ライフサイエンスコーパス: prostaglandin

1 mmunological factors, second messengers, and prostaglandins.

2 in E2 approximately 5 fold) as well as lower prostaglandins.

3 st guideline made a specific recommendation: prostaglandins.

4 or OAG or OHT; and no known nonresponders to prostaglandins.

5 s and AA is a precursor for pro-inflammatory prostaglandins.

6 tep in the metabolism of arachidonic acid to prostaglandins.

7 mation-initiating lipid mediators, including prostaglandins.

8 ream signaling through both nitric oxide and prostaglandins.

9 All were intubated and on prostaglandin, 24 (89%) were inotrope dependent, and 22

10 staglandins, 4.75 (CrI, 3.11 to 6.44); 2009: prostaglandins, 4.58 (CrI, 2.94 to 6.24).

11 staglandins, 5.43 (CrI, 3.38 to 7.38); 2004: prostaglandins, 4.75 (CrI, 3.11 to 6.44); 2009: prostagl

12 ic agonists, 5.64 (CrI, 1.73 to 9.50); 1999: prostaglandins, 5.43 (CrI, 3.38 to 7.38); 2004: prostagl

13 hannels serve as a portal for the release of prostaglandins, a critical process in mediating biologic

14 The role of prostaglandin A2 (PGA2) in modulation of vascular endoth

15 There are concerns that diminished prostaglandin action in fetal life could increase the ri

16 es (LNs) that was dependent on IL-17-induced prostaglandin activity.

17 was a significantly higher concentration of prostaglandins after FLACS relative to MCS (WMD, 198.34;

18 LPI group compared with 85.0% of eyes in the prostaglandin analog (PGA) group (P < 0.001), and qualif

19 f previously treated patients were receiving prostaglandin analog (PGA) monotherapy.

20 myopia, age-related macular degeneration, or prostaglandin analog use were not shown to increase risk

21 se of an untreated eye to monotherapy with a prostaglandin analogue at all daytime time points measur

22 ween 2007 and 2012 were analyzed to identify prostaglandin analogue monotherapy OAG patients with an

23 secretion through their effects on pituitary prostaglandin and BMP4 signaling.

24 AA play a critical role in the catalysis of prostaglandin and thromboxane synthesis.

25 oncoding dsRNA as an upstream coordinator of prostaglandin and Wnt levels in regeneration.

26 decreased levels of proinflammatory hepatic prostaglandins and 20-hydroxyeicosatetraenoic acid (20-H

27 and LCL may result from an imbalance between prostaglandins and leukotrienes, which may serve as targ

28 ERD, correlating with enhanced production of prostaglandins and leukotrienes.

29 Prostaglandins and their receptors have been implicated

30 nducible enzyme involved in the synthesis of prostaglandins, and has been implicated in many pathophy

31 rleukin(IL)-1beta treatment markedly induced prostaglandin biosynthesis in diseased compared to healt

32 TGS2, which codes for COX-2, a key enzyme in prostaglandin biosynthesis, and AREG, which codes for th

33 or-derived VEGF-C promoted expression of the prostaglandin biosynthetic enzyme COX-2 in lymphatics, a

34 lays a dual role by promoting the cPLA2alpha/prostaglandin/cAMP/PKA pathway and CREB phosphorylation

35 ical outcomes, it was associated with higher prostaglandin concentrations and higher rates of posteri

36 yptophan and other amino acids, fatty acids, prostaglandins, cyclic nucleotides, odorants, polyamines

37 Cyclopentenone prostaglandins (cyPGs) are reactive lipid mediators that

38 the production of endogenous cyclopentenone prostaglandins (CyPGs), Delta-12 prostaglandin J2 (Delta

39 ing, chemokine ligand 5 (CCL5) hematopoietic prostaglandin D synthase (HPGDS) and neuropeptide S rece

40 reater IL-5 and IL-13 than did hematopoietic prostaglandin D synthase-negative and CD161(-) cT(H)2 ce

41 H)2 cells-positive (CRTH2(+)), hematopoietic prostaglandin D synthase-positive CD161(hi) CD4 T cells.

42 AGN 211377 antagonizes prostanoid prostaglandin D2 (DP)1, DP2, prostaglandin E2 (EP)1, EP4

43 Also, levels of prostaglandin D2 (PGD2) and lipoxin A4 (LXA4) in patient

44 Effects of common pesticides on prostaglandin D2 (PGD2) inhibition in SC5 mouse Sertoli

45 monly used in the European Union to suppress prostaglandin D2 (PGD2) synthesis.

