ライフサイエンスコーパス: prostanoid

1 ions generated substantial quantities of the prostanoid.

2 receiving endothelin-receptor antagonists or prostanoids.

3 n mediator prostaglandin E2 (PGE2) and other prostanoids.

4 aglandin D2 and allows rapid access to other prostanoids.

5 iprocal increase in basal excretion of other prostanoids.

6 ivity and association with the ER but not on prostanoids.

7 staglandin J(2), act through 2 GPCRs, d-type prostanoid 1 and the chemoattractant receptor homologous

8 (1) and CysLT(2)) and the PGE(2) receptors E-prostanoid 1 to 4 (EP(1)-EP(4)) in bronchial biopsy spec

9 We identified 18 prostanoids, 12 hydroxy-fatty acids, 9 endocannabinoids

10 tor-beta-induced fibroblast activation via E prostanoid 2 (EP2) receptor binding.

11 ivo function of PGE2 signaling through its E-prostanoid 2 (EP2) receptor in murine innate immune resp

12 ance to decreased expression levels of the E prostanoid 2 (EP2) receptor.

13 neuronal localization of the PGE2 receptor E-prostanoid 2 (EP2).

14 AMP, generated mainly upon ligation of the E prostanoid 2 receptor and acting via protein kinase A (P

15 n was mediated by PGE(2) signaling via its E prostanoid 2 receptor and the second messenger cAMP.

16 e AM overproduction of PGE(2) and elevated E prostanoid 2 receptor expression, AM phagocytosis, killi

17 -stimulated liver NKT cells in a PGE2 E-type prostanoid 2/E-type prostanoid 4 receptor-mediated manne

18 receptors, the prostaglandin E(2) (PGE(2)) E-prostanoid 3 (EP3) receptor binds agonist with high affi

19 mpromised by concomitant activation of the E-prostanoid 3 (EP3) receptor.

20 We used mice lacking eicosanoid prostanoid 3 receptors (EP3R), breathing brainstem organ

21 em/progenitor egress resulted from reduced E-prostanoid 4 (EP4) receptor signalling.

22 2), autocrine activation of the macrophage E-prostanoid 4 (EP4) receptor, and subsequent triggering o

23 T cells in a PGE2 E-type prostanoid 2/E-type prostanoid 4 receptor-mediated manner.

24 In 9 patients on chronic intravenous prostanoids, 8 transitioned from intravenous prostanoids

25 Cyclooxygenase-derived prostanoids act in an autocrine or a paracrine fashion a

26 PGE2, a major immunomodulatory prostanoid, acts as a proinflammatory agent in several m

27 ion of PGE(2) and, to a lesser extent, other prostanoids after LPS.

28 Among several prostanoid agonists tested in combination with forskolin

29 COX-derived prostanoids also appear to be involved in the pathogenes

30 Cyclooxygenase-derived prostanoids also are involved in certain pathological pr

31 ors, including nitric oxide, endothelin, and prostanoids, among others.

32 noid synthase for the synthesis of bioactive prostanoid and (b) the interaction with its receptors th

33 e, small-molecule dual antagonist of human D-prostanoid and CRTH2.

34 Inhibition of strain-related prostanoid and nitric oxide production inhibits strain-r

35 phages revealed suppression of COX-2-derived prostanoids and augmented 5-lipoxygenase product formati

36 Various prostanoids and peroxisome proliferator-activated recept

37 OX) -1 and -2 metabolize arachidonic acid to prostanoids and reactive oxygen species, major players i

38 crophages, miR-466l overexpression increased prostanoids and SPMs (e.g., resolvin D1 [RvD1] and RvD5)

39 ical trials, but the COX isoform, downstream prostanoid, and cell compartment responsible for this ef

40 mmatory mediators, specifically neurokinins, prostanoids, and histamine.

