ライフサイエンスコーパス: prostacyclin

1 Ser-(Lys)(4) (Pam(3)CSK(4)), is resistant to prostacyclin.

2 cardioprotective prostagladins, particularly prostacyclin.

3 ells, a prominent source of atheroprotective prostacyclin.

4 n of prostaglandin H(2), an endoperoxide, to prostacyclin.

5 al despite current treatments including i.v. prostacyclin.

6 tion of PGIS in the isomerization of PGH2 to prostacyclin.

7 io-, vasculo-, and cytoprotective effects of prostacyclin.

8 omboprotection by elevating nitric oxide and prostacyclin.

9 PPARbeta is a putative receptor for prostacyclin.

10 ween platelet thromboxane A2 and endothelial prostacyclin.

11 ents with severe PH treated chronically with prostacyclin.

12 ssed Fzd9 expression, which was abrogated by prostacyclin.

13 ha can be directly correlated with levels of prostacyclin.

14 vation, a process antagonized by endothelial prostacyclin.

15 ression of the renal receptor Mas and plasma prostacyclin.

16 MP, which underpin the bioactivity of NO and prostacyclin.

17 ucing increased plasma nitric oxide (NO) and prostacyclin.

18 We hypothesized that prostacyclin (a COX-derived product) may directly mediat

19 hidonic acid is predominantly converted into prostacyclin, a potent vasodilator and inhibitor of plat

20 nd 2 contribute to production of endothelial prostacyclin, a vasodilator that inhibits platelet activ

21 In older males, CVC during prostacyclin administration was not influenced by l-NNA

22 were related to the disease and/or expected prostacyclin adverse events.

23 re, we make a weak recommendation for either prostacyclin agonist or endothelin receptor antagonist t

24 received approval, including a subcutaneous prostacyclin, an inhaled prostacyclin, and oral medicati

25 e tested the hypothesis that treprostinil, a prostacyclin analog approved for the treatment of pulmon

26 Activating PKA by injection of the prostacyclin analog iloprost reduced PAK activation and

27 The prostacyclin analog treprostinil is also efficacious by

28 lets after treatment with iloprost, a stable prostacyclin analog, for 0, 10, 30, and 60 seconds to ch

29 ition of inhaled treprostinil, a long-acting prostacyclin analog, might be a safe and effective treat

30 Additionally, we identified Iloprost, a prostacyclin analog, which initiates downstream signalin

31 M, resveratrol: IC50 approximately 5 muM) or prostacyclin analogs (IC50 approximately 5 muM) prevente

32 Prostacyclin analogs are widely used in the management o

33 efficacy and long-term tolerability of some prostacyclin analogs may be compromised by concomitant a

34 ecause one of the treatment options is using prostacyclin analogs, we hypothesized that prostacyclin

35 o assess the safety and efficacy of the oral prostacyclin analogue beraprost sodium during a 12-month

36 Chemoprevention in former smokers using the prostacyclin analogue iloprost reduces endobronchial dys

37 The addition of a long-acting prostacyclin analogue via the inhaled route might be a s

38 Treprostinil, a stable prostacyclin analogue with a half-life of 3 h, has been

39 Treprostinil (TRE), a prostacyclin analogue with extended half-life and chemic

40 Beraprost is the first orally active prostacyclin analogue.

41 Because prostacyclin analogues are effective treatments for clin

42 Prostacyclin analogues enhance Id1 expression in vitro a

43 ension may impair the therapeutic effects of prostacyclin analogues such as iloprost and carbaprostac

44 tors, soluble guanylate cyclase stimulators, prostacyclin analogues, and prostacyclin receptor agonis

45 of drugs approved for the treatment of PAH: prostacyclin analogues, endothelin receptor antagonists,

46 promising new therapeutic options, including prostacyclin analogues, endothelin-1-receptor antagonist

47 tic peptide bioactivity and is additive with prostacyclin analogues, PDE5 inhibitor, and NO.

