ライフサイエンスコーパス: PGF

1 PGF accounted for 23.4% (n=364) of all deaths (n=1555) i

2 PGF is a secreted factor that supports hypertrophy and c

3 PGF is induced in the heart after pressure-overload stim

4 PGF promoted metastasis of BCCs and also facilitated hom

5 PGF transgenic mice showed a more adaptive type of cardi

6 PGF was studied from the perspective of "hard outcomes"

7 PGF(2alpha) and 17,20beta-P thereby seemed to act throug

8 PGF(2alpha) and latanoprost acid induce coordinated alte

9 PGF(2alpha) at 8% WT levels was sufficient to induce coo

10 PGF(2alpha) has been implicated in wound healing and car

11 PGF(2alpha) increased the secretion of MMP-2 in a dose-d

12 PGF(2alpha) induces phosphorylation of JunD bound to the

13 PGF(2alpha) was also found to induce the expression of E

14 PGF(2alpha)-induced ERK1/2 phosphorylation was prevented

15 PGF-CTERM occurs in 29 archaeal species, some of which h

16 PGF-CTERM proteins include the major cell surface protei

17 Our results revealed that: (1) PGF varied depending on the pollinator species, and was

18 eroxide reductase activity and 9alpha,11beta-PGF(2) (PGF(2)(alphabeta)) from PGD(2) by the PGD(2) 11-

19 easured as PGD(2) reduction to 9alpha,11beta-PGF(2) by ELISA) were impaired by small interfering RNA

20 changes in leukotriene E(4) or 9alpha,11beta-PGF(2) levels after AD.

21 sed urinary tetranor PGDM > 2,3-dinor-11beta-PGF(2alpha) > 11beta-PGF(2alpha) in mice.

22 increased tetranor PGDM and 2,3-dinor-11beta-PGF(2alpha) in humans coincident with facial flushing.

23 elevated tetranor PGDM and 2,3-dinor-11beta-PGF(2alpha) in volunteers, coincident with a pyrexial an

24 respondingly, both PGDM and 2,3-dinor-11beta-PGF(2alpha) were suppressed by inhibition of COX-1 and C

25 tes, 11beta-PGF(2alpha) and 2,3-dinor-11beta-PGF(2alpha), in human urine and was the only endogenous

26 PGDM > 2,3-dinor-11beta-PGF(2alpha) > 11beta-PGF(2alpha) in mice.

27 abundant than the PGD(2) metabolites, 11beta-PGF(2alpha) and 2,3-dinor-11beta-PGF(2alpha), in human u

28 estion of higher urinary excretion of 11beta-PGF(2alpha) and a lower excretion of a PGE(2) metabolite

29 The same strong inter-15-PGF correlations were observed in plasma from healthy yo

30 All plasma 15-PGF isomers increased over time with in vitro cigarette

31 acidified, and total (free + esterified) 15-PGFs and AA were extracted with organic solvents.

32 itation of several 15-series PGF isomers (15-PGFs) and AA by high-performance liquid chromatography-t

33 ng HPLC-tandem MS applied to plasma total 15-PGFs.

34 0.83%) and lowest with P. rapae (2.71%); (2) PGF with B. ignitus depended on the distance between GM

35 reductase activity and 9alpha,11beta-PGF(2) (PGF(2)(alphabeta)) from PGD(2) by the PGD(2) 11-ketoredu

36 in levels of prostaglandin (PG)E(2), PGD(2), PGF(2alpha), and thromboxane B(2), as well as the expres

37 perfusion with 5 micromol/L PGE(2), PGD(2), PGF(2alpha), or carboprostacyclin.

