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 vation, a process antagonized by endothelial prostacyclin.

10 PPARbeta is a putative receptor for prostacyclin.

11 ween platelet thromboxane A2 and endothelial prostacyclin.

12 ents with severe PH treated chronically with prostacyclin.

13 ssed Fzd9 expression, which was abrogated by prostacyclin.

14 ression of the renal receptor Mas and plasma prostacyclin.

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

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

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

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

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

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

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

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

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

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

25 The prostacyclin analog treprostinil is also efficacious by

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

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

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

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

30 Prostacyclin analogs are widely used in the management o

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

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

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

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

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

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

37 Beraprost is the first orally active prostacyclin analogue.

38 Because prostacyclin analogues are effective treatments for clin

39 Prostacyclin analogues enhance Id1 expression in vitro a

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

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

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

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

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

45 rase inhibitors, endothelin antagonists, and prostacyclin analogues.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 The increased prostacyclin biosynthesis in smokers is derived largely

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 ate any antithrombotic role for COX1-derived prostacyclin from the prothrombotic effects of platelet

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

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

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

86 Prostacyclin has many effects in the vasculature; one of

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

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

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

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

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

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

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

94 o identify the role, if any, of COX1-derived prostacyclin in antithrombotic protection in vivo and co

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

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

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

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

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

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

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

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

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

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

105 Prostacyclin-induced increases in CVC were similar betwe

106 This prostacyclin-induced response may be diminished in older

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

108 antagonists for PGE(2) (EP(2) and EP(4)) and prostacyclin (IP) also enhanced the mannitol-induced bro

109 Prostacyclin is an antithrombotic hormone produced by th

110 Prostacyclin is an important antithrombotic hormone that

111 Intravenous prostacyclin is approved for treating pulmonary arterial

112 Increased prostacyclin is associated with elevated aortic vasculop

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

114 Prostacyclin is the major end product of cyclooxygenase-

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

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

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

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

119 s to inhibit platelet aggregation and plasma prostacyclin levels were reduced when COX1 was knocked o

120 in combination, did not significantly affect prostacyclin levels.

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

122 Using urinary prostacyclin markers some groups have proposed that vasc

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

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

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

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

127 rker of platelet COX-1 activity, and urinary prostacyclin metabolite (PGIM) excretion were measured a

128 -fold), as well as PGE(2) (6.3-fold) and the prostacyclin metabolite 6-keto PGF(1alpha) (5.7-fold).

129 ) levels vis-a-vis healthy subjects, whereas prostacyclin metabolite levels were diminished only weak

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

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

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

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

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

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

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

137 Conversely, exogenous prostacyclin or peroxisome proliferator-activated recept

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 0 mmol/l) switched angiotensin II-stimulated prostacyclin (PGI(2))-dependent relaxation into a persis

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

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

160 The GRIPHON trial (Prostacyclin [PGI(2)] Receptor Agonist In Pulmonary Arte

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

162 Prostacyclin (PGI2) analogues, which relax pulmonary ves

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

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

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

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

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

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

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

170 Prostacyclin (PGI2) modulates platelet activation to reg

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

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

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

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

175 Prostacyclin (PGI2), a vascular protector with vasodilat

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

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

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

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

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

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

182 Prostacyclin plays important roles in vascular homeostas

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

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

185 prostacyclin synthase, which is required for prostacyclin production after lipopolysaccharide stimula

186 e relative importance of COX1 versus COX2 in prostacyclin production and antithrombotic protection in

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

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

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

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

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

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

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

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

195 COX1 immunoreactivity and prostacyclin production were primarily associated with t

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

197 Moreover, aortic prostacyclin production, the ability of aortic rings to

198 otype that was independent of local vascular prostacyclin production.

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

200 s and avoiding suppression of antithrombotic prostacyclin production.

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

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

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

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

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

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

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

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

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

210 5b-KOs showed ex vivo significantly enhanced prostacyclin receptor (IP)-dependent relaxation, whereas

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

212 However, prostacyclin receptor activated with iloprost showed no

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

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

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

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

217 ccelerated thrombosis to a similar extent as prostacyclin receptor blockade.

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

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

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

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

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

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

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

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

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

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

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

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

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

231 s are activated upon depolarization, whereas prostacyclin receptors are not.

232 /2, cyclooxygenase COX-1 (but not COX-2) and prostacyclin receptors.

233 he release of prostacyclin and activation of prostacyclin receptors.

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

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

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

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

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

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

240 Finally, prostacyclin released from PVAT contributes to the vascu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 Prostacyclin synthase (PGIS) is tyrosine nitrated in dis

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

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

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

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

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

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

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

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

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

265 activation suppressed tyrosine nitration of prostacyclin synthase in diabetes.

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 tion factor Gata6 controls the expression of prostacyclin synthase, which is required for prostacycli

285 try analysis showed that CBP/p300 acetylates prostacyclin synthase, which regulates Treg differentiat

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

287 zymes, endothelial nitric oxide synthase and prostacyclin synthase.

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

289 ombosis, including through the activation of prostacyclin synthesis.

290 y isolated aortic ECs released >10-fold more prostacyclin than smooth muscle cells.

291 Prostacyclin, the major cyclooxygenase-derived product o

292 Postburn prostacyclin treatment appears to have no beneficial eff

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

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

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

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

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

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

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

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

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