48 rase inhibitors, endothelin antagonists, and prostacyclin analogues.

49 denosine monophosphate levels in response to prostacyclin and a substantial increase in basal Akt act

50 ne feedback pathway involving the release of prostacyclin and activation of prostacyclin receptors.

51 tudied of these are the inhaled prostanoids (prostacyclin and iloprost), and there is growing interes

52 uction of targeted PAH therapy consisting of prostacyclin and its analogs, endothelin antagonists, ph

53 This is mediated by increased levels of prostacyclin and nitric oxide as well as decreased level

54 to the mechanism whereby endothelial-derived prostacyclin and nitric oxide limit platelet activation

55 In contrast, treatment of platelets with prostacyclin and nitric oxide, which trigger inhibitory

56 urprisingly, apyrase was more effective than prostacyclin and NO at limiting secondary P2X1 activatio

57 d Mas overexpression produce elevated plasma prostacyclin and NO leading to acquired platelet functio

58 or Sirt1 inhibitor splitomicin lowers plasma prostacyclin and normalizes arterial thrombosis times.

59 asis is influenced in part by the balance of prostacyclin and thromboxane A2, many other substances a

60 Vascular drugs, such as nitroglycerine, prostacyclin, and bosentan, offer opportunities for impr

61 ons of ADP, collagen, thrombin, thromboxane, prostacyclin, and nitric oxide.

62 ding a subcutaneous prostacyclin, an inhaled prostacyclin, and oral medications in 2 separate classes

63 Bradykinin (BK) liberates nitric oxide, prostacyclin, and tissue plasminogen activator from endo

64 ry bypass, inhaled nitric oxide, and inhaled prostacyclin are all important tools for the anesthesiol

65 ) are mediated by non-NO vasodilators (i.e., prostacyclin) as evidenced by induction of COX-2.

66 olecules such as IL-6, cyclooxygenase-2, and prostacyclin, as determined by ELISA and Western blot.

67 ced up-regulation of the enzymes involved in prostacyclin biosynthesis in nontransformed rat intestin

68 The increased prostacyclin biosynthesis in smokers is derived largely

69 We hypothesized that the excess in prostacyclin biosynthesis in smokers was derived from th

70 ts have relied on immunoassays to detect the prostacyclin breakdown product, 6-keto-PGF1alpha and ant

71 en platelet thromboxane A(2) and endothelial prostacyclin, but this controversial issue will only be

72 roduction of prostaglandin (PG)F(2alpha) and prostacyclin by 2- and 13-fold, respectively.

73 BSDL also increased the production of prostacyclin by human endothelial cells.

74 ed pulmonary production of prostaglandin I2 (prostacyclin) by lung-specific overexpression of prostac

75 nhaled vasodilators such as nitric oxide and prostacyclin can be life-saving when perioperative right

76 When smoke is removed miR-31 is reduced, prostacyclin can increase Fzd9 expression, and progressi

77 we continue to investigate the mechanisms of prostacyclin chemoprevention and identify biomarkers for

78 mbination, lowered CVC in young males at all prostacyclin concentrations (P </= 0.05), with the excep

79 of endothelium-derived nitric oxide (NO) and prostacyclin contributes to PH pathogenesis, and current

80 t not absent, formation of prostaglandin I2 (prostacyclin; control 956 +/- 422 pg/ml vs. patient 196

81 exerts anti-inflammatory properties by both prostacyclin-dependent and prostacyclin-independent acti

82 in vitro and in vivo antifibrotic effects of prostacyclin derivatives and show that these effects are

83 We observed that, although prostacyclin does not mediate sweating in young and olde

84 We conclude that, although prostacyclin does not mediate sweating, it modulates cut

85 ension are reviewed, including nitric oxide, prostacyclin, endothelin-1, reactive oxygen species, and

86 increased the activity of isolated PGHS and prostacyclin formation by aortic endothelial cells.

87 cyclin synthase fusion protein that produces prostacyclin from arachidonic acid.