38 at vasodilatory prostaglandins (PGs) PGE(2), PGF(2alpha), and PGE(3) accompany the erythema in the fi

39 and COX-2 as well as their products PGE(2), PGF(2alpha), and thromboxane B(2) and their receptors fo

40 PGD(2), PGE(2), PGF(2alpha), carbaprostacyclin (cPGI(2); a stable prosta

41 IV-1, while 9,10-dihydro-15d-PGJ(2), PGE(2), PGF(2alpha), or PGD(2) that lack the reactive alpha,beta

42 nfluent OCCM cells were treated with PGE(2), PGF(2alpha), specific activators/inhibitors of the EP pr

43 both isoforms with prostaglandin F(2alpha) (PGF(2alpha)) activates the small G-protein Rho, leading

44 ormonal pheromones, prostaglandin F(2alpha) (PGF(2alpha)) and 17alpha,20beta-dihydroxy-4-pregnen-3-on

45 and regioisomers of prostaglandin F(2alpha) (PGF(2alpha)) and are used as biomarkers for lipid peroxi

46 mechanisms by which prostaglandin F(2alpha) (PGF(2alpha)) increases intracellular Ca2+ concentration

47 y demonstrated that prostaglandin F(2alpha) (PGF(2alpha)) induces a rapid and transient expression of

48 Prostaglandin F(2alpha) (PGF(2alpha)) is a potent antiadipogenic factor in cultur

49 e of the major PGs, prostaglandin F(2alpha) (PGF(2alpha)) is present in human urine in significant co

50 of prostaglandins E(2) (PGE(2)), F(2alpha) (PGF(2alpha)), lipoxin A(4) (LXA(4)) and its receptor FPR

51 receptors that bind prostaglandin F(2alpha) (PGF(2alpha)), resulting in the activation of an inositol

52 ogical activator is prostaglandin-F(2alpha) (PGF(2alpha)).

53 re stereoisomers of prostaglandin F(2alpha) (PGF(2alpha)).

54 hly effective ocular hypotensive agent, is a PGF(2)(alpha) analogue that inhibits both the PGD(2) 11-

55 Travoprost acid, PGF(2alpha,) unoprostone, and S-1033 were tested in addi

56 approximately 30% enhancement by activating PGF(2alpha) receptor or thromboxane receptor, or approxi

57 ured in expression of PAPPA, FLT1, ENG, AFP, PGF, and LGALS14, but not LGALS13 or the lineage marker

58 how the regulation of EGR-1 expression after PGF(2alpha) activation of FP receptors and suggests that

59 Prostaglandin F(2)alpha (PGF(2)alpha) binding to its receptor on the rat corpus l

60 luteolytic mediator prostaglandin F2-alpha (PGF) significantly increased TNF in the ovaries when com

61 Although PGF transgenic mice did not have a baseline phenotype or

62 Furthermore, although PGF(2alpha) increases intracellular cyclic AMP via Galph

63 t cryptococcal production of both PGE(2) and PGF(2 alpha) can be chemically inhibited by caffeic acid

64 red colonic motility index, lower TxA(2) and PGF(2) and higher PGE(2) levels than controls.

65 on of 9 alpha,11 beta-PGF(2) from PGD(2) and PGF(2)(alpha) from PGH(2) in the presence of NADPH.

66 31 and increased the synthesis of PGE(2) and PGF(2)alpha.

67 f PGE(2) and PGF(2alpha) and that PGE(2) and PGF(2alpha) act as paracrine factors that stimulate mela

68 PGE(2) and PGF(2alpha) alter cell function by binding and activatin

69 ocyte PAR-2 stimulates release of PGE(2) and PGF(2alpha) and that PGE(2) and PGF(2alpha) act as parac

70 The prostaglandins (PG) E(2) and PGF(2alpha) are important cytokines in periodontal physi

71 In this study, we examined the PGE(2) and PGF(2alpha) effects on the immortalized cementoblastic O

72 We conclude that PGE(2) and PGF(2alpha) exert an anabolic effect on OCCM mineralizat

73 endricity observed in response to PGE(2) and PGF(2alpha) is cAMP-independent.

74 PGE(2) and PGF(2alpha) significantly increased mineralization of OC

75 nocytes, as well as by release of PGE(2) and PGF(2alpha) that stimulate melanocyte dendricity through

76 dins involved in inflammation are PGE(2) and PGF(2alpha).

