ライフサイエンスコーパス: PGI2

1 ate cyclooxygenase to generate prostacyclin (PGI2).

2 as few as three loci (pilA, abcZ, and pip or pgi2).

3 s of the vasodilatory molecule prostacyclin (PGI2).

4 a stable hydrolysis product of prostacyclin (PGI2).

5 ic oxide (iNO) and intravenous prostacyclin (PGI2).

6 hesis of nitric oxide (NO) and prostacyclin (PGI2).

7 increasing the biosynthesis of prostacyclin (PGI2).

8 tion, and arrest under flow by prostacyclin (PGI2).

9 er protective vascular-derived prostacyclin (PGI2).

10 sion of COX-1-derived PGE2 and prostacyclin (PGI2).

11 ysis in part via the autocrine production of PGI2.

12 hannel blockers, were treated with long-term PGI2.

13 rt-term vasodilator testing with intravenous PGI2.

14 gery, if operable) were treated with chronic PGI2.

15 49 to 460+/-99 m (P=0.13, n=14) on long-term PGI2.

16 phospholipase A2, leading to the release of PGI2.

17 taglandin E2, but increasing biosynthesis of PGI2.

18 raction, which it may then use to synthesize PGI2.

19 (TXA2), in addition to increased amounts of PGI2.

20 platelets, reduced the inhibitory effects of PGI2.

21 ynthase 1 (mPGES-1) and in the receptors for PGI2.

22 Ad infection, as was production of PGE2 and PGI2.

23 vasodilatory and anti-aggregatory effects of PGI2.

24 dilation to the prostaglandins (PG) PGE2 and PGI2.

25 tes of both TxA2, 2,3-dinor TxB2 (Tx-M), and PGI2, 2,3-dinor 6-keto PGF(1alpha) (PGI-M), only PGI-M w

26 was used in 46 of 206 patients who received PGI2 (22.2%) and 1682 of 6021 who did not (27.9%).

27 Thirty-four patients who received PGI2 (23.3%) and 63 who did not (42.9%) received ECLS.

28 scular resistance also improved on long-term PGI2: 3.5+/-2.0 to 5.9+/-2.7 L. min-1.m-2 (P<0.01, n=16)

29 ary artery pressure decreased 21% on chronic PGI2: 77+/-20 to 61+/-15 mm Hg (P<0.01, n=16).

30 The role of prostaglandin I2 (PGI2), a cyclooxygenase (COX) pathway metabolite, in mod

31 roduced just prior to labor is prostacyclin (PGI2), a smooth muscle relaxant.

32 Prostacyclin (PGI2), a vascular protector with vasodilation and antith

33 PGI2 acts on its endothelial receptors to increase cAMP,

34 PGI2 acts through its G protein-coupled receptor IP.

35 None of the patients acutely responded to PGI2 administration.

36 ed autocrine production of prostaglandin I2 (PGI2, also called prostacyclin) in Cav-1 KO EC, and this

37 component in the synthesis of prostacyclin (PGI2), an important vasodilator and antithrombotic molec

38 In contrast, the PGI2 analog cicaprost attenuated the anti-tolerance effe

39 red with IL-33 and IL-2 and treated with the PGI2 analog cicaprost.

40 ere cultured with IL-33 and treated with the PGI2 analog cicaprost.

41 he concentration and time of exposure to the PGI2 analog iloprost and was blocked by both RO3244794 a

42 In addition, exogenous administration of a PGI2 analog inhibited Alternaria extract-induced lung IL

43 Finally, a PGI2 analog inhibited IL-5 and IL-13 expression by human

44 Both PGE2 and iloprost, a stable PGI2 analog, evoke human umbilical vein endothelial cell

45 Our results show that cicaprost, a stable PGI2 analog, significantly reduced basal, maximal, and s

46 PGI2 analogs promoted the differentiation of naive T cel

47 osure of baroreceptor neurones to the stable PGI2 analogue carbacyclin significantly inhibited the st

48 We also showed that the PGI2 analogue cicaprost inhibited CD4 T cell proliferati

49 red with control hMSCs or iloprost (a stable PGI2 analogue).