46 Furthermore, we also show how prostaglandin D2 (PGD2), which is upregulated in balding

47 activation, including abundant production of prostaglandin D2 (PGD2).

48 mphopoietin [TSLP]) and mast cell mediators (prostaglandin D2 [PGD2]) are critical activators of ILC2

49 Prostaglandin D2 levels were measured with ELISA.

50 set of patients with AERD is associated with prostaglandin D2 overproduction.

51 esulted in over 50% decrease in KLA-elicited prostaglandin D2 production.

52 that fevipiprant (QAW039), an antagonist of prostaglandin D2 receptor 2, might reduce eosinophilic a

53 d, compound 1 (AGN 211377), that antagonizes prostaglandin D2 receptors (DPs) DP1 (49) and DP2 (558),

54 ible and competitive with the native agonist prostaglandin D2(PGD2).

55 ls, along with increased production of IL-5, prostaglandin D2, and eosinophil and T-helper type 2 cel

56 Release of beta-hexosaminidase, prostaglandin D2, and GM-CSF and changes in reactive oxy

57 ed in combination with niacin to abolish the prostaglandin D2-(PGD2)-induced flushing.

58 peT(H)2 but not cT(H)2 cells produced prostaglandin D2.

59 eating focal wounds in the colonic mucosa of prostaglandin-deficient mice.

60 his effect was mediated by an increase in 15-prostaglandin dehydrogenase (15-Pgdh) activity, which ox

61 The enzyme 15-prostaglandin dehydrogenase (15-PGDH) catalyzes the firs

62 sed tendon cells, we also found increased 15-Prostaglandin Dehydrogenase (15-PGDH) expression as well

63 to the nucleus for repression of 15-hydroxy prostaglandin dehydrogenase (15-PGDH).

64 e inflammation, joint destruction, cartilage prostaglandin depletion, osteoclast activity, and Th17 p

65 Prostaglandin E Receptor EP1 transfection or treatment w

66 Results show that only prostaglandin E receptor-4 (EP4) was involved and mediat

67 Prostaglandin E receptor-4 receptor mediates endothelial

68 g carcinoma cells reveal that Gas6 increases prostaglandin E synthase (Ptges) expression in endotheli

69 By contrast, deletion of microsomal prostaglandin E synthase 1 (mPGES-1) confers analgesia,

70 type I receptor (IL-1RI), COX-2, microsomal prostaglandin E synthase 1 (mPGES-1), and EP receptors,

71 PTGES, which encodes the prostaglandin E synthase, has also been linked to asthma

72 tion of a virus vector expressing microsomal prostaglandin E synthase-1 (mPGES-1) into the median pre

73 creening hit was found to inhibit microsomal prostaglandin E synthase-1 (mPGES-1) with an IC50 of 17.

74 xpression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 and reduces 15-hydroxyprostag

75 Inhibiting COX-2 or microsomal prostaglandin E synthase-1 suppressed the 6-OHDA-trigger

76 m of COX-1 that synthesizes PgE2 (microsomal prostaglandin E synthase-1) depends critically for its v

77 Genetic ablation of cyclooxygenases (COX) or prostaglandin E synthases in Braf(V600E) mouse melanoma

78 Using a connectivity map, we identified prostaglandin E1 (PGE1) as a small molecule that partly

79 timulated phosphoprotein phosphorylation and prostaglandin E1-induced increase in cyclic adenosine mo

80 izes prostanoid prostaglandin D2 (DP)1, DP2, prostaglandin E2 (EP)1, EP4, prostaglandin F2alpha, and

81 h and bone density (P <0.01), enhanced 7-day prostaglandin E2 (P <0.01), and reduced 28-day inflammat

82 enase-2 (COX-2) and its prostanoid products, prostaglandin E2 (PGE2 ) in particular, are key contribu

83 89 +/- 17.47 pg/mg protein; P <0.05); and 3) prostaglandin E2 (PGE2) (LPS: 159.20 +/- 38.70 pg/mg wet

84 The two synthetic pathways are connected by prostaglandin E2 (PGE2) activation of the aromatase enzy

85 Here we demonstrate in vivo that prostaglandin E2 (PGE2) can differentially increase the

86 Inflammation-induced release of prostaglandin E2 (PGE2) changes breathing patterns and t

87 cell activation via producing high level of prostaglandin E2 (PGE2) due to their thousands-fold high

88 ase (mPGES)-1 is responsible for the massive prostaglandin E2 (PGE2) formation during inflammation.