77 rachidonate metabolites (PGD(2), PGE(2), and PGF(2)) by the action of three groups of enzymes.

78 rachidonate metabolites (PGD(2), PGE(2), and PGF(2)) by the action of three groups of enzymes.

79 ers and ethanolamides of PGE(2), PGD(2), and PGF(2alpha) were major products of the endocannabinoid-d

80 ay, prostanoids (PGE(2), PGD(2), TXB(2), and PGF(2alpha)) by gas chromatography-negative ion chemical

81 GH(2) mimetic (U-51605), PGD(2,) PGJ(2), and PGF(2alpha).

82 By using cyclosporin A and PGF(2)alpha treatment, we established that inhibition of

83 g on PGHS-1 pathways involving PGD, PGE, and PGF.

84 t levels of PGE(2), PGD(2), thromboxane, and PGF(2alpha), but not PGI(2).

85 d catalyzes the formation of 9 alpha,11 beta-PGF(2) from PGD(2) and PGF(2)(alpha) from PGH(2) in the

86 dogenic-associated gene (VEGF, VEGFR2, BFGF, PGF, HGF, Ang-1, VWF, PECAM-1 and ENOS) expression analy

87 Bound PGF(2alpha) isomers are derivatized by 1-pyrenyldiazomet

88 e loss of 20alpha-HSD promoter activation by PGF(2)alpha.

89 ong the 414 heart transplants complicated by PGF, 354 (85.5%) recipients died and 60 (14.5%) were ret

90 Thus, induction of EGR-1 expression by PGF(2alpha) was blocked using dominant-negative construc

91 blocked the induction of EGR-1 expression by PGF(2alpha).

92 PGE(2) treatment or, to a lesser extent, by PGF(2alpha), but not by other prostaglandins, such as PG

93 ased uveoscleral outflow of aqueous humor by PGF(2alpha).

94 vation of ERK1/2 mediates nur77 induction by PGF(2alpha).

95 t-negative JunD abolished nur77 induction by PGF(2alpha).

96 that activation of the human FP receptor by PGF(2alpha) could induce the expression of EGR-1 and fou

97 lpha-HSD promoter that confers regulation by PGF(2)alpha in ovarian primary cells.

98 ents contraction of rat uterus stimulated by PGF(2alpha) and induces relaxation of aorta previously c

99 sites, but its binding is not stimulated by PGF(2alpha).

100 FP receptor stimulation by PGF(2alpha) induced the phosphorylation of C-Raf, MEK1/2

101 iadipogenic properties possibly supported by PGF(2alpha) synthase activity.

102 Cloprostenol (PGF(2alpha) agonist) administration to Akr1b7(-/-) mice

103 ure, two model structures of PGFS containing PGF(2)(alpha) and PGH(2) were built.

104 In contrast, PGF(2alpha) levels remained unchanged and were three-fol

105 e Trp53 induces preterm birth through a COX2/PGF synthase/PGF(2alpha) pathway.

106 f cells with bisindolylmaleimide I decreased PGF(2alpha)-stimulated phosphorylation of the FP(A) isof

107 CRP significantly decreased PGF-1alpha release from HAECs under basal (48% decrease,

108 Akr1b7 loss was associated with decreased PGF(2alpha) WAT contents.

109 An important difference between COX-derived PGF(2alpha) and the IsoPs is that the former is an optic

110 ese findings have implications for designing PGF(2alpha) analogs for treating disease states.

111 le resolution in the separation of different PGF(2alpha) isomers and can be used not only for sample

112 PKC inhibitor bisindolylmaleimide I enhanced PGF(2alpha)-stimulated IP accumulation in transfected ce

113 pects to PGF(2alpha) and its enantiomer, ent-PGF(2alpha), are formed in equal amounts esterified in t

114 pared by centrifugation and esterified 8-epi PGF(2alpha) measured at the start and finish of each tre

115 resulted in a significant decrease in 8-epi PGF(2alpha) production, from 38.8 (95% CI 24.9 to 52.7)

116 tion on 8-epi prostaglandin F(2alpha) (8-epi PGF(2alpha)) content and the effect of concurrent oral a

117 in an increase in platelet-esterified 8-epi PGF(2alpha), a free radical and cyclooxygenase-dependent

118 ficant increase in platelet-esterified 8-epi PGF(2alpha), from 32.9 (95% confidence interval [CI] 11.