50 vity in response to the stable prostacyclin (PGI2) analogue carbacyclin (cPGI) in culture.

51 ubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.

52 d incubation with the COX-2 product PGE2 and PGI2 analogues or the COX substrate arachidonic acid, su

53 Prostacyclin (PGI2) analogues, which relax pulmonary vessels mainly th

54 ly tipping a "balance" between COX-2-derived PGI2 and COX-1-derived platelet thromboxane is misplaced

55 Primary mouse muscle cells both secrete PGI2 and express the PGI2 receptor, IP, at various stage

56 dephosphorylation of SPL tyrosine residues, PGI2 and forskolin cause phosphorylation of SPL Ser94 wi

57 ization and airway inflammation suggest that PGI2 and its analogue iloprost, both Food and Drug Admin

58 To determine the role of the eicosanoid PGI2 and its receptor IP during allergic airway sensitiz

59 PGI2 and NO effects are mediated by cyclic nucleotides,

60 ed at 120 hours, only a marginal increase in PGI2 and PGE2 levels was detected.

61 rotein, and cardioprotective prostaglandins (PGI2 and PGE2).

62 tical COX2-derived prostanoids, particularly PGI2 and PGE2, play critical roles in maintaining blood

63 renal COX-1 and PGIS protein expression and PGI2 and prostaglandin E2 (PGE2) levels in the kidney an

64 The inhibitory effects of PGI2 and the IP signaling pathway on CD4 T cell activati

65 d 6-keto PGF1alpha (the stable metabolite of PGI2) and inhibited ex vivo human platelet aggregation t

66 Endothelial cells release prostacyclin (PGI2) and nitric oxide (NO) to inhibit platelet function

67 y addition of both carbacyclin (an analog of PGI2) and PGE2, whereas the addition of each alone had l

68 uppressing the biosynthesis of prostacyclin (PGI2) and prostaglandin E2.

69 , the stable metabolite of prostaglandin I2 (PGI2) and thromboxane B2 (TXB2), the stable metabolite o

70 nt Ang II via release of vasodilators NO and PGI2, and the vasoconstriction effects due to Ang II are

71 An imbalance in vasodilating (prostacyclin [PGI2]) and vasoconstricting (thromboxane A2 [TxA2]) eico

72 early stage of sepsis, mediators other than PGI2 appear to play a major role in producing the hyperd

73 ines of evidence suggest that the effects of PGI2 are mediated by its activation of the nuclear hormo

74 We have identified PGI2 as a novel regulator of myogenesis in vitro.

75 eting the prostanoids, specifically PGE2 and PGI2, as well as the leukotrienes is now being considere

76 When PGI2 became available for long-term administration, all

77 The loss of high-affinity PGI2 binding led to the failure of PGI2 to inhibit the p

78 recognition and inhibition of high-affinity PGI2 binding to platelets was due to an anti-prostacycli

79 reflects a loss in venular nitric oxide and PGI2 bioavailability, associated with the chronic elevat

80 Specifically upregulating PGI2 biosynthesis is an ideal model for the prevention a

81 Specific upregulation of PGI2 biosynthesis through expression of the engineered s

82 No homeostatic increase in PGI2 biosynthesis was detected.

83 d in vivo thromboxane (TX) and prostacyclin (PGI2) biosynthesis and their determinants, as well as as

84 Suppression of prostacyclin (PGI2) biosynthesis may explain the increased incidence o

85 al anti-inflammatory drugs (NSAIDs), inhibit PGI2 but not TxA2.

86 Increased PGI2 by Adv-COPI protects the kidney against I/R-induced

87 ts cardiac hypertrophy, whereas formation of PGI2 by the same isozyme ameliorates the phenotype.

88 lease of nitric oxide (NO) and prostacyclin (PGI2) by elevated glucose and insulin were investigated

89 production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-2).

90 ession of these prostaglandins, particularly PGI2, by cyclooxygenase-2 inhibition or deletion of its

91 -1 receptor, showed increased sensitivity to PGI2/cAMP signaling and diminished PDE3A activity, which

92 This study demonstrates that PGI2 can reverse key platelet functions after their init

93 alytic step 1), PGH2 (catalytic step 2), and PGI2 (catalytic step 3).

