding to EP4.

247 The developed DPV on PGE method constitutes a simple and inexpensive tool for

248 phenolic contents (TPCs) evaluated by DPV on PGE were 35.81, 34.59 and 31.21 mg caffeic acid equivale

249 Self-assembly of PNPs on PGE surface and adhesion of DLD-1 cancer cells on this s

250 Using the emission profile based on PGEs and ambient quantification, mass balancing revealed

251 of human THP-1 cell-derived m with PGE(2) or PGE-M caused dose-dependent induction of OSM.

252 PS-induced production of IL-6, TNF-alpha, or PGE(2), especially under the high glucose conditions.

253 ning and labor with prostaglandin (PG) E2 or PGE analogs, often requiring many hours of hospitalizati

254 duction by PBMCs through EP(2) but not other PGE(2) receptors.

255 ine and morphine bonded on dsDNA/MWCNTs-PDDA/PGE was used to obtain an analytical signal.

256 ents in whom the urinary metabolite of PGE2 (PGE-M) is suppressed.

257 The two major PGs, PGE(2) and PGD(2), are synthesized by the prostanoid iso

258 PNP/PGEs acted as a sensitive platform for simple and rapid

259 Py) modified pencil graphite electrodes (PPy/PGE).

260 diators nitric oxide (NO) and prostaglandin (PGE(2)) was significantly inhibited by treatment of EGCG

261 The prostanoid PGE(2), which induces angiogenesis and vasodilation, is

262 y mediated through the EP1 and EP3 G protein PGE(2) receptors.

263 er, these data indicate that SphK1 regulates PGE(2) production by mPGES-1 expression via the p38 MAPK

264 represents a promising candidate to replace PGE(2) in DC maturation protocols for cancer vaccination

265 In this study, we report PGE concentrations and osmium isotope ((187)Os/(188)Os)

266 rGO-PGEs were then utilized for electrochemical monitoring o

267 The electrochemical behavior of rGO-PGEs was examined by cyclic voltammetry (CV).

268 MSCs constitutively secrete PGE(2), which is augmented in allogeneic reactions.

269 phrine before the addition of PAF suppressed PGE(2) release, treatment with epinephrine after PAF sti

270 Paradoxically low tendon PGE(2) levels in early injury may be attributed to incre

271 ned unchanged and were three-fold lower than PGE(2).

272 We previously demonstrated that PGE(2) synthesis by F. tularensis-infected macrophages r

273 These findings indicate that PGE(2) helps MSC-induced IL-10(+)IFN-gamma(+)CD4(+) T(R)

274 ific TCR are also protected, indicating that PGE(2) acts primarily after challenge with inhaled Ag.

275 It is likely that PGE is widespread in Psocodea, including human lice.

276 As recent studies have shown that PGE are bioavailable in the environment and pose health

277 We show in this study that PGE(2), in combination with LPS, is able to promote an a

278 The results suggest that PGE emitted from automotive catalytic converters are lik

279 The results of our study suggest that PGE(2) may have a pathogenic role in diabetic retinopath

280 This suggests that PGE(2) released from muscle fibres and PGI(2) released f

281 of these transcription factors abrogated the PGE(2) increase of DNMT3a expression.

282 tors 1 and 2 (CysLT(1) and CysLT(2)) and the PGE(2) receptors E-prostanoid 1 to 4 (EP(1)-EP(4)) in br

283 Subcutaneous injection of the PGE(2) analog misoprostol decreased M-CSFR expression in

284 as correlated with a distinct pattern of the PGE(2) receptors expressed, with EP4 being preferentiall

285 These data demonstrate a novel role of the PGE(2)-EP4 axis in CD46 functions, which might at least

286 of activated STAT1 and STAT6 related to the PGE(2) production of tumor cells.

287 Topical treatment of diabetic mice with the PGE analog misoprostol improved host defense against MRS

288 Thus, PGE(2) inhibition is both an independent candidate thera

289 om cellular phospholipids to be converted to PGE(2).

290 ted cAMP accumulation, yet were resistant to PGE(2)-mediated suppression of LT generation.

291 This response to PGE(2) was mediated chiefly through the EP1 receptor and

292 eration and inversely with responsiveness to PGE(2)-mediated suppression of LTB(4).

293 )Os/(188)Os composition can be used to trace PGE sources.

294 and OATP4A1 transporters, known to transport PGE(2).

295 sis was performed regarding baseline urinary PGE-M and outcomes.

296 patients with a >/= 50% decrease in urinary PGE-M after 5 days of treatment with apricoxib could enr

297 In vitro PGE(2) inhibited cytokine production by PBMCs through EP

298 el DC progenitor regulatory pathway in which PGE(2) signaling through EP1/EP3 receptors regulates Flt

299 , MSC-induced T(R)1-like cells combined with PGE(2), but not either alone, significantly reduced TA a

300 olar smooth-muscle hyperplasia compared with PGE(2)-sufficient controls when challenged intranasally

301 Treatment of human THP-1 cell-derived m with PGE(2) or PGE-M caused dose-dependent induction of OSM.