119 tane, 8-epi-prostaglandin F(2)(alpha) (8-epi-PGF(2)(alpha)), a biomarker of in vivo lipid peroxidatio

120 Plasma levels of 8-epi-PGF(2alpha) (8-IP) were somewhat increased in CBS(-/+) m

121 the levels of the isoprostane product, 8-epi-PGF(2alpha).

122 e, and 2 microg PGF(2alpha)-isopropyl ester (PGF(2alpha)-IE) was applied to the other eye of cynomolg

123 Because extracellular PGF(2alpha) may compete for binding between FP receptors

124 and MSCs expressed placental growth factor (PGF) and its cognate receptor VEGFR1, respectively, in a

125 VEGF family member placental growth factor (PGF) as an aldosterone-regulated vascular MR target gene

126 , VEGFD (FIGF), and placental growth factor (PGF); VEGF receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VE

127 Primary graft failure (PGF) is the most common cause of short-term mortality af

128 sculopathy (CAV), and primary graft failure (PGF).

129 iments to measure pollen-mediated gene flow (PGF) in the absence and presence of pollinators (Bombus

130 a a transporter, which has high affinity for PGF(2alpha) and PGE(2), but not prostacyclin (PGI(2)).

131 the g-HCM cells than in the n-HCM cells (for PGF(2alpha), 60% vs. 151%).

132 at the necessary and sufficient elements for PGF(2alpha) induction of Nur77 promoter activity are loc

133 as the likely protein-processing enzyme for PGF-CTERM.

134 cloprostenol); the corresponding values for PGF(2)(alpha) and cloprostenol were 23 nM (91% relative

135 pathway indicates that a single pathway from PGF(2alpha) receptor to CREB is responsible for inducing

136 In recipients with prompt graft function (PGF), the mean cold storage time was 22+/-9 hr versus 29

137 All four PG-Gs (PGE(2)-G, PGD(2)-G, PGF(2alpha)-G, and 6-keto-PGF(1alpha)-G) and the prostag

138 on were in the following order: CCh > ET-1 > PGF(2alpha).

139 7 nM) > bimatoprost acid (EC(50) = 112 nM) > PGF(2alpha) (EC(50) = 120 nM) >> unoprostone (UF-021; EC

140 In summary, we have identified PGF as what we believe to be a novel downstream target o

141 There was no significant difference in PGF at 90 days or recipient mortality after up to 5 year

142 the expression of both genes was not seen in PGF(2)alpha receptor knockout mice.

143 Secondary outcomes included PGF and other postoperative events, such as renal failur

144 the anti-substituted isoprostanes, including PGF(2)(alpha), were, however, observed in the product mi

145 mulated Pgf gene transcription and increased PGF protein expression and secretion in the mouse vascul

146 nerated cardiac-specific and adult inducible PGF-overexpressing transgenic mice and analyzed Pgf(-/-)

147 otic human vessels, MR antagonists inhibited PGF expression.

148 Urinary F(2)-iPs, PGF(2alpha) isomers derived from arachidonic acid (AA) a

149 -1); P < 0.05) at day 14 and the renal 8-iso PGF(2alpha) excretion (3.53 +/- 0.71 pg. d(-1); P < 0.05

150 Renal excretion of 8-iso PGF(2alpha) was increased in AngII400 group at day 12 (2

151 For example, iPF(2alpha)-III (8-iso PGF(2alpha)) and iPE(2)-III modulate platelet function a

152 h ketorolac (1 and 10 mg/kg) abolished 8-iso-PGF sensitization and reduced the effects of 8-iso-PGE.