89 Prostaglandin E2 (PGE2) has emerged as a principal media

90 ical hyperalgesia and marked prolongation of prostaglandin E2 (PGE2) hyperalgesia, a key feature of h

91 Here we identified prostaglandin E2 (PGE2) in the tumor as a key mediator o

92 Here we show that Prostaglandin E2 (PGE2) is an inflammatory cytokine that

93 n strongly linked to adhesion formation, and Prostaglandin E2 (PGE2) is associated with both adhesion

94 Prostaglandin E2 (PGE2) is associated with proliferation

95 Prostaglandin E2 (PGE2) is derived from arachidonic acid

96 cholamines induce inflammation by increasing prostaglandin E2 (PGE2) levels in ovarian cancer cells.

97 Modulating levels of prostaglandin E2 (PGE2) or PGB2 restricted distal segmen

98 vitalization of the cyclooxygenase (COX) and prostaglandin E2 (PGE2) pathway.

99 fibroblast via the cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) pathway.

100 We tested the hypothesis that astrocytic prostaglandin E2 (PgE2) plays a key role for cerebrovasc

101 endothelial cells, we demonstrate that local prostaglandin E2 (PGE2) production in deep brain areas,

102 on of cyclooxygenase 2 (COX-2) and resultant prostaglandin E2 (PGE2) production.

103 ase-2 (COX-2) activity and activation of the prostaglandin E2 (PgE2) receptors EP2 and EP4.

104 ge (0.57-fold Nrf-2 and 0.34-fold HO-1), and prostaglandin E2 (PGE2) release was increased in samples

105 ypersensitivity was impaired, and subsequent prostaglandin E2 (PGE2) response was blunted.

106 ion of infected apoptotic cells (IACs) drive prostaglandin E2 (PGE2) secretion to generate Th17 cells

107 e results from LPS-induced the production of prostaglandin E2 (PGE2) show that, esculetin, curcumin a

108 pithelial cell culture system, we found that prostaglandin E2 (PGE2) signaling through one of its rec

109 In human aortic smooth muscle cells, prostaglandin E2 (PGE2) stimulates adenylyl cyclase (AC)

110 Prostaglandin E2 (PGE2) stimulates HSC renewal and engra

111 dothelium followed by COX1-mediated cerebral prostaglandin E2 (PGE2) synthesis.

112 eurological conditions, mainly via producing prostaglandin E2 (PGE2) that activates four membrane rec

113 TLR4 ligand, induces macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and micr

114 Fever occurs upon binding of prostaglandin E2 (PGE2) to EP3 receptors in the median p

115 COX-2 overexpression or Prostaglandin E2 (PGE2) treatment increased beta1-integr

116 significantly increased, while the level of prostaglandin E2 (PGE2) was decreased.

117 ls overexpress cyclooxygenase-2, overproduce prostaglandin E2 (PGE2), and exhibit defective intracell

118 Although immunoregulatory factors, such as Prostaglandin E2 (PGE2), and their mechanisms of action

119 looxygenases (COXs) and their final product, prostaglandin E2 (PGE2), are known to play important rol

120 scued by the addition of arachidonic acid or prostaglandin E2 (PGE2), indicating a phospholipase-depe

121 valuate levels of four major labor triggers, prostaglandin E2 (PGE2), interleukin (IL)-1beta, IL-6, a

122 rs, such as vasoactive intestinal peptide or prostaglandin E2 (PGE2), regulate intestinal anion/fluid

123 Previously, we revealed that prostaglandin E2 (PGE2), released during hypercapnic cha

124 at the key products of NOS2 and COX2, NO and prostaglandin E2 (PGE2), respectively, promote feed-forw

125 al cells with M27 increases the secretion of prostaglandin E2 (PGE2), the enzymatic product of Ptges,

126 nd were treated with vehicle, diclofenac, or prostaglandin E2 (PGE2), the most important COX-2 produc

127 We observed that prostaglandin E2 (PGE2), through its receptor EP4, is do

128 ted macrophages and expressed high levels of prostaglandin E2 (PGE2)-forming enzymes microsomal PGE2

129 iety of lipid signaling molecules, including prostaglandin E2 (PGE2).