88 ial cells may have use as a means to enhance prostacyclin function and reduce endothelial barrier per

89 butyric acid) were restored after ELPC-based prostacyclin gene therapy.

90 Furthermore, we also demonstrate that prostacyclin generation can arise via transcellular coll

91 Prostacyclin has many effects in the vasculature; one of

92 es of prostacyclin PGI(2), namely benzindene prostacyclins, has been achieved via the stereoselective

93 inone, inhaled nitric oxide, and intravenous prostacyclin have the greatest support in the literature

94 thin the third cytoplasmic loop of the human prostacyclin (hIP) receptor were detected: 1) R212C (CGC

95 ed by ligand-induced activation of the human prostacyclin (hIP) receptor, a seven-transmembrane-domai

96 By contrast, direct-acting nitroglycerine or prostacyclin improved cell engraftment and also kinetics

97 synovitis via production of proinflammatory prostacyclin in an autoimmune arthritis model.

98 All four sites were coadministered with prostacyclin in an incremental manner (0.04, 0.4, 4, 40

99 rget that may mediate some of the effects of prostacyclin in blood.

100 epression of the major urinary metabolite of prostacyclin in COX-2 null mice was only partially rescu

101 r hypothesized that if the overproduction of prostacyclin in smokers were restraining platelet activa

102 plore which isoform drives the production of prostacyclin in vitro and in vivo.

103 clearly needed to support the use of inhaled prostacyclins in severe respiratory failure, encouraging

104 alpha (the stable metabolic product of PGI2; prostacyclin) in a gene dose-dependent manner in Het and

105 ction of prostaglandin I2 (PGI2, also called prostacyclin) in Cav-1 KO EC, and this PGI2 increase app

106 roperties by both prostacyclin-dependent and prostacyclin-independent actions; heparin interferes wit

107 on and sweating, and this may be mediated by prostacyclin-induced activation of nitric oxide synthase

108 hough NOS and KCa channels contribute to the prostacyclin-induced cutaneous vasodilatation in young m

109 although NOS and KCa channels contribute to prostacyclin-induced cutaneous vasodilatation in young m

110 Prostacyclin-induced increases in CVC were similar betwe

111 This prostacyclin-induced response may be diminished in older

112 are under oxidative stress and that chronic prostacyclin infusion has an antiinflammatory effect on

113 Prostacyclin is an antithrombotic hormone produced by th

114 Prostacyclin is an important antithrombotic hormone that

115 Intravenous prostacyclin is approved for treating pulmonary arterial

116 Increased prostacyclin is associated with elevated aortic vasculop

117 biosynthesis of both thromboxane (Tx) A2 and prostacyclin is increased.

118 Prostacyclin is the major end product of cyclooxygenase-

119 PGI(2) (prostacyclin) is a lipid mediator with vasodilatory and

120 Prostaglandin (PG) I(2) (PGI(2), prostacyclin) is a PGH(2) metabolite with anti-inflammat

121 tabolism and (like another important target, prostacyclin) is downstream of cyclooxygenase-2.

122 produced by the uterus just prior to labor, prostacyclin, is a smooth muscle relaxant.

123 ins (e.g. PGE(1), PGE(2), 8-iso-PGF(2alpha), prostacyclin), leukotrienes (e.g. LTB(4), LTC(4), LTD(4)

124 in combination, did not significantly affect prostacyclin levels.

125 as become the indicator of choice to measure prostacyclin levels.

126 carcinogens reduced expression of Fzd9 while prostacyclin maintained or increased expression.

127 Using urinary prostacyclin markers some groups have proposed that vasc

128 t that some of the antithrombotic actions of prostacyclin may be mediated via activation of PPARs.