153 (PG) E(1) and 8-iso-PGE(2), but not by 8-iso-PGF(1alpha), 8-iso-PGF(2alpha), and 8-iso-PGF(3)alpha.

154 of cells with TP antagonists, whereas 8-iso-PGF(2 alpha) was without effect.

155 rostane using an antibody specific for 8-Iso-PGF(2) (15-F(2t)-IsoP).

156 (P<0.01) and diastolic BP (P<0.01) and 8-iso-PGF(2alpha) decreased (P<0.05), whereas urinary NO(X) in

157 atterns, chromatographic separation of 8-iso-PGF(2alpha) from its isomers is necessary for its quanti

158 was optimized for rapid measurement of 8-iso-PGF(2alpha) in urine, and it is ideally suited for clini

159 menadione and alphaEE showed increased 8-iso-PGF(2alpha) levels compared with untreated controls, whe

160 assay had a linear range of 1-40 pg of 8-iso-PGF(2alpha) on column and can quantify as little as 40 p

161 eated controls, whereas no increase in 8-iso-PGF(2alpha) was detected in kidneys of alphaEE-treated g

162 jor urinary metabolite of 15-F2t-IsoP (8-iso-PGF(2alpha)) is 2,3-dinor-5,6-dihydro-15-F2t-IsoP (15-F2

163 ease in 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) levels compared with untreated controls.

164 urinary 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), a biomarker of lipid peroxidation.

165 insulin, 8-isoprostaglandin F(2alpha) (8-iso-PGF(2alpha)), and glucose measurements.

166 -PGE(2), but not by 8-iso-PGF(1alpha), 8-iso-PGF(2alpha), and 8-iso-PGF(3)alpha.

167 of prostaglandin F(2alpha), including 8-iso-PGF(2alpha), following derivatization with 1-pyrenyldiaz

168 r prostaglandins (e.g. PGE(1), PGE(2), 8-iso-PGF(2alpha), prostacyclin), leukotrienes (e.g. LTB(4), L

169 biomarkers than the commonly measured 8-iso-PGF(2alpha).

170 so-PGF(1alpha), 8-iso-PGF(2alpha), and 8-iso-PGF(3)alpha.

171 ostane E(2) (8-iso-PGE) and F(2alpha) (8-iso-PGF) sensitize nociceptors and capsaicin-sensitive DRG n

172 8-Isoprostane PGF(2alpha) and malonyldialdehyde were measured in group

173 and 6-keto prostaglandin F(1alpha) (6-kepto PGF(1alpha)).

174 ons in urinary excretion of 2,3-dinor 6-keto PGF(1alpha) (PGI-M) and 11-dehydro thromboxane B(2) (Tx-

175 inor TxB2 (Tx-M), and PGI2, 2,3-dinor 6-keto PGF(1alpha) (PGI-M), only PGI-M was depressed by the COX

176 g/ml for control and 10(-6) M NOC/oFQ 6-Keto PGF(1alpha) and TXB(2), respectively).

177 y increased cerebrospinal fluid (CSF) 6-Keto PGF(1alpha) and TXB(2), the stable breakdown products of

178 ex vivo, depressed urinary 2,3 dinor 6-keto PGF(1alpha) by approximately 60% but had no effect on th

179 NOC/oFQ-stimulated release of 6-Keto PGF(1alpha) was blocked while such release of TXB(2) was

180 depressed, whereas urinary 2,3-dinor 6-keto PGF(1alpha), but not 2,3-dinor-TxB(2), was increased in

181 immunoassay of its stable metabolite, 6-keto PGF(1alpha), that was abolished by diclofenac.

182 -1 levels, but not LPS, TNF-alpha, or 6-keto PGF(1alpha), were lower during CVVH (p = 0.042).

183 content of prostaglandin (PG)E(2) and 6-keto-PGF(1alpha) (+250 +/- 85% and +259 +/- 107%, respectivel

184 rothromboxane B2 (Tx-M) and 2'3-donor-6-keto-PGF(1alpha) (PGI-M).