41 Renal medullary COX2-derived prostanoids appear to have an antihypertensive effect in

42 Prostanoids are a large family of bioactive lipids deriv

43 Prostanoids are prominent, yet complex, components in th

44 Prostanoids are suggested to participate in diabetes pat

45 ralization of PGE2 in AEC-CM implicated this prostanoid as the major AEC-derived factor mediating enh

46 A polypharmacologic approach to prostanoid based anti-inflammatory therapeutics was unde

47 ooxygenase (COX) catalyzes the first step in prostanoid biosynthesis and exists as two isoforms.

48 a patient hypothesized to have an inherited prostanoid biosynthesis deficiency due to his multiple,

49 of the effect of mPGES-1 genetic deletion on prostanoid biosynthesis in fibroblast lineage cells and

50 Ibuprofen, an inhibitor of prostanoid biosynthesis, is a common pharmacological age

51 genase (COX)-2, the inducible key enzyme for prostanoid biosynthesis, is overexpressed in most colore

52 to prostaglandin H2 in the committed step of prostanoid biosynthesis.

53 se (COX)-1 and -2 catalyze the first step in prostanoid biosynthesis.

54 ecreased cell cycle-regulating cyclin D1 and prostanoid biosynthetic enzyme cyclooxygenase-2 in micro

55 the production of cytokines, chemokines, and prostanoids by immune and non-immune cells.

56 Cyclooxygenase (COX)-2-derived prostanoids can influence several processes that are lin

57 s, we only found a modest down regulation in prostanoid concentrations, whereas it led to significant

58 The prostanoid content of arthritic ankles was assessed in a

59 Vasodilator prostanoid contribution to endothelium-dependent relaxat

60 -induced degranulation by acting through the prostanoid D receptor 1 (DP1).

61 lts show that, like viruses, bacteria induce prostanoid-dependent beta2 -AR desensitization on ASM ce

62 tion in human bronchial epithelial cells and prostanoid-dependent bronchodilation.

63 ition, we also examined the effects of other prostanoids derived from COX-2 oxygenation of eCBs on mI

64 s, but the role of its two receptors, D-type prostanoid (DP) and, in particular, chemoattractant rece

65 expressed on T(H)2 cells (CRTH2), and D-type prostanoid (DP) receptor.

66 -2 (COX-2) and the prostaglandin E receptor, prostanoid E receptor subtype 1, are involved in seizure

67 ult of the reduced COX-derived production of prostanoids (e.g., prostacyclin) rather than the decreas

68 is generated through enzymatic metabolism of prostanoid endoperoxides by specific PGE synthases (PGES

69 Therapy with prostanoids, endothelin-1 inhibitors and phosphodiestera

70 Here we report in vitro specificities of prostanoid enzymes and receptors toward EPA-derived, 3-s

71 (PGH2) is also a command substrate for other prostanoid enzymes that produce distinct eicosanoids, su

72 re in the monkey, the prototypical selective prostanoid EP(4) receptor agonist (3,7-dithia PGE(1)) wa

73 ists to S1P(1) and S1P(2) receptors, and the prostanoid EP(4) receptor agonist 3,7-dithia PGE(1).

74 ng 4 distinct G protein-coupled receptors, E prostanoid (EP) 1 to 4.

75 yl PGE(2), or of selective agonists of the E-prostanoid (EP) 1, EP2, and EP3 receptors, respectively,

76 four distinct G protein-coupled receptors, E-prostanoid (EP) 1-4.

77 erived PGE(2) signals via up-regulation of E prostanoid (EP) 2 and down-regulation of EP3 receptors t

78 Studies with the E prostanoid (EP) 2 receptor antagonist AH-6809 and EP2-nu

79 andin (PG) E2 and diminished expression of E-prostanoid (EP) 2 receptor, are closely linked.

80 regulatory function in MSCs by triggering E-Prostanoid (EP) 2 receptor.

81 We observed that activation of E-type prostanoid (EP) 4 receptor by PGE(2) or an EP4-selective

82 , we investigated the function of the PGE2 E-prostanoid (EP) 4 receptor in the CNS innate immune resp

83 These mixed effects relate to 4 E-prostanoid (EP) receptor subtypes (EP1, 2, 3 and 4) expr

84 the activation of the G(s) protein-coupled E prostanoid (EP) receptors EP2 and EP4 (macrophages) or E

85 Interestingly, the E prostanoid (EP) receptors EP2 and EP4 are elevated on do

86 nd evaluate the significance of individual E prostanoid (EP) receptors in mediating the fibroprolifer

87 of prostaglandin (PG) E(2) or of specific E prostanoid (EP) receptors is not known.