129 othelium-dependent nitric oxide-mediated and prostacyclin-mediated dilations to serotonin and arachid

130 Endothelium-independent and prostacyclin-mediated endothelium-dependent relaxations

131 ss and compromises nitric oxide-mediated and prostacyclin-mediated vasomotor function via LOX-1 activ

132 For example, prostacyclin metabolites were strongly reduced (18.4% of

133 olecules showed that cysteinyl leukotrienes, prostacyclin metabolites, and PGE2 were all increased to

134 We previously reported that the prostacyclin mimetic, cicaprost, selectively inhibits cy

135 right ventricular failure, mitral stenosis, prostacyclin, nitric oxide, sildenafil, dopamine, dobuta

136 erived growth factor, von Willebrand factor, prostacyclin, NO, endothelin-1, and chemokines and the e

137 or in response to binding of agonists to the prostacyclin or beta-adrenergic receptors.

138 f male patients and those never treated with prostacyclin or its analogs.

139 Conversely, exogenous prostacyclin or peroxisome proliferator-activated recept

140 Modulation of SIRT1 and hence TF by prostacyclin/peroxisome proliferator-activated receptor-

141 f biologically important stable analogues of prostacyclin PGI(2), namely benzindene prostacyclins, ha

142 and neutrophils, (c) hypoxia and (d) altered prostacyclin (PGI(2)) and enhanced isoprostane formation

143 rse effects by suppression of PGHS-2-derived prostacyclin (PGI(2)) and PGE(2).

144 PGES-1 deletion augmented expression of both prostacyclin (PGI(2)) and thromboxane (Tx) synthases in

145 Prostacyclin (PGI(2)) and thromboxane (TxA(2)) are biolo

146 Prostacyclin (PGI(2)) is a major PG with antiapoptotic a

147 ic activity and the subsequent production of prostacyclin (PGI(2)) is an important mechanism responsi

148 pression of cyclooxygenase 2 (COX-2)-derived prostacyclin (PGI(2)) is sufficient to explain most elem

149 Prostacyclin (PGI(2)) is the major prostaglandin generat

150 Prostacyclin (PGI(2)) is widely used to treat pulmonary

151 stimulated endothelial nitric oxide (NO) and prostacyclin (PGI(2)) production.

152 increase in prostanglandin E(2) (PGE(2)) and prostacyclin (PGI(2)) production.

153 by the endothelial cell COX-2 coupled to the prostacyclin (PGI(2)) synthase (PGIS) activates the nucl

154 inhibitors of cyclooxygenase (COX)-2 depress prostacyclin (PGI(2)) without a concomitant inhibition o

155 yometrial PG produced just prior to labor is prostacyclin (PGI(2)), a smooth muscle relaxant.

156 on of vasoregulatory proteins, production of prostacyclin (PGI(2)), and cAMP were determined.

157 ir contribution to the production of PGE(2), prostacyclin (PGI(2)), and thromboxane A(2) in human cor

158 hat evoked by iloprost, a stable analogue of prostacyclin (PGI(2)), or by an NO donor.

159 roduct of vascular Cyclooxygenase-2 (COX-2), prostacyclin (PGI(2)), restrains atherogenesis, inhibiti

160 0 mmol/l) switched angiotensin II-stimulated prostacyclin (PGI(2))-dependent relaxation into a persis

161 ar side effects, likely due to inhibition of prostacyclin (PGI(2)).

162 platelet cAMP normally caused by endothelial prostacyclin (PGI(2)).

163 d chemosensitivity in response to the stable prostacyclin (PGI2) analogue carbacyclin (cPGI) in cultu

164 Prostacyclin (PGI2) analogues, which relax pulmonary ves

165 Endothelial cells release prostacyclin (PGI2) and nitric oxide (NO) to inhibit pla

166 lammation by suppressing the biosynthesis of prostacyclin (PGI2) and prostaglandin E2.

167 We investigated in vivo thromboxane (TX) and prostacyclin (PGI2) biosynthesis and their determinants,

168 Suppression of prostacyclin (PGI2) biosynthesis may explain the increas

169 Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and p

170 idated the protective mechanism of increased prostacyclin (PGI2) derived from adenoviral cyclo-oxygen

171 The prostanoid prostacyclin (PGI2) inhibits aortic smooth muscle cell p

172 Prostacyclin (PGI2) modulates platelet activation to reg

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

174 glandin H2) mimic (U46619) to the engineered prostacyclin (PGI2) synthase (PGIS) in solution.