185 significantly increased secretion of 6-keto-PGF(1alpha) and PGE(2).

186 S-398 nor celecoxib lowered PGE(2) or 6-keto-PGF(1alpha) levels in the nonischemic region of precondi

187 e cardiac prostaglandin (PG) E(2) and 6-keto-PGF(1alpha) levels were significantly decreased in heart

188 Levels of 6-keto-PGF(1alpha), a stable metabolite of prostacyclin, were r

189 sgenics exhibited only an increase in 6-keto-PGF(1alpha), not a decrease in PGE(2).

190 GE(2)-G, PGD(2)-G, PGF(2alpha)-G, and 6-keto-PGF(1alpha)-G) and the prostaglandins (PGs) that are for

191 crease in tissue levels of PGE(2) and 6-keto-PGF(1alpha).

192 In this report we show, using mice lacking PGF(2)alpha receptor and pregnant rats, that PGF(2)alpha

193 o commands for the vector graphics languages PGF/TikZ that can be compiled into scalable vector graph

194 n required for potency in the natural ligand PGF(2)(alpha) yet retain binding affinity for the hFP re

195 [9,11-dideoxy-9 alpha,11 alpha-methanoepoxy PGF(2 alpha) (U46619)] in CHO cells transfected with the

196 s topically applied to one eye, and 2 microg PGF(2alpha)-isopropyl ester (PGF(2alpha)-IE) was applied

197 crease in the Fura PE-3 signal to 0.1 microM PGF(2alpha) was abolished, whereas 10 microM PGF(2alpha)

198 au rise in [Ca2+]i in response to 0.1 microM PGF(2alpha) was insensitive to diltiazem, and was abolis

199 The [Ca2+]i response to 0.1 microM PGF(2alpha) was mimicked by the FP receptor agonist flup

200 han that seen for the response to 0.1 microM PGF(2alpha), and were also much less sensitive to U-7312

201 Both responses became maximal at 0.1 microM PGF(2alpha).

202 he rises in [Ca2+]i in response to 10 microM PGF(2alpha) and 0.01 microM U-46619 were partially inhib

203 PGF(2alpha) was abolished, whereas 10 microM PGF(2alpha) and 0.05 microM U-46619 still caused substan

204 fluprostenol, whilst the effect of 10 microM PGF(2alpha) was mimicked by the TP receptor agonist U-46

205 U-46619 and 10-100 microM PGF(2alpha) cause a TP receptor-mediated Ca2+ influx inv

206 ls: PGE2 (3.7+/-0.7 versus 1.1+/-0.2 pg/mL), PGF(1alpha) (16.2+/-2.8 versus 7.2+/-1.2 pg/mL), and bra

207 ng that links a specific pheromone molecule (PGF(2alpha)) to neurogenesis in a vertebrate animal.

208 upport targeting the vascular aldosterone/MR/PGF/Flt1 pathway as a therapeutic strategy for ischemic

209 The addition of 1 muM PGF(2alpha) also increased MMP-2 secretion in a time-dep

210 the expression of EGR-1 and found that 1 muM PGF(2alpha) produced a time-dependent induction of both

211 Neither PGF(2alpha) or PGE(2) elevated cAMP in human melanocytes

212 s showed that 24 hours of exposure to 100 nM PGF(2alpha) significantly increased mRNA for MMP-1 and -

213 cleral tissues were exposed to 100 to 500 nM PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 (the

214 The secretory action of PGF(2alpha) was inhibited by pretreatment with a protein

215 The addition of PGF(2alpha) and latanoprost acid increased ERK1/2 activi

216 Interestingly, addition of PGF(2alpha), which was not known to affect lymphocytes,

217 (2alpha)-G but is observed after addition of PGF(2alpha).

218 donate independent of COX and is composed of PGF(2alpha) and its enantiomer, although the latter comp

219 e results suggest that low concentrations of PGF(2alpha) act via FP receptors to cause IP3-dependent

220 At higher concentrations of PGF(2alpha), a further slower rise in [Ca2+]i was superi

221 e mixture (10:1), fluorescent derivatives of PGF(2alpha) remain bound to cellulose while a significan

222 1- or 5-year mortality or the development of PGF (odds ratio, 1.11; 95% CI, 0.88-1.39; P = .37).