130 -2) pathway and the concomitant increases in prostaglandin E2 (PGE2).

131 Cyclooxygenase and lipoxygenase metabolites prostaglandin E2 (vasodilator) and 12-hydroxyeicosatetra

132 Although suppression of prostaglandin E2 accounts for the protective effect of m

133 PPARgamma) activator rosiglitazone (Rosi) or prostaglandin E2 analog (16,16-dimethyl PGE2) to adipose

134 n were performed and included measurement of prostaglandin E2 and cytosolic phospholipase A2 activity

135 isruption of the protein's ability to induce prostaglandin E2 and cytosolic phospholipase A2 synthesi

136 demonstrated increased urinary excretion of prostaglandin E2 and metabolites.

137 tantly, MKO(GFAP) mice exhibit reduced brain prostaglandin E2 and pro-inflammatory cytokine levels up

138 tion initiating mediators leukotriene B4 and prostaglandin E2 and pro-resolving mediators resolvin D1

139 We show that COX-2 and prostaglandin E2 are required for C1P-mediated increases

140 ia-synapse cross talk requires production of prostaglandin E2 by microglia, leading to the activation

141 dsRNA-induced WIHN and Wnt7b, and exogenous prostaglandin E2 can rescue WIHN and Wnt7b.

142 ponses to capsaicin but reduced responses to prostaglandin E2 compared with healthy volunteers.

143 Both AREG and prostaglandin E2 converge to activate signaling through

144 , increased free water reabsorption, urinary prostaglandin E2 excretion, and reduced excretion of ser

145 UV-induced prostaglandin E2 has been implicated as an intermediary

146 Prostaglandin E2 increased in controls and EPI group and

147 on of cultured small-diameter DRG neurons by prostaglandin E2 is also prevented and reversed by HMWH.

148 In other tissues, prostaglandin E2 is an important effector of regeneratio

149 Functionally, aortic Leukotriene B4 and Prostaglandin E2 levels correlated with traits of plaque

150 Plaa-null mice were generated and prostaglandin E2 levels were measured in different tissu

151 Urinary metabolite of prostaglandin E2 may be able to identify patients who co

152 omponents, the enantioselective synthesis of prostaglandin E2 methyl ester has been achieved through

153 els of acquired AI resistance indicated that prostaglandin E2 receptor 4 (PTGER4) is upregulated afte

154 Further, mice lacking the prostaglandin E2 receptor EP3 selectively on serotonergi

155 n D2 receptors (DPs) DP1 (49) and DP2 (558), prostaglandin E2 receptors (EPs) EP1 (266) and EP4 (117)

156 resistance protein 4, and G-protein-coupled prostaglandin E2 receptors 1 and 2), abolished P-glycopr

157 Increased cyclooxygenase-2 expression and prostaglandin E2 release could be abrogated in metastati

158 oxyprostaglandin dehydrogenase, resulting in prostaglandin E2 release in human breast cancer.

159 g components in the cyclooxygenase-2 (COX-2)/prostaglandin E2 signaling cascade (phospholipase A2, CO

160 a mechanism involving caspase activation and prostaglandin E2 signaling.

161 Microsomal prostaglandin E2 synthase (mPGES)-1 is responsible for t

162 Microsomal prostaglandin E2 synthase type 1 (mPGES-1) is responsibl

163 also been linked to asthma, where deficient prostaglandin E2 synthesis has been associated with airw

164 lic phospholipase A2, which was reflected in prostaglandin E2 synthesis.

165 sion induced by inflammatory pain depends on prostaglandin E2 that is synthesized by cyclooxygenase 2

166 t of diffusible signaling molecules, such as prostaglandin E2 The capability of human or murine CAFs

167 erinatal lethal with reduced brain levels of prostaglandin E2 The non-functional phospholipase A2-act

168 reversed hyperalgesia induced by intrathecal prostaglandin E2 To distinguish between a peripheral/spi

169 The whipworm (Trichuris suis) secretes prostaglandin E2 to suppress proinflammatory properties

170 We propose that tick salivary prostaglandin E2 triggers antibody class switching in ma

171 r the formation of the potent lipid mediator prostaglandin E2 under proinflammatory conditions, and t

172 We also evaluated prostaglandin E2 urinary metabolite (PGE-M) in an indepe

173 However, responses to prostaglandin E2 were decreased by CS exposure.

174 ls pulsed in vitro for 2 hours with dimethyl prostaglandin E2 were functionally similar to those from

175 sphatidylcholine, lysophosphatidic acid, and prostaglandin E2) recapitulated M1 phenotype in iPLA2bet

176 ammatory lipid mediators, Leukotriene B4 and Prostaglandin E2, and a concomitant decrease of resolvin

177 evelopmentally regulated by the inflammatory prostaglandin E2, but in different ways.