88 different cell types are mediated by four E prostanoid (EP) receptors, EP(1)-EP(4).

89 Among the four E-prostanoid (EP) receptors, EP3 is unique in that it exis

90 crophages through G protein-coupled E-series prostanoid (EP) receptors.

91 onchodilator response was inhibited by the E prostanoid (EP) subtype 4 receptor antagonist ONO-AE3-20

92 ng ex vivo is controlled heterologously by E prostanoid (EP)(1) and EP(2) receptor-dependent signalin

93 A stable PGE2 analog and a selective E prostanoid (EP)2 receptor agonist blocked the responses

94 d small-interfering RNA approaches, a PGE2/E prostanoid (EP)2/adenylate cyclase pathway was implicate

95 cytokine release from human macrophages, the prostanoid EP1 receptor played a permissive role in supp

96 Activation of prostanoid EP2 receptor exacerbates neuroinflammatory an

97 Cyclooxygenase-derived prostanoids exert complex and diverse functions within t

98 ted the role of PGE(2), which binds to the E-prostanoid family of G protein-coupled receptors through

99 enes differentially induced by the synthetic prostanoid fluprostenol and IL-1 in cementoblastic cells

100 owever, the contribution of these enzymes in prostanoid formation varies depending on the stimuli and

101 PGE(2) was found as the main prostanoid formed by the pancreas.

102 Thromboxane A(2) (TxA(2)) is a prostanoid formed by thromboxane synthase using the cycl

103 pressure in WT mice via activation of the F prostanoid (FP) receptor.

104 and the prostaglandin F2alpha (PGF2alpha) F prostanoid (FP) receptors are both potent regulators of

105 Production of 2-series prostanoids from AA by PGHS-2 would be expected to decre

106 remain unclear, though stimulated release of prostanoids from neighboring vascular cells has been imp

107 egulation of COX-2 induction and its role in prostanoid generation after a pro-inflammatory challenge

108 luence of PTEN was observed on alternative E prostanoid GPCRs.

109 Prostanoids have been proposed as potent adipogenic horm

110 Endogenous prostanoids have been suggested to modulate sensitizatio

111 le in the regulation of COX-2 expression and prostanoid homeostasis in vascular endothelium.

112 , its influence on cyclooxygenases (COX) and prostanoid homeostasis is not well understood.

113 se of corresponding arachidonic acid-derived prostanoids, implying that these effects are not mediate

114 rostaglandin (PG)E2, a major proinflammatory prostanoid in the cardiovascular system, is a potent sti

115 OX-1 activity within the body as it produces prostanoids in an explosive burst that does not reflect

116 Although the role of prostanoids in itch was actively studied a decade ago, i

117 ble enzyme that converts arachidonic acid to prostanoids in the brain.

118 E(2) (PGE(2)) is one of the most ubiquitous prostanoids in the kidney, where it may influence a wide

119 These sex differences in the role of these prostanoids in the PVAT-induced contraction can be expla

120 etermined the role of cyclooxygenase-derived prostanoids in this contractile response and determined

121 ess this question, we measured production of prostanoids, including 6-keto-PGF1alpha, by isolated ves

122 indomethacin pellets, suggesting a role for prostanoids, including prostaglandin E(2), in differenti

123 ictor responses to PGE2 and all other tested prostanoids, including the EP1/EP3 receptor agonist 17-p

124 ed families of natural products, such as the prostanoids, indole alkaloids, and macrolide antibiotics

125 The eCB-derived prostanoid-induced responses appeared to be different fr

126 and synthesis of a new series of potent non-prostanoid IP receptor agonists that showed oral efficac

127 The biological effect of each prostanoid is controlled at multiple levels, including (

128 gesting that this powerful anti-inflammatory prostanoid is part of an endogenous defence mechanism to

129 s, PGE(2) and PGD(2), are synthesized by the prostanoid isomerases, PGE synthases (PGES) and PGD synt

130 ion profile and the individual role of these prostanoid isomerases-mediated inflammation in macrophag

131 -cAMP), stimulation of adenylate cyclase, or prostanoids known to drive cAMP response.

