ライフサイエンスコーパス: thromboxane

1 stanes) and inflammation (prostaglandins and thromboxanes).

2 s of the bioactive lipids prostaglandins and thromboxane.

3 al macrophages and increased biosynthesis of thromboxane.

4 -iso-PGF2 was diminished and that for pinane thromboxane A nonexistent when Galpha12 was the reporter

5 Pinane thromboxane A(2) (PTA(2)) activates G(q) in preference t

6 mplicated by the feedback effects of ADP and thromboxane A(2) (TxA(2)) and by the overlap with the re

7 ERK1/2 plays an important role in regulating thromboxane A(2) (TXA(2)) generation in platelets, we in

8 telet PGH synthase 1-derived (PGHS1-derived) thromboxane A(2) (TxA(2)) has been implicated in its pat

9 -dose aspirin incompletely inhibits platelet thromboxane A(2) (TXA(2)) in the majority of ET patients

10 Thromboxane A(2) (TxA(2)) is a prostanoid formed by thro

11 tive cardiac sympathetic afferents, and that thromboxane A(2) (TxA(2)) is one of the mediators releas

12 This enhanced signaling was detected as thromboxane A(2) (TxA(2)) production and granule secreti

13 c acid from glycerophospholipids, leading to thromboxane A(2) (TxA(2)) production.

14 The human thromboxane A(2) (TXA(2)) receptor (TP) is known to medi

15 s showed significantly lower agonist-induced thromboxane A(2) (TXA(2)) release through reduced extrac

16 racellular signal-regulated kinase-dependent thromboxane A(2) (TxA(2)) release.

17 release of VEGF, but not endostatin whereas, thromboxane A(2) (TXA(2)) released endostatin but not VE

18 ) receptor (TP), two critical components for thromboxane A(2) (TXA(2)) signaling, have been suggested

19 entrations of thrombin receptor agonists and thromboxane A(2) (TXA(2)), but not collagen or VWF.

20 ion, Rac1 activation, and release of ADP and thromboxane A(2) (TxA(2)).

21 cted, human endothelial cells (ECs) released thromboxane A(2) (TXA(2)).

22 looxygenase-2 and catalyzes the synthesis of thromboxane A(2) (TXA(2)).

23 As reported previously, TP activation by the thromboxane A(2) analog U46619 caused inhibition of Maxi

24 activation of platelets by collagen and the thromboxane A(2) analog U46619.

25 Aging selectively attenuated thromboxane A(2) and Ang II-induced IAS contraction.

26 characterize IAS smooth muscle cells (SMCs): thromboxane A(2) and angiotensin II type 1.

27 d cyclooxygenase-2 expression, and increased thromboxane A(2) and prostacyclin production.

28 Macrophage-COX-2, primarily a source of thromboxane A(2) and prostaglandin (PG)E(2), promotes at

29 n the setting of PGE(2) deficiency depend on thromboxane A(2) and signaling through the T prostanoid

30 ough cyclooxygenase-2 (COX-2) pathways while thromboxane A(2) formed by platelets from AA via cycloox

31 uction of PGE(2), prostacyclin (PGI(2)), and thromboxane A(2) in human coronary artery endothelial ce

32 ntractions induced by angiotensin II and the thromboxane A(2) mimetic, U46619, and had no significant

33 her IBOP or U46619, two structurally related thromboxane A(2) mimetics, significantly reduced insulin

34 In summary, the data support a role for the thromboxane A(2) pathway in the pathogenesis of bladder

35 liberates AA and elicits LTC(4), PGD(2), and thromboxane A(2) production by bone marrow-derived mast

36 In contrast, histamine did not stimulate thromboxane A(2) production in resting or LPS-activated

37 AYPGKF-induced thromboxane A(2) production in wild-type and P2Y(12) def

38 reas a marked inhibition of thrombin-induced thromboxane A(2) production was observed, which was foun