178 accelerate thrombogenesis, while suppressing prostaglandin E2, but increasing biosynthesis of PGI2.

179 inhibited mechanical hyperalgesia induced by prostaglandin E2, carrageenan-induced hyperalgesia, and

180 induced by diverse pronociceptive mediators, prostaglandin E2, epinephrine, TNFalpha, and interleukin

181 Elevation of baseline urinary metabolite of prostaglandin E2, indicating activation of the COX-2 pat

182 Thus, the glyceryl ester of prostaglandin E2, PGE2-G, mobilizes Ca(2+) and activates

183 Plasma levels of histamine, leukotriene B4, prostaglandin E2, prostaglandin F2, pH, and HCO3 were me

184 s activators of PKA, including adenosine and prostaglandin E2, results in a profound delay of neutrop

185 DUSP2 led to overproduction of COX-2-derived prostaglandin E2, which promoted cancer stemness via the

186 synaptic inhibition occur partially through prostaglandin E2- (PGE2-) and PKA-dependent phosphorylat

187 terminal to mediate a marked prolongation of prostaglandin E2-induced hyperalgesia.

188 phorylation of PREX1 after isoproterenol and prostaglandin E2-mediated GPCR activation is partially P

189 oncentrations counterregulated adenosine and prostaglandin E2-mediated inhibition of ERK1/2 activatio

190 rly induces the beta-catenin pathway through prostaglandin E2.

191 the biosynthesis of prostacyclin (PGI2) and prostaglandin E2.

192 ction of proinflammatory effectors including prostaglandin E2.

193 LPS-stimulated prostaglandin-E2 production was dysregulated in macropha

194 tion and lipid deposition, and to controlled prostaglandin-E2 production.

195 Prostaglandin endoperoxide H synthase-2 (PGHS-2), also c

196 Prostaglandin endoperoxide H synthases (PGHSs), also cal

197 chanisms of damage involve the activities of prostaglandin-endoperoxide synthase 1 (PTGS1 or cyclooxy

198 ionship between levels of MIC1 and levels of prostaglandin-endoperoxide synthase 2 expression (PTGS2

199 with its primary mode of action in mammals (prostaglandin-endoperoxide synthases) but modulated gene

200 and proven anabolic selective agonist of the prostaglandin EP4 receptor, compound 5, and alendronic a

201 coding variant that alters expression of the prostaglandin EP4 receptor.

202 roup and decreased in 4-aminopyridine group; prostaglandin F2 increased in controls but decreased in

203 histamine, leukotriene B4, prostaglandin E2, prostaglandin F2, pH, and HCO3 were measured.

204 signaling and also reduces expression of the prostaglandin F2a receptor negative regulator (PTGFRN),

205 In this work, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) was analysed in

206 ell as products of lipid peroxidation (8-iso-prostaglandin F2alpha (8-isoPF2alpha) and 4-hydroxy-2-no

207 alpha,20beta-dihydroxyprogesterone (DHP) and prostaglandin F2alpha (PGF2alpha) levels rise in teleost

208 inflammation-initiating mediators including prostaglandin F2alpha and leukotriene B4 and pro-resolvi

209 E2 receptors (EPs) EP1 (266) and EP4 (117), prostaglandin F2alpha receptor (FP) (61), and thromboxan

210 inflammation-initiating mediators (including prostaglandin F2alpha) and select proresolving pathways

211 D2 (DP)1, DP2, prostaglandin E2 (EP)1, EP4, prostaglandin F2alpha, and thromboxane A2 receptors but

212 t aggregate inhibitor and two members of the prostaglandin family of compounds by catalytic cross-met

213 th a mechanism downstream of proinflammatory prostaglandin formation, acetaminophen also reversed hyp