175 nown that Ptgs2 expression and Ptgs2-derived prostacyclin (PGI2) synthesis at implantation sites are

176 yometrial PG produced just prior to labor is prostacyclin (PGI2), a smooth muscle relaxant.

177 Prostacyclin (PGI2), a vascular protector with vasodilat

178 rate-limiting component in the synthesis of prostacyclin (PGI2), an important vasodilator and antith

179 ted to suppression of COX-1-derived PGE2 and prostacyclin (PGI2).

180 cid and stimulate cyclooxygenase to generate prostacyclin (PGI2).

181 erived TXA2 over protective vascular-derived prostacyclin (PGI2).

182 lytic enzyme is introduced to stably produce prostacyclin (PGI2-hMSCs).

183 -regulate the production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (C

184 Prostacyclin plays important roles in vascular homeostas

185 ek randomized trial examining the effects of prostacyclin plus conventional therapy compared with con

186 s, we establish that paracrine production of prostacyclin proceeds in the absence of cyclooxygenase-2

187 size that localized jugular vein delivery of prostacyclin-producing cells may provide sustained thera

188 contrast to VEGF-A, VEGF-D weakly stimulated prostacyclin production and gene expression, had little

189 It is widely believed that COX-2 drives prostacyclin production and that this explains the cardi

190 th the idea that COX-2 in endothelium drives prostacyclin production in healthy individuals removed,

191 itions it is COX-1 and not COX-2 that drives prostacyclin production in the cardiovascular system, an

192 and that urinary metabolites do not reflect prostacyclin production in the systemic circulation.

193 As the rate-limiting step in prostacyclin production is the generation of free arachi

194 bition of 11betaHSD2 did not reduce systemic prostacyclin production or accelerate atherosclerosis in

195 er COX-1 results in preferential decrease in prostacyclin production over thromboxane A2 production,

196 ld increase risk (for example, inhibition of prostacyclin production), and some could decrease risk (

197 pression, and increased thromboxane A(2) and prostacyclin production.

198 s and avoiding suppression of antithrombotic prostacyclin production.

199 OX-1, not COX-2, is responsible for vascular prostacyclin production.

200 in F1alpha, the stable hydrolysis product of prostacyclin (prostaglandin I2).

201 In mouse resident peritoneal macrophages, prostacyclin, prostaglandin E2 and leukotriene C4 were p

202 s diminished, and the urinary metabolites of prostacyclin, prostaglandin E2, prostaglandin D2, and th

203 COX-derived production of prostanoids (e.g., prostacyclin) rather than the decreased sensitivity of p

204 The human prostacyclin receptor (hIP) has recently been recognized

205 The human prostacyclin receptor (hIP) is a seven transmembrane-spa

206 n = 1,761) to search for dysfunctional human prostacyclin receptor (hIP) variants, we recently discov

207 The human prostacyclin receptor (hIP), a G protein-coupled recepto

208 athways involving a cyclooxygenase-2 (COX-2)/prostacyclin receptor (IP receptor) autocrine loop and a

209 first intracellular loop (iLP1) of the human prostacyclin receptor (IP) and G alpha s protein have be

210 ellular loop (iLP1, residues 39-51) of human prostacyclin receptor (IP) was proposed to be involved i

211 in endothelial cells preferentially enhances prostacyclin receptor (versus other GPCR)-stimulated cAM

212 eceptors, respectively, with and without the prostacyclin receptor agonist iloprost.

213 ase stimulators, prostacyclin analogues, and prostacyclin receptor agonists.

214 ha, Csf1) were increased by treatment with a prostacyclin receptor antagonist and protein kinase A in

215 Treatment of wild-type mice with a prostacyclin receptor antagonist or a peroxisome prolife

216 most comprehensive characterization of human prostacyclin receptor genetic variants to date.