39 ibited by activation of the vasoconstricting thromboxane A(2) prostanoid receptor (TP), a mechanism s

40 Thromboxane synthase (TXAS) and thromboxane A(2) receptor (TP), two critical components

41 ecretion induced by arachidonic acid and the thromboxane A(2) receptor (TxA(2)R) agonist U46619 were

42 G(q) and G(13) (of the G(12) family) by the thromboxane A(2) receptor alpha (TPalpha), via agonist-e

43 Blockade of thromboxane A(2) receptor did not affect the serotonin r

44 on, localization, and functional coupling to thromboxane A(2) receptors (TPRs) during oligodendrocyte

45 Platelet phospholipase A(2) and thromboxane A(2) significantly decreased and vasodilator

46 erythrocytes blocked its ability to inhibit thromboxane A(2) synthesis and platelet aggregation.

47 Moreover, A23187-induced thromboxane A(2) synthesis, platelet aggregation, and se

48 ages with bacterial LPS increased PGI(2) and thromboxane A(2) to varied extents.

49 In contrast, production of thromboxane A(2) was significantly reduced, whereas prod

50 Neutrophil-produced thromboxane A(2) was the key eicosanoid controlling both

51 platelet aggregation induced by thrombin and thromboxane A(2) were also reversed by supplementing ADP

52 iene [LT] C(4), prostaglandin [PG] D(2), and thromboxane A(2)), which mediate vascular leak, bronchoc

53 elet recruitment, platelet isoprostanes, and thromboxane A(2), and increased vasodilator-stimulated p

54 expression; HMGB1 release; and secretions of thromboxane A(2), CXCL7, and IL-33 by mouse platelets we

55 The antagonism of the thromboxane A(2), cyclooxygenase-1/cyclooxygenase-2, or

56 elet recruitment, platelet isoprostanes, and thromboxane A(2), platelet Nox2, Rac1, p47(phox), protei

57 platelets bind collagen and release ADP and thromboxane A(2), recruiting additional platelets to a g

58 e concentrations of the prothrombic mediator thromboxane A(2), reduced brain infarcts, and decreased

59 ox2 and ultimately platelet isoprostanes and thromboxane A(2).

60 gregation induced by thrombin, collagen, and thromboxane A(2).

61 sence of exogenous adenosine diphosphate and thromboxane A(2).

62 quantified by ELISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expression determined by We

63 X-2) and the vasoconstrictor prostaglandins, thromboxane A2 (TXA2 ) and prostaglandin F2alpha (PGF2al

64 ion of vasoconstrictive prostanoids, such as thromboxane A2 (TXA2 ), contributes to endothelial dysfu

65 ation depends on secondary mediators such as thromboxane A2 (TxA2) and ADP, which are agonists for G-

66 de-out signaling because granular secretion, Thromboxane A2 (TxA2) generation, as well as fibrinogen

67 py, and dependent on inhibition of the COX-1/thromboxane A2 (TXA2) pathway.

68 olic phospholipase A2 (cPLA2) and consequent thromboxane A2 (TXA2) production.

69 S18886 is an orally active thromboxane A2 (TXA2) receptor (TP) antagonist in clinic

70 VPC31143 increased thromboxane A2 (TXA2) release from TA of wild-type, TP-K

71 VWF-induced Erk2 phosphorylation and thromboxane A2 (TXA2) release were completely blocked by

72 olipase C (PLC) inhibitor] or furegrelate [a thromboxane A2 (TXA2) synthesis inhibitor] 5 min prior t

73 pathway is unclear but is thought to involve thromboxane A2 (TXA2) synthesis.

74 Thromboxane A2 (TXA2) was the prostanoid product of COX-

75 dent of Syk, adenosine diphosphate (ADP), or thromboxane A2 (TXA2), in addition to their recognized r

76 adenosine triphosphate (ATP) secretion in a thromboxane A2 (TxA2)- and Ca2+-dependent manner.