132 ncubation of DPTL with small molecules (e.g. prostanoids, leukotrienes, lipids, biogenic amines) foll

133 nd to LPS by a COX-2-dependent production of prostanoids, mainly vasoactive PGE(2), and suggest that

134 est a novel mechanism through which reactive prostanoids may activate nociceptive neurons independent

135 Prostanoids mediate many of their physiological effects

136 olypharmacological approach for treating the prostanoid-mediated component of inflammatory diseases w

137 Thus, PVCs provide both prostanoid-mediated drive to the HPA axis and an anti-in

138 The HSD augmented in all strains urinary prostanoid metabolite excretion, with the exception of t

139 This cascade requires prostanoid/nitric oxide production and is independent of

140 In the prostanoid/NO protocol: (1) ketorolac (Keto), (2) NG-nit

141 Here, we examined the effects of this prostanoid on apoptosis and apoptosis pathways in normal

142 tion with endothelin receptor antagonists or prostanoids, or both.

143 f treatment with intravenous or subcutaneous prostanoids, or worsening of pulmonary arterial hyperten

144 Renal cortical COX2-derived prostanoids, particularly PGI2 and PGE2, play critical r

145 -1 inhibition versus other mechanisms in the prostanoid pathway.

146 aimed at identifying specific COX-2-derived prostanoid pathways.

147 Conversely, treatment with Cox-derived prostanoids PGD(2) or 15-deoxy-Delta(12,14)-PGJ(2) induc

148 f the pro-inflammatory cytokine IL-8 and the prostanoid PGE(2) are regulated by NF-kappaB, this could

149 The prostanoid PGE(2), which induces angiogenesis and vasodi

150 Ra triggers production of high levels of the prostanoid PGE(2), which promotes protection against mit

151 ell count and IS supernatant (ISS) levels of prostanoids, PGE(2) , 8-iso-PGE(2) , tetranor-PGE-M, 8-i

152 Prostanoids play important physiological roles in the ca

153 Through these actions, prostanoids play important roles in maintaining renal fu

154 y reduced prostaglandin E2 (PGE(2)), a major prostanoid produced downstream of COX-2 and an important

155 Thromboxane A2 (TXA2) was the prostanoid product of COX-1 responsible for this antimet

156 volving endothelial nitric oxide synthase or prostanoid production (indomethacin).

157 to stimuli (lipopolysaccharide) that engaged prostanoid production by ECs as well.

158 tly elevate bacterially induced inflammatory prostanoid production by isolated cultures of these cell

159 PGES-1 gene deletion results in diversion of prostanoid production from PGE2 to 6-keto PGF1alpha (the

160 g them with wild-type sPLA(2) fully restored prostanoid production to anticipated levels.

161 effects of histamine on COX-2 expression and prostanoid production were mediated through H(1) recepto

162 antiinflammatory agents (NSAIDs) that reduce prostanoid production, for example, selective inhibitors

163 id stimulated cyclooxygenase-2 induction and prostanoid production.

164 alytic activity by a COX-2 inhibitor blocked prostanoid production.

165 se in lipoxygenase-derived hydroxylation and prostanoid production.

166 , which correlated well with COX-2-dependent prostanoid production.

167 the enzyme cyclooxygenase-2 (COX-2) and its prostanoid products, prostaglandin E2 (PGE2 ) in particu

168 AGN 211377 antagonizes prostanoid prostaglandin D2 (DP)1, DP2, prostaglandin E2

169 ooxygenase-2 (COX-2) produces novel types of prostanoids: prostaglandin glycerol esters (PG-Gs) and p

170 ted moderate selectivity to EP2 over the DP1 prostanoid receptor ( approximately 10-fold) and low aqu

171 it functions through two major receptors, D prostanoid receptor (DP) and chemoattractant receptor-li

172 ittle is known about other aspects of E-type prostanoid receptor (EP) 1 receptor signaling.

