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 er protective vascular-derived prostacyclin (PGI2).

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

9 ysis in part via the autocrine production of PGI2.

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

11 rt-term vasodilator testing with intravenous PGI2.

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

13 49 to 460+/-99 m (P=0.13, n=14) on long-term PGI2.

14 phospholipase A2, leading to the release of PGI2.

15 taglandin E2, but increasing biosynthesis of PGI2.

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

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

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

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

20 vasodilatory and anti-aggregatory effects of PGI2.

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

22 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

23 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)

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

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

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

27 PGI2 acts on its endothelial receptors to increase cAMP,

28 None of the patients acutely responded to PGI2 administration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 PGI2 and NO effects are mediated by cyclic nucleotides,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 No homeostatic increase in PGI2 biosynthesis was detected.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 Chronic PGI2 improves hemodynamics and quality of life in patien

113 blockers, continuous intravenous infusion of PGI2 improves survival.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 2 or carbaprostacyclin (a stable analogue of PGI2) into LPA3-deficient female mice rescued delayed im

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

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

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

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

137 PGI2 is a potent vasodilator and inhibitor of platelet a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 Prostacyclin (PGI2) modulates platelet activation to regulate haemosta

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

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

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

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

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

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

161 PGI2 or iloprost at the IP receptor inhibited basal ERK

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Most of these compounds inhibit induced PGI2 production.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 2 synthesis, cholesterol enrichment enhanced PGI2 release in response to AlF4-, GTPgammaS, and ATP.

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

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

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

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

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

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

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

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

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

217 more variable immunohistological pattern of PGI2-S expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 2 expression and Ptgs2-derived prostacyclin (PGI2) synthesis at implantation sites are needed for imp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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