223 .14; P =.18) mortality or the development of PGF (odds ratio, 1.11; 95% CI, 0.88-1.39; P =.37).

224 sted predictive model for the development of PGF was formulated in a similar fashion.

225 ion has been well studied, but the effect of PGF(2alpha) on mucin production remains poorly understoo

226 The 1-pyrenylmethyl esters of PGF(2alpha) can be quantitatively extracted from cellulo

227 quantification of 1-pyrenylmethyl esters of PGF(2alpha) isomers at picogram level are complicated by

228 The purified 1-pyrenylmethyl esters of PGF(2alpha) were quantitatively analyzed by reverse-phas

229 clerosis, aldosterone enhanced expression of PGF and its receptor, FMS-like tyrosine kinase 1 (Flt1).

230 has dual catalytic activities: formation of PGF(2)(alpha) from PGH(2) by the PGH(2) 9,11-endoperoxid

231 Formation of PGF(2)(alpha) from PGH(2) most likely involves a direct

232 idate the effect and underlying mechanism of PGF(2alpha) on MUC5AC production, we investigated the si

233 Low concentrations (0.01-1 microM) of PGF(2alpha) caused a transient followed by a plateau ris

234 roxyprostaglandin dehydrogenase oxidation of PGF(2 alpha)-G was observed.

235 The low prevalence of PGF has limited efforts at identifying risk factors for

236 of follow-up, nor any difference in rates of PGF at 90 days and CAV at 5 years between recipients of

237 own to coordinate the specific regulation of PGF in human trophoblast cell lines.

238 The regulation of PGF(2alpha)-induced MUC5AC expression by CREB was furthe

239 The release of PGF-1alpha, a stable product of PGI2, was also assayed i

240 we now report that following the removal of PGF(2 alpha) the reversal of cell rounding is much slowe

241 Following the removal of PGF(2alpha), however, FP(A)-expressing cells show rapid

242 edure of derivatization includes sorption of PGF(2alpha) isomers from solution in a hexane:ethyl acet

243 , we investigated the signal transduction of PGF(2alpha) associated with this effect using normal hum

244 d CXCL10 expression by MSCs was dependent on PGF expression by BCCs.

245 tors independently have a positive effect on PGF gene expression, when combined, DLX3 acts as an anta

246 simultaneous effect of multiple variables on PGF.

247 cinoma cell line, with HGF, IL-6, PGE(2), or PGF(2)alpha resulted in significantly increased cell gro

248 hout increasing recipient mortality, CAV, or PGF.

249 erved after addition of PGE(2), PGD(2)-G, or PGF(2alpha)-G but is observed after addition of PGF(2alp

250 erefore, controlling tissue levels of HRG or PGF might be a promising strategy in chronic inflammator

251 PGE(2) release were in the following order: PGF(2alpha) > CCh > ET-1; and their effects on inositol

252 and g-HCM cells were in the following order: PGF(2alpha) > ET-1 > CCh; their effects on PGE(2) releas

253 O2, VO2, HCO3, K+, phosphate, lactate, PGE2, PGF(1alpha), and bradykinin) potentially involved in erg

254 receptor agonists fluprostenol and 17-phenyl PGF(2alpha).

255 o 100 to 500 nM PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 (the active form of latanoprost)

256 n), exposure to PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 each increased scleral permeabili

257 h exposure to PGF(2alpha) or 17-phenyltrinor-PGF(2alpha).

258 bition of NUR77 DNA binding in vivo prevents PGF(2)alpha induction of the 20alpha-HSD gene in the cor

259 n matrix adhesion, we demonstrate a profound PGF(2alpha)-induced alteration in cytoskeletal remodelli

260 spectrometry, the vast majority of putative PGF(2alpha) in human urine is derived from the free radi

261 determined, however, that levels of putative PGF(2alpha) in urine cannot be suppressed by nonsteroida

262 of their functional antagonism in regulating PGF promoter activity.