173 re mediated by the combined action of E-type prostanoid receptor (EP) 2 and EP4 receptors, which were

174 einyl leukotriene receptor 1 (CysLT1R) and E-prostanoid receptor (EP) 3, enhanced extracellular signa

175 ty of Ishikawa cells stably expressing the F-prostanoid receptor (FPS) to adhere to vitronectin.

176 er augmented by coincident deletion of the I prostanoid receptor (n=10-18).

177 ion of the vasoconstricting thromboxane A(2) prostanoid receptor (TP), a mechanism supported by MaxiK

178 D prostanoid receptor 1 (DP(1)) or the thromboxane-like pr

179 The D prostanoid receptor 2 (DP2; also known as chemoattractan

180 his is mediated by a cyclooxygenase-PGE(2)-E prostanoid receptor 2 (EP2)-adenylyl cyclase-cyclic AMP

181 h2 cells by signaling through its receptor E-prostanoid receptor 2 (EP2).

182 However, cyclooxygenase-1 and prostanoid receptor 2-4 levels were comparable in pups w

183 GE2, which induces IL-1beta production via E prostanoid receptor 2/4-cAMP-PKA-NFkappaB-dependent mech

184 Prostanoid receptor agonists and the combination thereof

185 ptors for prostaglandin E2 (PGE2) and that E-prostanoid receptor agonists, including PGE2, induce the

186 ooxygenase-2 inhibition or deletion of its I prostanoid receptor also predisposes to accelerated athe

187 xpression of the G(alphas) protein-coupled I prostanoid receptor and greater cAMP generation in PMs t

188 The D-prostanoid receptor and the chemoattractant receptor hom

189 ere reversed by cyclooxygenase inhibition or prostanoid receptor antagonism.

190 of prostanoid synthesis or highly selective prostanoid receptor blockade.

191 therapy could be targeted through a specific prostanoid receptor downstream of COX-2.

192 Prostanoid receptor EP2 can play a proinflammatory role,

193 The prostanoid receptor EP2 was overexpressed in human prost

194 ed to the expression of IL-6 mediated by the prostanoid receptor EP2.

195 Adult mice carrying a null mutation of the prostanoid receptor EP3R (EP3R(-/-) mice) exhibit increa

196 l assays with respect to most members of the prostanoid receptor family and a more modest 30- to 50-f

197 By contrast, deletion of the I prostanoid receptor had no effect on the attenuation of

198 The EP1 prostanoid receptor is one of four subtypes whose cognat

199 Here we show that the EP(3) prostanoid receptor is specifically activated by ricinol

200 ons demonstrate the first working example of prostanoid receptor polypharmacology for potentially saf

201 n, and we now suggest how targeting specific prostanoid receptor signaling pathways could be exploite

202 broblasts; (ii) PGE(2) activation of the EP3 prostanoid receptor stimulates the activation of JNK.

203 dating the role of prostaglandin E2 (PGE2) E-prostanoid receptor subtype 1 (EP1) in regulating blood

204 In contrast, E-prostanoid receptor subtype 2 (EP2) activation, which se

205 Cooperativity of E-prostanoid receptor subtypes in regulating signaling and

206 ion of PGI2, we generated mice lacking the I prostanoid receptor together with mPges-1 on a hyperlipi

207 Whereas compounds selective for a single prostanoid receptor typically exhibited modest but stati

208 landin E activating the EP3 isoform of the E prostanoid receptor, appears to be up-regulated in insul

209 Hence, prostanoid receptor-1 and tumour necrosis factor-alpha a

210 Cyclooxygenase-2 or prostanoid receptor-1 inhibition reduced tumour necrosis

211 Cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha in

212 tion or suppression of downstream molecules--prostanoid receptor-1 or tumour necrosis factor-alpha--m

213 treated with inhibitors of cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha; a

214 ssion of cyclooxygenase-2, prostaglandin E2, prostanoid receptor-1, tumour necrosis factor-alpha and

215 promising new outlook for the examination of prostanoid receptor-G-protein interactions in greater de

216 indomethacin or by null mutation of the EP3 prostanoid receptor.