217 usters (analysis via a rhodopsin-based human prostacyclin receptor homology model).

218 those seen in response to activation of the prostacyclin receptor IP.

219 n the cyclooxygenase-2 inhibition studies or prostacyclin receptor knockout mice studies.

220 Polymorphisms of the human prostacyclin receptor potentially may be important predi

221 ical approaches, we conclude that diminished prostacyclin receptor signaling may contribute, in part,

222 smembrane-located cysteine residues in human prostacyclin receptor structure-function.

223 We report that a prostacyclin receptor variant (R212C) is defective in ad

224 ion instigated further genetic screening for prostacyclin receptor variants on 1455 human genomic sam

225 aining the structural integrity of the human prostacyclin receptor, as 7 of 12 extracellular and tran

226 RMICs do not express the prostacyclin receptor, but they do express the prostacyc

227 In the case of the human prostacyclin receptor, such alterations may reduce the c

228 Using a naturally occurring mutation in the prostacyclin receptor, we report for the first time that

229 Using multiple strategies, including prostacyclin receptor-targeted small interfering RNA, we

230 lecular pharmacogenetic studies of the human prostacyclin receptor.

231 /2, cyclooxygenase COX-1 (but not COX-2) and prostacyclin receptors.

232 he release of prostacyclin and activation of prostacyclin receptors.

233 s were not similarly altered in mice lacking prostacyclin receptors.

234 the antagonists of EP4, prostaglandin D2, or prostacyclin receptors.

235 reate an 'imbalance' between thromboxane and prostacyclin (reduction of prostacyclin), resulting in a

236 th the conclusion that COX-1 drives vascular prostacyclin release and puts the sparse expression of C

237 vation of VEGFR(1-2) inhibits VEGF-A-induced prostacyclin release, phosphorylation of ERK1/2 MAP kina

238 ups have proposed that vascular COX-2 drives prostacyclin release.

239 Finally, prostacyclin released from PVAT contributes to the vascu

240 At low agonist concentrations, the prostacyclin-resistant Ca(2+) response was predominantly

241 ostacyclin receptor, but they do express the prostacyclin responsive nuclear transcription factor per

242 n thromboxane and prostacyclin (reduction of prostacyclin), resulting in a prothrombic state; however

243 r, during the late postburn endotoxic phase, prostacyclin seems to significantly improve hepatic tota

244 port for the first time that a deficiency in prostacyclin signaling through its G protein-coupled rec

245 anism involving Gbetagamma/calcium/ERK/COX-1/prostacyclin signaling, and (ii) this PKA activation pro

246 Inhaled prostacyclins, similar to inhaled nitric oxide, are not

247 ised and mediated by increased receptor Mas, prostacyclin, Sirt1, and KLF4, leading to reduced vascul

248 from pregnant women near term and found that prostacyclin stimulation, which raises cAMP levels that

249 und II in analogy with plant AOS (CYP74) and prostacyclin synthase (CYP8A1).

250 ived from adenoviral cyclo-oxygenase (COX)-1/prostacyclin synthase (PGIS) (Adv-COPI) gene transfer in

251 The eicosanoid pathway enzymes prostacyclin synthase (PGIS) and inducible prostaglandin

252 s to determine whether tyrosine nitration of prostacyclin synthase (PGIS) contributes to retinal cell

253 Prostacyclin synthase (PGIS) is a membrane-bound class I

254 Prostacyclin synthase (PGIS) is tyrosine nitrated in dis

255 The most significant interaction was at prostacyclin synthase (PGIS) rs5602 (OR = 0.34, 95% CI 0

256 sis via tyrosine nitration and inhibition of prostacyclin synthase (PGIS), an enzyme with antithrombo

257 rdinate up-regulation of cPLA(2), COX-2, and prostacyclin synthase (PGIS).

258 uced insulin-resistant mice--inactivation of prostacyclin synthase and eNOS was prevented by inhibiti

259 tivated 2 important antiatherogenic enzymes, prostacyclin synthase and eNOS.