77 alphaIIbbeta3 and elicits ATP secretion in a thromboxane A2 (TxA2)-dependent manner.

78 s that produce distinct eicosanoids, such as thromboxane A2 (TXA2).

79 me processing arachidonic acid to synthesize thromboxane A2 (TxA2).

80 us, the autocrine and paracrine functions of thromboxane A2 act downstream of LTC4/type 2 cysLT recep

81 induced in 8 pigs by intravenous infusion of thromboxane A2 analogue.

82 h plasma (PRP) and caused their secretion of thromboxane A2 and CXCL4.

83 logically and pathophysiologically important thromboxane A2 and endothelin-1 receptors.

84 ude that in a clinical setting in which both thromboxane A2 and iPF2alpha-III are elevated, suppressi

85 ate that this pathway requires production of thromboxane A2 and signaling through both hematopoietic

86 edback agonists adenosine 5'-diphosphate and thromboxane A2 are mandatory for platelet aggregation.

87 Andoh et al. demonstrate that the prostanoid thromboxane A2 elicits scratching through its TP recepto

88 ate platelet aggregation, ATP secretion, and thromboxane A2 generation by low doses of collagen (<1 m

89 integrin signaling, platelet secretion, and thromboxane A2 generation.

90 n platelets, with functional implications in thromboxane A2 generation.

91 f PKCdelta dramatically blocked PAR-mediated thromboxane A2 generation.

92 with U-46619, a stable mimetic of endogenous thromboxane A2 implicated in the etiology of cerebral va

93 ction, elevated oxidant stress and increased thromboxane A2 improve perfusion-based outcomes.

94 exes, suggesting a possible role of platelet thromboxane A2 in microvascular occlusion.

95 ory vascular reactions but is independent of thromboxane A2 levels, changes in blood pressure, or lip

96 Urinary thromboxane A2 metabolites, in contrast, were significan

97 platelet-rich plasma (PRP) treated with the thromboxane A2 mimetic U46619, collagen and thrombin in

98 evidence: (i) inhibition of MaxiK current by thromboxane A2 mimetic, U46619, occurs even when G-prote

99 lar metabolism before the resulting products thromboxane A2 or LTC4 can activate their cognate recept

100 -based activation motif pathway, and ADP and thromboxane A2 pathways.

101 eatment reduced interleukin-1beta-stimulated thromboxane A2 production in the pulmonary epithelial ce

102 ergic constriction combined with an elevated thromboxane A2 production may contribute to impaired fun

103 Interestingly, thromboxane A2 production was markedly increased in resp

104 are more susceptible to an increase in RVSP, thromboxane A2 production, and vascular remodeling than

105 ial decrease in prostacyclin production over thromboxane A2 production, thus leading to less gastric

106 rostaglandin F2alpha receptor (FP) (61), and thromboxane A2 receptor (TP) (11) while sparing EP2, EP3

107 structural flexibility of the purified human thromboxane A2 receptor (TP) was characterized by spectr

108 Human thromboxane A2 receptor (TP), a G protein-coupled recept

109 ted to elucidate the molecular mechanisms of thromboxane A2 receptor (TP)-induced insulin resistance

110 racterization of the signaling properties of thromboxane A2 receptor (TPalpha) -Galpha12 and -Galpha1

111 n interacting partner of the beta-isoform of thromboxane A2 receptor (TPbeta) by yeast two-hybrid scr

112 Thromboxane A2 receptor (TPr) stimulation induces cellul

113 d created by oxidative stress, activates the thromboxane A2 receptor (TXAR) and the Rho-associated ki

114 e to inhibit vasoconstriction induced by the thromboxane A2 receptor agonist U46619, which suggest a

115 We explore here, using the thromboxane A2 receptor TPalpha, the ability of G12 and

116 Here, we show that vasopressive thromboxane A2 receptors (TP) can intimately couple with

117 in E2 (EP)1, EP4, prostaglandin F2alpha, and thromboxane A2 receptors but not anti-inflammatory EP2,

118 (S)-HETE, in addition to prostanoids such as thromboxane A2 Releasates from activated platelets cause

119 LPA1 receptor-mediated thromboxane A2 release is responsible for lysophosphatid

120 Thus, thromboxane A2 signaling within the intact cerebral vasc

121 g that inhibits phosphodiesterase as well as thromboxane A2 synthase.