214 clooxygenase-2 catalyses the biosynthesis of prostaglandins from arachidonic acid but also the biosyn

215 rachidonic acid but also the biosynthesis of prostaglandin glycerol esters (PG-Gs) from 2-arachidonoy

216 vo effects of pharmacological agonism of the prostaglandin I2 (IP) receptor in pancreatic beta-cells

217 so observed enhanced autocrine production of prostaglandin I2 (PGI2, also called prostacyclin) in Cav

218 ptor antagonists, indicating a role for both prostaglandin I2 and E2 Activation of ERKs and p38, but

219 ceptor (TP) (11) while sparing EP2, EP3, and prostaglandin I2 receptors (IPs); Kb values (in nanomole

220 I2, E1, E2, and A2, while in HRGEC only more prostaglandin I2 was detected.

221 production of the counteracting eicosanoids prostaglandin I2, E1, E2, and A2, while in HRGEC only mo

222 A2 receptors but not anti-inflammatory EP2, prostaglandin I2, or EP3 receptors.

223 ein kinases triggers the rapid production of prostaglandins I2 and E2 through cyclooxygenase (COX)-1

224 Here, we have investigated the role of prostaglandins in the affective dimension of pain using

225 High concentrations of adenosine and prostaglandins in the fetal and neonatal circulation ham

226 talyzes the first step in the degradation of prostaglandins including PGE2.

227 Inhibiting nitric oxide (l-NAME) and prostaglandin (indomethacin) synthesis increased CGRP EC

228 ignaling lipid molecule 15-deoxy-delta 12,14 prostaglandin J2 (15-d-PGJ2) and confers cytoprotection

229 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) is naturally produced in the

230 yclooxygenase (COX)-dependent cyclopentenone prostaglandin J2 (15d-PGJ2) plays a key role.

231 J2 (Delta(12)-PGJ2), and 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2).

232 lopentenone prostaglandins (CyPGs), Delta-12 prostaglandin J2 (Delta(12)-PGJ2), and 15-deoxy-Delta12,

233 and increases of its product 15-deoxy Delta-prostaglandin J2 as well as cyclooxygenase 2/15-deoxy De

234 azone, troglitazone, and 15-deoxy-Delta12,14-prostaglandin J2) decrease levels of beta-catenin.

235 olvement of cyclooxygenase 2, 15-deoxy Delta-prostaglandin J2, and peroxisome proliferator-activated

236 2 as well as cyclooxygenase 2/15-deoxy Delta-prostaglandin J2-dependent activation of peroxisome prol

237 ury involves cyclooxygenase 2/15-deoxy Delta-prostaglandin J2-dependent activation of peroxisome prol

238 data suggest roles for 15-deoxy-Delta(12,14)-prostaglandin-J2 and lipoxin A4, both of which are poten

239 A series of Delta(12)-prostaglandin J3 (Delta(12)-PGJ3) analogues and derivati

240 ation of eicosanoids and docosanoids such as prostaglandins, leukotrienes, thromboxanes, isoprostanes

241 n cyclopenthenone groups, which recapitulate prostaglandin-like structure, cause sustained enhancemen

242 c screen using zebrafish and discovered that prostaglandins, lipid mediators involved in many physiol

243 natural product class: terpenes, alkaloids, prostaglandins, macrolides, and tetracyclines.

244 Collectively, our findings show that prostaglandin-mediated modulation of serotonergic transm

245 Women with known allergies to prostaglandins or pregnancy complications were excluded.

246 However, suppression of these prostaglandins, particularly PGI2, by cyclooxygenase-2 i

247 utic effect superior to global inhibition of prostaglandin (PG) biosynthesis by aspirin-like drugs.

248 Prostaglandin (PG) D2 is an early-phase mediator in infl

249 Prostaglandin (PG) D2 is the dominant COX product of mas

250 potent pro-resolving mediators, such as the prostaglandin (PG) D2-derived cyclopentenone metabolite,

251 ERD), reduced expression/production of COX-2/prostaglandin (PG) E2 and diminished expression of E-pro

252 s; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin (PG) E2 are generated at the site of infla

253 Prostaglandin (PG) E2 is a bioactive lipid that plays pr

254 Prostaglandin (PG) E2 is involved in the Mo/Mp-mediated

255 nduction of cervical ripening and labor with prostaglandin (PG) E2 or PGE analogs, often requiring ma

256 Cyclooxygenase-prostaglandin (PG) E2 signaling within the ventrolateral

257 otypes were distinguished by thromboxane B2, prostaglandin (PG) E2, and PGD2 production, in addition

258 the asthma phenotype; however, the effect of prostaglandin (PG) I2 on ILC2 function is unknown.