260 d ELPCs (expressing cyclooxygenase isoform 1-prostacyclin synthase and nuRFP) were tested in rats wit

261 y, we observed that COX-2 deletion decreased prostacyclin synthase and production and peroxisome prol

262 tacyclin) by lung-specific overexpression of prostacyclin synthase decreases lung tumor incidence and

263 ressing a human cyclooxygenase isoform 1 and prostacyclin synthase fusion protein that produces prost

264 activation suppressed tyrosine nitration of prostacyclin synthase in diabetes.

265 ypothesized that pulmonary overexpression of prostacyclin synthase may prevent the development of mur

266 addition of AICAR reduced both O(2).(-) and prostacyclin synthase nitration caused by high glucose,

267 lting in the inhibition of both O(2).(-) and prostacyclin synthase nitration in diabetes.

268 P-2 expression and reduced both O(2).(-) and prostacyclin synthase nitration in diabetic wild-type mi

269 CP-2 significantly ablated both O(2).(-) and prostacyclin synthase nitration triggered by high glucos

270 ) increased superoxide anions (O(2).(-)) and prostacyclin synthase nitration.

271 Transgenic FVB/N mice with lung-specific prostacyclin synthase overexpression were exposed to mai

272 We hypothesized that pulmonary prostacyclin synthase overexpression would prevent lung

273 ransfected with the cyclooxygenase isoform 1-prostacyclin synthase plasmid and labeled with lentiviru

274 We demonstrated differences of prostacyclin synthase promoter activities dependent on t

275 Prostacyclin synthase promoter haplotypes' transcription

276 g prostacyclin analogs, we hypothesized that prostacyclin synthase promoter sequence variants associa

277 Prostacyclin synthase promoter sequence variants exhibit

278 We identified a comprehensive set of prostacyclin synthase promoter variants and tested their

279 in reaction approaches were used to genotype prostacyclin synthase promoter variants in more than 300

280 To determine the distribution of prostacyclin synthase promoter variants in PAH, unaffect

281 iscovered a significant bias for more active prostacyclin synthase promoter variants in unaffected ca

282 HIF-responsive genes (VEGF-A, PPARgamma, and prostacyclin synthase) due to an insufficient increase i

283 NA and protein levels of cPLA(2), COX-2, and prostacyclin synthase, as well as the promoter and enzym

284 Cyclooxygenase isoform 1-prostacyclin synthase-expressing ELPCs reversed MCT-indu

285 zymes, endothelial nitric oxide synthase and prostacyclin synthase.

286 by stimulating Cox-2 expression, leading to prostacyclin synthesis and an IP-dependent inhibition of

287 ombosis, including through the activation of prostacyclin synthesis.

288 Prostacyclin, the major cyclooxygenase-derived product o

289 Administration of inhaled prostacyclin to decrease pulmonary artery pressures and

290 Postburn prostacyclin treatment appears to have no beneficial eff

291 In addition, prostacyclin treatment attenuated burn- and endotoxin-in

292 Nitric oxide (NO) and prostacyclin trigger well-defined vasodilator pathways;

293 A neovessel-derived signal mediated by prostacyclin triggers axonal sprouting and functional re

294 failure of the endothelial nitric oxide and prostacyclin vasodilator pathways, coupled with dysregul

295 The systemic biosynthesis of TxA2 and prostacyclin was assessed by analysis of their respectiv

296 Inhaled prostacyclin was started at a dosage of 50 ng/kg/min, an

297 The relative importance of PGE2 and PGI2 (prostacyclin) was determined using mice deficient in mic

298 antagonistic efficacy of endothelial-derived prostacyclin, we determined how Iloprost reverses ADP-me

299 l platelet inhibitors is endothelium-derived prostacyclin which stimulates the platelet cyclic adenos

300 that postburn treatment with the vasodilator prostacyclin would be beneficial for hepatic perfusion a