94 nd that treatment of adherent platelets with PGI2 caused inhibitory phosphorylation of RhoA, reduced

95 Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic s

96 It was hypothesised that PGI2 could reverse platelet spreading by actin cytoskele

97 despite the direct vasodilator properties of PGI2, deletion of the I prostanoid receptor (Ipr) suppre

98 was modulated in an NO-dependent manner, and PGI2 derived from COX-2 might contribute to the antiprol

99 tective mechanism of increased prostacyclin (PGI2) derived from adenoviral cyclo-oxygenase (COX)-1/pr

100 aglandin E2 (PGE2) PGI2 > PGF2a > TxA2, only PGI2 enhanced RMIC viability following hypertonic stress

101 lly, whereas mice incapable of responding to PGI2 exhibited a significantly attenuated arthritis cour

102 ata suggest a novel pathway for ET-1-induced PGI2 formation in the rat aorta involving activation of

103 ipases (PLs) A2, C, and/or D in ET-1-induced PGI2 formation in the rat aorta, measured as immunoreact

104 atalytic functions could directly synthesize PGI2 from AA with a Km of approximately 3.2 microM.

105 -dependent increase in the release of NO and PGI2 from isolated bovine retinal vessels, indicating th

106 lene blue (MelB), attenuated the NO-mediated PGI2 from the EC by at least 70%.

107 also stimulates production of prostacyclin (PGI2) from arachidonic acid.

108 nd 6-keto-PG-F1alpha (a stable metabolite of PGI2) from isolated bovine retinal vessels.

109 PGI2 generation by the vessel wall is an agonist for cyc

110 who received ECLS were included in the early PGI2 group if PGI2 was started prior to ECLS.

111 ugh RMICs synthesize prostaglandin E2 (PGE2) PGI2 > PGF2a > TxA2, only PGI2 enhanced RMIC viability f

112 G, MMF, anti-CD40L mAb, CVF, pIL3, pSCF, and PGI2 had no effect on purified baboon platelet aggregati

113 long-term therapy; after 1987, prostacyclin (PGI2) has been available for long-term intravenous use.

114 Although long-term prostacyclin (PGI2) has been shown to improve hemodynamics, quality of

115 We conclude that PGE2 and PGI2 have a synergistic role in restoration of intestina

116 the other hand, prostaglandin E2 (PGE2) and PGI2 have also been implicated as determinants of renin

117 hesis of nitric oxide (NO) and prostacyclin (PGI2) have been investigated in human umbilical vein end

118 )--or with potential adjuncts, prostacyclin (PGI2), heparin, methylprednisolone, and eptifibatide (a

119 involves long noncoding RNA H19 in promoting PGI2-hMSC-associated survival and proliferation of host

120 Transplanted PGI2-hMSCs do not incorporate long term into host tissue

121 We show that PGI2-hMSCs facilitate perfusion recovery and enhance run

122 gether, our data reveal the novel ability of PGI2-hMSCs to stimulate host regenerative processes and

123 s introduced to stably produce prostacyclin (PGI2-hMSCs).

124 nts showed that plasma TSP-1 did not correct PGI2 hypersensitivity in TSP-1-/- platelets.

125 Chronic PGI2 improves hemodynamics and quality of life in patien

126 blockers, continuous intravenous infusion of PGI2 improves survival.

127 uous intravenous epoprostenol (prostacyclin, PGI2) improves haemodynamics and exercise tolerance, and

128 ivity of vW factor, increased with long-term PGI2 in adults from an abnormally low level (0.6+/-0.2)

129 cetin cofactor also decreased with long-term PGI2 in both groups (P<.02).

130 sible role for combined therapy with iNO and PGI2 in infants with severe PPHN.

131 data demonstrate a hitherto unknown role for PGI2 in regulating the number and properties of NK cells

132 the studies reported herein, cells generated PGI2 in response to AlF4-, GTPgammaS, and ATP in a dose-

133 uated arthritis course, confirming a role of PGI2 in this arthritis model.