217 ct was abrogated by an antagonist of the DP1 prostanoid receptor.

218 but its action and the roles of the 2 D-type prostanoid receptors (DPs) DP1 and DP2 (also called chem

219 Inhibition of the PG receptors E-prostanoid receptors 2 and 4 prevented the tolerogenic e

220 , we studied mice with selective deletion of prostanoid receptors and generated conditionally immorta

221 xygenase-2, its derivative prostaglandin E2, prostanoid receptors and pro-inflammatory cytokines were

222 roblasts (18Co) through Gs protein-coupled E-prostanoid receptors and the cyclic AMP/protein kinase A

223 FP prostanoid receptors are G-protein-coupled receptors who

224 ibitory approach to perform the screening of prostanoid receptors as potential candidates that mediat

225 anner, 3) exhibits high selectivity over all prostanoid receptors as well as 157 other receptors and

226 Agonists of E prostanoid receptors EP2 (butaprost) and EP1/3 (sulprost

227 e show the ERG-mediated up-regulation of the prostanoid receptors EP2 and EP3.

228 fferent functions and cell distribution of E prostanoid receptors explain the difficulty encountered

229 In vivo studies validating multitargeting of prostanoid receptors for achieving superior anti-inflamm

230 obesity and suggest that targeting specific prostanoid receptors may represent a novel strategy for

231 COXs, prostanoid synthases, and prostanoid receptors should provide fruitful targets for

232 receptor pathways, beta(2)-adrenoceptors and prostanoid receptors that are expressed endogenously in

233 product of arachidonic acid that activates D prostanoid receptors to modulate vascular, platelet, and

234 Multitargeting of selected prostanoid receptors yielded a prototype compound, compo

235 While BF cultures expressed all four prostanoid receptors, direct addition of sulprostone but

236 It is known that PGE2 signals via the E prostanoid receptors, EP1-4, but the role that each rece

237 isolated from obese-diabetic mice expressed prostanoid receptors, EP2 and DP1, and contained signifi

238 se findings reveal that blockade of multiple prostanoid receptors, with absent antagonism of EP2 and

239 al and uterine smooth-muscle cells via EP(3) prostanoid receptors.

240 hat these effects are not mediated via known prostanoid receptors.

241 mmatory properties attributed to the various prostanoid receptors.

242 in) rather than the decreased sensitivity of prostanoid receptors.

243 9 possess high selectivity relative to other prostanoid receptors.

244 These results reveal a mechanism by which prostanoids regulate cell movement, which may be relevan

245 from which arise cyclopentenones such as the prostanoid-related clavulones.

246 a predetermined stereogenic center into the prostanoid ring, resulting in the synthesis of 15R-methy

247 to exogenous mechanical stimuli secondary to prostanoid signaling and Akt/mTOR (mammalian target of r

248 xide-, or cytochrome p450-derived vasoactive prostanoid signaling but is associated with vascular hyp

249 pholipid EPA/AA ratios in cells would dampen prostanoid signaling with the largest effects being on P

250 muscle, alterations in both nitric oxide and prostanoid signalling underlie endothelial dysfunction.

251 The data indicate that bioactive prostanoids significantly impair membrane phospholipid p

252 Targeting the prostanoids, specifically PGE2 and PGI2, as well as the

253 However, the prostanoid strongly inhibited CCL17-induced chemotaxis o

254 erived, 3-series versus AA-derived, 2-series prostanoid substrates and products.

255 c acid (HETE) and 15(S)-HETE, in addition to prostanoids such as thromboxane A2 Releasates from activ

256 pendent production of COX-derived endogenous prostanoids, such as Delta(12)-PGJ2 and 15d-PGJ2, may re

257 Increased production of vasoconstrictive prostanoids, such as thromboxane A2 (TXA2 ), contributes

258 catalyzed sequentially by cyclooxygenase and prostanoid synthase for the synthesis of bioactive prost

259 COXs, prostanoid synthases, and prostanoid receptors should pr

260 rent diets will likely affect both base-line prostanoid synthesis and responses to COX inhibitors.