263 method for quantitation of several 15-series PGF isomers (15-PGFs) and AA by high-performance liquid

264 es preterm birth through a COX2/PGF synthase/PGF(2alpha) pathway.

265 shed, using luteinized granulosa cells, that PGF(2alpha) stimulates in vitro nur77 expression in a ti

266 Our research confirmed that PGF depended on pollinator species, distance between pla

267 Our results demonstrated that PGF(2alpha) induces MUC5AC overproduction via a signalin

268 PGF(2)alpha receptor and pregnant rats, that PGF(2)alpha is responsible for the rapid and massive exp

269 Mechanistically, we show that PGF does not have a direct effect on cardiomyocytes but

270 The PGF(2alpha)- and latanoprost-acid-induced ERK1/2 activat

271 ty was less intense in the sections from the PGF(2alpha)-IE-treated eyes compared with the vehicle-tr

272 Pressure reductions of 5 mm Hg in the PGF(2alpha)-IE-treated eyes were confirmed.

273 , a TNF-neutralizing antibody, inhibited the PGF-induced decrease in P4 and delayed luteal regression

274 role in ovarian physiology by mediating the PGF(2alpha) induction of 20alpha-HSD, a steroidogenic en

275 Proteomics suggests that the PGF-CTERM region is removed.

276 era to prostaglandin (PG)F(2alpha) or to the PGF(2alpha) analogue latanoprost acid alters mRNA for ma

277 treatment with PGF and were resistant to the PGF-induced decrease in P4.

278 Therefore, PGF(2alpha) seemed to modulate male brain plasticity tha

279 Moreover, we show that these PGF(2alpha)-induced alterations in adhesion and morpholo

280 osure to PhXA85 and similar with exposure to PGF(2alpha) or 17-phenyltrinor-PGF(2alpha).

281 (-6) cm/sec for 70 kDa dextran), exposure to PGF(2alpha), 17-phenyltrinor PGF(2alpha), or PhXA85 each

282 ts of compounds identical in all respects to PGF(2alpha) and its enantiomer, ent-PGF(2alpha), are for

283 Moreover, IOP-lowering topical PGF(2alpha)-IE treatment decreases the amount of TIGR pr

284 nce between GM and non-GM cottons; (3) total PGF to Shiyuan321 (8.61%) was higher than to Hai7124 (4.

285 ator of WAT development through at least two PGF(2alpha)-dependent mechanisms: inhibition of adipogen

286 d in understanding the mechanisms underlying PGF and in matching recipients with donors in efforts to

287 the nonsupplemented group; P<0.001); urinary PGF(2-alpha) excretion was also highest in the JO group

288 the renal-cell membrane and elevated urinary PGF(2-alpha) excretion, and the precipitous fall in inul

289 Thus, quantification of urinary PGF(2alpha) actually reflects oxidative stress status as

290 The elucidation that urinary PGF(2alpha) in humans is derived from the IsoP pathway h

291 Exposure to waterborne PGF(2alpha) induced a multitude of changes in male goldf

292 was to evaluate risk factors associated with PGF after heart transplantation.

293 s of pretransplant variables associated with PGF included: ischemic time, donor gender, donor age, mu

294 nd donor characteristics are associated with PGF.

295 ute treatment of FP(B)-expressing cells with PGF(2alpha) leads to a subcellular reorganization of bet

296 ansporter (hPGT), stimulation of the FP with PGF(2alpha) (1 nM-1 microM), or the less potent FP agoni

297 were significantly better in recipients with PGF (90% and 74%) versus DGF (79% and 54%) (P<0.002).

298 d for 24 hours with medium supplemented with PGF(2a), latanoprost acid, or vehicle.

299 Treatment with PGF also reduced serum progesterone (P4) concentrations

300 luteal regression 24 h after treatment with PGF and were resistant to the PGF-induced decrease in P4