134 lease of nitric oxide (NO) and prostacyclin (PGI2) in porcine aortic endothelial cells cultured and s

135 tions of nitric oxide (NO) and prostacyclin (PGI2) in the in vivo antiplatelet effects of clinically

136 hrs after CLP, and plasma concentrations of PGI2, in the form of its stable product 6-keto-PGF1alpha

137 alled prostacyclin) in Cav-1 KO EC, and this PGI2 increase appeared to stimulate cAMP/PKA pathways, c

138 In vivo, PGI2 increased retinal blood flow (RBF) in control and d

139 Previous studies indicate that prostacyclin (PGI2) increases the activity of baroreceptor afferent fi

140 This mechanism may contribute to the PGI2-induced increase in baroreceptor activity demonstra

141 f this study was to test the hypothesis that PGI2 inhibits Ca(2+)-activated K+ current (IK(Ca))in iso

142 We demonstrate that PGI2 inhibits IL-5 and IL-13 protein expression by IL-33

143 We conclude that PGI2 inhibits proliferation of aortic smooth muscle cell

144 The prostanoid prostacyclin (PGI2) inhibits aortic smooth muscle cell proliferation b

145 2 or carbaprostacyclin (a stable analogue of PGI2) into LPA3-deficient female mice rescued delayed im

146 effects are absent in Th2 cells lacking the PGI2 IP receptor (IP knockout [KO]).

147 mice lacking a functional IP receptor (i.e., PGI2 IP receptor-deficient [IP(-/-)]) were compared with

148 on abrogated immune tolerance by suppressing PGI2 IP signaling, suggesting that PGI2 signaling promot

149 PGI2 is a member of the family of prostaglandins (PG), a

150 and pharmacological approaches, we show that PGI2 is a negative regulator of myoblast migration that

151 PGI2 is a potent vasodilator and inhibitor of platelet a

152 deletion in atherosclerosis, augmentation of PGI2 is the dominant contributor to its favorable thromb

153 Prostacyclin (PGI2) is a key mediator of pulmonary vasodilation in the

154 Prostaglandin I2 (PGI2) is a lipid mediator known to inhibit T helper 2 (T

155 Prostacyclin (PGI2) is a therapeutic option to treat congenital diaphr

156 Prostacyclin (PGI2) is a vasodilator that inhibits platelet function.

157 trate herein that COX2-derived prostacyclin (PGI2) is the primary PG that is essential for implantati

158 Results also reveal that PGE2, but not PGI2, is the major PG at implantation sites where Ptgs2

159 Prostacyclin (prostaglandin I2 [PGI2]) is a key mediator of pulmonary vascular function

160 lted in the loss of high-affinity binding of PGI2 (Kd1 = 9.1 +/- 2.0 nM; n1 = 170 +/- 32 sites per ce

161 for oral activity, "shunt" effect to elevate PGI2 level, and absence of agonist activity.

162 Thus, PGI2 may act as a "brake" on migrating cells to facilita

163 These results suggest that PGI2 may be a potential therapy to reduce the ILC2 respo

164 th primary pulmonary hypertension, long-term PGI2 may have an important role in the treatment of pati

165 indings establish a mechanistic link between PGI2-mediated immunoregulation and metabolic reprogrammi

166 critical role in optimizing the capacity for PGI2-mediated pulmonary vasodilation at birth, and it ma

167 We therefore propose that PGI2-mediated upregulation of contractile proteins and c

168 Herein, we examine if COX-2-derived PGI2 might condition the response of the vasculature to

169 We report here that the PGI2 mimetic, cicaprost, inhibits the induction of cycli

170 Thus, PGI2 modulates platelet-vascular interactions in vivo an

171 Prostacyclin (PGI2) modulates platelet activation to regulate haemosta

172 d distal tubules and significantly increased PGI2, not PGE2, production in the renal venous plasma an

173 suggest that the known excitatory effect of PGI2 on baroreceptor and vagal afferent fibres is mediat