122 nd PGD2 synthase, and also between COX-1 and thromboxane A2 synthase.

123 lin, prostaglandin E2, prostaglandin D2, and thromboxane A2 were also reduced.

124 PGF2alpha and a purported antagonist (pinane thromboxane A2), was silent.

125 Prostaglandin E2 and thromboxane A2, as well as total APP levels, were found

126 hed eicosanoid synthesis in platelets (e.g., thromboxane A2, control 20.5 +/- 1.4 ng/ml vs. patient 0

127 d in part by the balance of prostacyclin and thromboxane A2, many other substances are involved in th

128 serum thromboxane B2, a stable metabolite of thromboxane A2, may be implicated in post-PCI microvascu

129 Platelet activation by thrombin, thromboxane A2, or ADP stimulates the association of 14-

130 g to RGS18 even in the presence of thrombin, thromboxane A2, or ADP.

131 e absence of Grb2 can be compensated through thromboxane A2-induced G protein-coupled receptor signal

132 with exogenous cyclic nucleotides inhibited thromboxane A2-induced MYPT1 membrane association, RhoA

133 etion, and aggregation, but not with ADP and thromboxane A2-mediated pathways.

134 e thrombin generation plus aspirin to reduce thromboxane A2-mediated platelet activation is superior

135 evels can be increased through activation of thromboxane A2-prostanoid (TP) receptors on neurons.

136 GS in these cell lines blocked thrombin- and thromboxane A2-stimulated cell invasion.

137 sphatidic acid, sphingosine-1-phosphate, and thromboxane A2.

138 soluble agonists such as thrombin, ADP, and thromboxane A2.

139 Furthermore, SQ29548, a thromboxane A2/prostaglandin H2 receptor antagonist, sig

140 -)- and ONOO(-)-dependent PGIS nitration and thromboxane A2/prostaglandin H2 receptor stimulation.

141 vasoconstriction by way of activation of the thromboxane-A2 /prostaglandin-endoperoxide (TP) receptor

142 uced vasoconstriction was dependent on a non-thromboxane agonist of the thromboxane receptor, whereas

143 tometry, without and with stimulation by the thromboxane analog U46619 or ADP.

144 from euglycemic pigs to endothelin-1 (ET-1), thromboxane analog U46619, and norepinephrine were media

145 han the predominantly Galpha(12/13)-mediated thromboxane analog U46619.

146 induced only by 5 muM ADP and 10 muM of the thromboxane analog, U46619.

147 rthermore, 5,6-EET could be metabolized to a thromboxane analog.

148 ated the constriction with serotonin and the thromboxane-analog U-46619 in arteries +E.

149 kg; i.v.) inhibited COX-1, measured as blood thromboxane and COX-2, measured as lung PGE2.

150 identified that the cyclooxygenase products thromboxane and PGF2alpha are released from coronary art

151 e-2 inhibitors create an 'imbalance' between thromboxane and prostacyclin (reduction of prostacyclin)

152 duct formation, while triggering prostanoid (thromboxane and prostaglandin D(2) and E(2) ) production

153 coronary vasoconstrictor after stenting, and thromboxane and TNFalpha somewhat potentiate the seroton

154 , and norepinephrine were mediated by ET(A), thromboxane, and alpha(2)-adrenergic receptors, respecti

155 atory eicosanoids, including prostaglandins, thromboxanes, and leukotrienes, are critical mediators o

156 M, and the effect was not altered by a DP(2)/thromboxane antagonist or by a peroxisome proliferator-a

157 Thromboxane appears to mediate the PVAT-induced contract

158 Prostaglandins (PGs) and thromboxanes are produced in vivo both from the omega 6

159 f proinflammatory cysteinyl leukotrienes and thromboxanes at the feeding site.