259 Analgesics which affect prostaglandin (PG) pathways are used by most pregnant wo

260 idespread reduction (between 50% and 90%) in prostaglandin (PG) profiles in fish tissues and plasma w

261 h a modest reliance on nitric oxide (NO) and prostaglandin (PG) synthesis.

262 Prostaglandin (PG)E2 accumulates in inflamed periodontal

263 ass spectrometry identified this compound as prostaglandin (PG)E2.

264 IR ), and synthesis of nitric oxide (NO) and prostaglandins (PG).

265 butyrate, leading to increased production of prostaglandin PGE2, a secreted autacoid that maintains r

266 Prostaglandins (PGs) are mediators of inflammation with

267 )), to examine the role of ATII cell-derived prostaglandins (PGs) in these processes.

268 Interestingly, other prostaglandins (PGs) inhibited the enzyme, including non

269 nd receptors which are critical not only for prostaglandin production and activity but also for estra

270 proinflammatory cytokine known to stimulate prostaglandin production and EP3 expression.

271 s 2-31, (H)Gly-Gly-Phe-Leu(OMe) (30) reduced prostaglandin production of COX-2 with an IC50 of 60 nM

272 bition of beta-hydroxybutyrate signalling or prostaglandin production similarly abolishes PGC1alpha-d

273 , these results demonstrate a novel role for prostaglandin receptor EP4 in the mediation of barrier-e

274 A activator 6-benzoyl-cAMP, and agonists for prostaglandin receptors IP, EP2, and EP4 in infected but

275 ry rate-based statistics identified a higher prostaglandin reductase 2 expression at early reperfusio

276 ), an enzyme involved in production of these prostaglandins, results in delayed parturition in mice.

277 entify cells in the brain that transduce the prostaglandin signal to mate and show that the gonadal s

278 negative regulator (PTGFRN), an inhibitor of prostaglandin signaling and follicle-stimulating hormone

279 rafish embryonic kidney, thus revealing that prostaglandin signaling may have implications for renal

280 Prostaglandins stimulate uterine contractions and are cl

281 ators such as hydroperoxides and EPA-derived prostaglandins, such as 12-HpHEPE/15-HpHEPE and PGD3/PGE

282 The divergent effects on these prostaglandins suggest that inhibitors of mPGES-1 may be

283 nase (COX) inhibitors that inhibit mammalian prostaglandin synthesis affected the worm's motility but

284 ity, because specific fatty acids may affect prostaglandin synthesis and steroidogenesis.

285 nto the intestinal lumen, where they promote prostaglandin synthesis and Wnt signaling.

286 Perturbation of prostaglandin synthesis by manipulating Cox1 or Cox2 act

287 ENT By using mice with selective deletion of prostaglandin synthesis in brain endothelial cells, we d

288 Inhibiting NO and prostaglandin synthesis increased CGRP EC50 in Young and

289 dation of 2-AG in astrocytes provides AA for prostaglandin synthesis promoting LPS-induced neuroinfla

290 mmatory effects are rather caused by reduced prostaglandin synthesis than by activation of cannabinoi

291 upting chemicals have been found to suppress prostaglandin synthesis, but to our knowledge, pesticide

292 chidonic acid, phospholipases (PLA2G10), and prostaglandin synthesis-related enzymes (PTGD/PTGS2S).

293 ice and in mice with genetic deletion of the prostaglandin synthesizing enzyme cyclooxygenase-2 in th

294 ated with inflammation and known to activate prostaglandins that are implicated in the progression of

295 dothelium-derived hyperpolarizing factor, or prostaglandins to cause vasodilation.

296 Ks, by C. albicansacted synergistically with prostaglandins to induce expression of Il10,Nr4a2, and P

297 n with a variant in SLCO2A1, which encodes a prostaglandin transporter in the distal nephron.

298 The role of prostaglandin transporter OATP2A1/SLCO2A1 in colon cance

299 Prostaglandin use and previous retinal detachment were n

300 degeneration, retinal detachment repair, and prostaglandin use.