174 We evaluated the protective effect of PGI2 on hypoxia/reoxygenation-induced tubular cells inju

175 The effects of PGI2 on stress fibres were mimicked by the adenylyl cycl

176 ce to the inhibitory effect of prostacyclin (PGI2) on the platelet stimulation of thrombin generation

177 Suppression of COX-2-derived PGI2 or deletion of IP profoundly influences the archite

178 PGI2 or iloprost at the IP receptor inhibited basal ERK

179 ric oxide (NO), adenosine, or prostaglandins PGI2 or PGF2, all of which are putative KATP channel ope

180 activation by exposure to prostaglandin I2 (PGI2) or forskolin, both of which increase platelet cycl

181 ostol but not with 10(-6) M PGF2alpha, PGD2, PGI2, or butaprost, suggesting a principal dependence on

182 roduction of the glyceryl esters of PGE2 and PGI2 over 60 min.

183 Our data demonstrates that post-flow of PGI2 over activated and spread platelets on fibrinogen,

184 ted with arachidonic acid produced 100% more PGI2 (P<0.01), 400% more prostaglandin E2 (PGE2) (P<0.01

185 The cortical COX2-derived PGI2 participates in the pathogenesis of renal vascular

186 with an early increase in the production of PGI2, PGE2, PGE1 (known to cause vasodilation), and cAMP

187 With long-term PGI2, platelet aggregation normalized in 83% of the adul

188 A new study suggests that PGI2 plays a critical role in stimulating renin release

189 wn whether prostacyclin or prostaglandin I2 (PGI2) plays a significant role in modulating the hyperdy

190 AMs also produce increased prostacyclin (PGI2) post-BMT.

191 We tended to augment PGI2 production by intrarenal arterial Adv-COPI administ

192 Because inhibition of PGI2 production did not prevent the occurrence of the hy

193 of L-arginine transport and increased NO and PGI2 production in cells exposed to 5 mM glucose.

194 n OZR than LZR and significantly higher than PGI2 production in either following arachidonic acid cha

195 This mechanism may modulate pulmonary PGI2 production in the perinatal period, and it may also

196 ed by two observations: (1) G-protein-linked PGI2 production is inhibited by calphostin, and (2) chol

197 ng PGI2 signaling by drugs that either block PGI2 production or restrain IP signaling may augment STA

198 conditioned media dramatically increased REC PGI2 production, a response inhibited by blocking PSF wi

199 l/L for 48 hours) caused a 93% fall in basal PGI2 production, and bradykinin- and A23187-stimulated P

200 Our results show that reduced PGI2 production, but not increased TxA2 production, occu

201 arteries, COX-1 gene transduction increases PGI2 production, induces durable vasodilation, and reduc

202 Thus, NO preferentially stimulates PGI2 production, suggesting that production of NO by VSM

203 gs shown to release AA from cells and affect PGI2 production-e.g., thiazolidinediones and statins are

204 Most of these compounds inhibit induced PGI2 production.

205 umulation but had no effect on the depressed PGI2 production.

206 (index of NO synthesis) and 75% decrease in PGI2 production.

207 2 (PGE2) dominance to enhanced prostacyclin (PGI2) production via activation of C5a receptor 2 (C5aR2

208 induce expression of COX-2 and prostacyclin (PGI2) production, but not expression of COX-1, in human

209 e metabolic pathway leading to prostacyclin (PGI2) production.

210 The relative importance of PGE2 and PGI2 (prostacyclin) was determined using mice deficient

211 o PGF1alpha (the stable metabolic product of PGI2; prostacyclin) in a gene dose-dependent manner in H

212 Disruption of this C5aR2-PGI2-R axis was a hallmark of pathologically persistent

213 n mice that are genetically deficient in the PGI2 receptor (IP) but are depressed in mice genetically

214 Deletion of the PGI2 receptor (IP) or suppression of PGI2 with the selec

215 rgic airway inflammation, we identified that PGI2 receptor (IP) signaling was critical for indomethac

216 wever, here we have shown that activation of PGI2 receptor (IP) upregulated the expression of several

217 tors induced autocrine signaling through the PGI2 receptor and expression of the interleukin-1 (IL-1)

218 that was dependent on signaling through the PGI2 receptor IP.