261 Prostanoid synthesis in mammalian tissues is regulated a

262 ge conditions (interleukin-1) that activated prostanoid synthesis only in PVCs, while enhancing these

263 ammatory activity than global suppression of prostanoid synthesis or highly selective prostanoid rece

264 Prostanoid synthesis via cyclooxygenase (COX)-2 inductio

265 genase-2 (COX-2), a rate-limiting enzyme for prostanoid synthesis, has been implicated in the neuroto

266 ctive cyclooxygenase-2 inhibitors that block prostanoid synthesis.

267 proteins that catalyze the committed step in prostanoid synthesis.

268 rs, we aimed to establish whether endogenous prostanoids synthesised by cyclooxygenase (COX) affect r

269 ght the potential pathogenic contribution of prostanoids synthesized via COX-1, in particular PGI2, t

270 Cyclooxygenase-2 (COX-2) is a prostanoid-synthesizing enzyme that is critically implic

271 interaction between the endocannabinoid and prostanoid systems.

272 lly constitutively expressed and synthesizes prostanoids that mediate homeostatic functions; and (ii)

273 es of injury or inflammation and synthesizes prostanoids that mediate inflammation, pain and fever.

274 prostaglandin (PG) F(2alpha) and PGF(2alpha) prostanoids that sustain the growth of myeloid precursor

275 acid metabolism mediating the production of prostanoids that, among other actions, have strong vasoa

276 predictive of outcome; patients initiated on prostanoid therapy showed the greatest improvement in RV

277 d of right heart failure received parenteral prostanoid therapy.

278 d the transition from intravenous to inhaled prostanoid therapy.

279 Andoh et al. demonstrate that the prostanoid thromboxane A2 elicits scratching through its

280 sion and product formation, while triggering prostanoid (thromboxane and prostaglandin D(2) and E(2)

281 Aspirin impairs the biosynthesis of all prostanoids through the irreversible inhibition of both

282 KCa) channels, and (2) nitric oxide (NO) and prostanoids to cutaneous reactive hyperaemia.

283 prostanoids, 8 transitioned from intravenous prostanoids to inhaled iloprost, which continued during

284 se-1 [COX1 knockout (KO)] or the thromboxane prostanoid (TP) receptor (TP KO).

285 d receptor 1 (DP(1)) or the thromboxane-like prostanoid (TP) receptor did not play a role in mediatin

286 thromboxane A(2) and signaling through the T prostanoid (TP) receptor.

287 creased through activation of thromboxane A2-prostanoid (TP) receptors on neurons.

288 nded on platelet-adherent granulocytes and T-prostanoid (TP) receptors.

289 h hematopoietic and lung tissue-associated T prostanoid (TP) receptors.

290 in vitro in a PGE2-dependent manner via the prostanoid type E receptor-2 (EP2), effects not seen wit

291 yclooxygenase (COX)-mediated biosynthesis of prostanoids, various widely used nonsteroidal anti-infla

292 that mediates the inhibitory actions of this prostanoid via cAMP.

293 terase type-5 inhibitors and oral or inhaled prostanoids was permitted for WHO functional class III/I

294 f the receptor for PGI(2), but not for other prostanoids, was depressed by HSD in WT and even more so

295 lin-receptor antagonists or (nonintravenous) prostanoids were eligible.

296 Prostanoids were responsible for the rapid entry of neut

297 sma aldosterone level, and urinary and heart prostanoids were similar in apoE(-/-) and GV DKO mice af

298 ealed a nexus between metalloproteinases and prostanoids whereby MMP-1 and MMP-3, commonly found in i

299 to the production of TNFalpha, IL-1beta, and prostanoids, which are likely responsible for the mainte

300 As PGE2 is a multifunctional prostanoid with diverse roles in respiratory disease, ou