219 Deletion of the PGI2 receptor removed the atheroprotective effect of est

220 ng of [3H]PGE1 to the high-affinity platelet PGI2 receptor, demonstrates that the specific recognitio

221 scle cells both secrete PGI2 and express the PGI2 receptor, IP, at various stages of myogenesis.

222 rted bone marrow ILC2s of wild-type (WT) and PGI2 receptor-deficient (IP(-/-)) mice were cultured wit

223 the binding of [3H]PGE1 to the high-affinity PGI2 receptors of normal platelets.

224 is study was to examine the effect of CRP on PGI2 release from HAECs and human coronary artery endoth

225 Thus, CRP decreases PGI2 release from HAECs by inactivating PGIS via nitrati

226 The enhancement of PGI2 release in cholesterol-enriched cells was augmented

227 2 synthesis, cholesterol enrichment enhanced PGI2 release in response to AlF4-, GTPgammaS, and ATP.

228 In contrast, PGI2 release was inhibited in diabetic cells exposed to

229 ells underwent little or no cytotoxicity and PGI2 release when exposed to MAC.

230 -driven cyclooxygenase activation (and hence PGI2), release contributes to the marked anti-platelet e

231 with long-term PGI2 suggests that long-term PGI2 remodels the pulmonary vascular bed with subsequent

232 th evidence that inhibition of COX-2-derived PGI2 removes a protective constraint on thrombogenesis,

233 hat PSF expressed by ocular cells can induce PGI2, retinal vascular dilation, and increased retinal b

234 nisms underpinning this effect revealed that PGI2 reversed stress fibre formation in adherent platele

235 rent sizes of the pulmonary arteries express PGI2-S differently and that the loss of expression of PG

236 n = 2) lungs exhibited a marked reduction in PGI2-S expression, involving all size ranges of pulmonar

237 more variable immunohistological pattern of PGI2-S expression.

238 h concentric lesions showed complete lack of PGI2-S expression.

239 and in situ hybridization was used to assess PGI2-S mRNA expression.

240 stern blot analysis were used to assess lung PGI2-S protein expression, and in situ hybridization was

241 fferently and that the loss of expression of PGI2-S represents one of the phenotypic alterations pres

242 In the normal pulmonary circulation (n = 7), PGI2-S was expressed in 48% of small, 67% of medium, and

243 ession of the critical enzyme PGI2 synthase (PGI2-S) in the lung may represent an important manifesta

244 In addition, inhibiting PGI2 signaling by drugs that either block PGI2 productio

245 These findings reveal an inhibitory role of PGI2 signaling in trained ILC2 responses, emphasizing it

246 mass and membrane potential, suggesting that PGI2 signaling inhibits Th2 cell metabolism by reducing

247 lls, but not in IP KO cells, indicating that PGI2 signaling is essential for these metabolic changes.

248 ppressing PGI2 IP signaling, suggesting that PGI2 signaling promotes immune tolerance and that clinic

249 with severe asthma exacerbations, endogenous PGI2 signaling significantly inhibited lung IL-5 and IL-

250 ted that 6-keto-PGF1alpha (EC50 = 80 nM) and PGI2 stable analogues (EC50 = 280 nM) activate the same

251 ent in hemodynamic parameters with long-term PGI2 suggests that long-term PGI2 remodels the pulmonary

252 ecrease in expression of the critical enzyme PGI2 synthase (PGI2-S) in the lung may represent an impo

253 CRP had no effect on PGI2 synthase (PGIS) mass.

254 cyclooxygenase (COX, the first enzyme) with PGI2 synthase (PGIS, the second enzyme) using arachidoni

255 Inhibition of PGI2 synthase activity did not prevent the occurrence of

256 In additional studies, a PGI2 synthase inhibitor, tranylcypromine, was administer

257 The NO and PGI2 synthase inhibitors, 1-NOARG and flurbiprofen, resp

258 eme proteins such as cytochrome P450 2B1 and PGI2 synthase, through the nitration of tyrosine residue

259 mic (U46619) to the engineered prostacyclin (PGI2) synthase (PGIS) in solution.

260 Hypertonic stress increased PGI2 synthesis 330% above base line and also activated a

261 After the inhibition of endogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively

262 Similarly, PGI2 synthesis from arachidonic acid fell 86% with DEX;

263 all after birth and glucocorticoids decrease PGI2 synthesis in certain nonpulmonary cell types.

264 n cause upregulation of COX-1 expression and PGI2 synthesis in fetal PAEC via activation of PAEC ER.

265 corticoids downregulate COX-1 expression and PGI2 synthesis in fetal PAECs through the activation of

266 during late gestation and estrogen enhances PGI2 synthesis in nonpulmonary vascular cells.

267 The process of enhanced PGI2 synthesis is stimulated, in part, by G-protein-coup

268 study was to determine whether inhibition of PGI2 synthesis prevents the occurrence of the hyperdynam

269 otein expression and a threefold increase in PGI2 synthesis stimulated by bradykinin, the calcium ion

270 PGI2 synthesis, since ATP- and PDGF-induced PGI2 synthesis was inhibited by pertussis toxin.

271 xpression and on arachidonic acid-stimulated PGI2 synthesis, and ER expression was evident in the PAE

272 t reduced arachidonic acid- and PDGF-induced PGI2 synthesis, cholesterol enrichment enhanced PGI2 rel

273 onors increased COX-2 protein expression and PGI2 synthesis, had no effect on TXA2 production, and de

274 i subunits mediate G-protein agonist-induced PGI2 synthesis, since ATP- and PDGF-induced PGI2 synthes

275 een hypothesized to alter G-protein-mediated PGI2 synthesis.

276 2 expression and Ptgs2-derived prostacyclin (PGI2) synthesis at implantation sites are needed for imp

277 Transgene expression and prostaglandin I2 (PGI2) synthesis by the injured arteries were determined.

278 s for TxA2 (the TP), PGF2alpha (the FP), and PGI2 (the IP) were upregulated and urinary 8,12-iso-iPF2

279 duration among patients with CDH who started PGI2 therapy during the first week of life.

280 Early PGI2 therapy was defined as initiation of PGI2 within th

281 ere measured at baseline and after 1 year of PGI2 therapy.

282 s (18 adults, 24 children) after one year of PGI2 therapy.

283 s and 38 children) with PPH before long-term PGI2 therapy.

284 618 [42%] female), 206 (3.3%) received early PGI2 therapy.

285 -affinity PGI2 binding led to the failure of PGI2 to inhibit the platelet-stimulated thrombin generat

286 c AMP level, mediated through the binding of PGI2 to low-affinity receptors in platelets, was unaffec

287 tanoids synthesized via COX-1, in particular PGI2, to inflammatory arthritis.

288 Survival was also better in 24 PGI2-treated nonresponders compared with 22 nonresponder

289 c-fos induction and pericyte growth, whereas PGI2 was ineffective.

290 CLS were included in the early PGI2 group if PGI2 was started prior to ECLS.

291 kinin, but agonist-induced release of NO and PGI2 was still detectable.

292 ntracellular cGMP levels, whereas release of PGI2 was unaffected.

293 ders compared with 22 nonresponders for whom PGI2 was unavailable (P=0.0005) as well as in all childr

294 e release of PGF-1alpha, a stable product of PGI2, was also assayed in the absence and presence of a

295 address the cardioprotective contribution of PGI2, we generated mice lacking the I prostanoid recepto

296 ction, and bradykinin- and A23187-stimulated PGI2 were diminished 96% and 94%, respectively.

297 and 6-keto-PGF1alpha (a stable metabolite of PGI2) were detected in arthritic joint tissues, correlat

298 levels of prostaglandins E2 and I2 (PGE2 and PGI2), which are critical for implantation.

299 of the PGI2 receptor (IP) or suppression of PGI2 with the selective COX-2 inhibitor, nimesulide, bot

300 ly PGI2 therapy was defined as initiation of PGI2 within the first week of life.