160 ion risk score, clopidogrel use), both serum thromboxane B(2) >3.1 ng/mL and PFA-100 collagen-ADP CT

161 (PFA)-100, and levels of urinary 11-dehydro-thromboxane B(2) (11-dh-TxB(2)).

162 ns PGD(2) and PGE(2) from RAW264.7 cells and thromboxane B(2) (TXB(2)) from human alveolar macrophage

163 California), and urine levels of 11-dehydro-thromboxane B(2) (UTXB(2)).

164 al platelet COX-1 function measured by serum thromboxane B(2) and COX-1-independent platelet function

165 platelet function directly (eg, via reducing thromboxane B(2) and modulating phosphatidylserine expre

166 l as their products PGE(2), PGF(2alpha), and thromboxane B(2) and their receptors following stimulati

167 ia increased vitreous levels of ET-1 but not thromboxane B(2) In conclusion, both in vitro and in viv

168 sis, COX-1-dependent assays, including serum thromboxane B(2) level, were not associated with adverse

169 iene E(4), prostaglandin D(2) metabolite, or thromboxane B(2) levels; and did not display increases i

170 icantly increased and prostaglandin E(2) and thromboxane B(2) significantly decreased in the airways,

171 injury, produced more prostaglandin E(2) and thromboxane B(2), and had greater expression of prostagl

172 Serotonin, thromboxane B(2), and TNFalpha release into aspirate pla

173 se of catecholamines, endothelin, serotonin, thromboxane B(2), and tumor necrosis factor (TNF)alpha w

174 taglandin (PG)E(2), PGD(2), PGF(2alpha), and thromboxane B(2), as well as the expression of proinflam

175 rations at dosages that did not affect serum thromboxane B(2), consistent with a selective COX-2 effe

176 derivatization method allows prostaglandins, thromboxane B(2), leukotriene B(4), hydroxyeicosatetraen

177 Platelet function was tested by (1) serum thromboxane B(2); (2) arachidonic acid-stimulated platel

178 ionship between PCSK9 and urinary 11-dehydro-thromboxane B2 (11-dh-TxB2), a marker of platelet activa

179 F=3.64; P=0.01334) and correlated with serum thromboxane B2 (rho=0.31; P=0.0413) in control but not i

180 Serum thromboxane B2 (sTXB2), a validated biomarker of platele

181 Levels of PGF2alpha and thromboxane B2 (TXB2 ) were quantified by ELISA, and PGF

182 etter understand aspirin "resistance," serum thromboxane B2 (TXB2) and flow cytometric measures of ar

183 y the rate and extent of inhibition of serum thromboxane B2 (TXB2) generation.

184 e P-selectin, soluble CD40 ligand, and serum thromboxane B2 (TxB2) were measured.

185 lipopolysaccharide: prostaglandin E2 (PGE2)>thromboxane B2 (TxB2)>6-keto prostaglandin F1alpha (PGF1

186 yl leukotrienes, leukotriene B4 , 11-dehydro-thromboxane B2 , and prostaglandins E2 , D2 , and F2alph

187 Levels of thromboxane B2 and 12-hydroxyeicosatetraenoic acid produ

188 ines (TNF-alpha, IL-6, CXCL8), IL-12, CCL11, thromboxane B2 and immunoglobulin E at 24 h after local

189 and isofuranes, markers of oxidative stress, thromboxane B2 and immunoglobulin E were measured in bro

190 nd activation were assessed by aggregometry, thromboxane B2 assay, or FACS.

191 lush grade=3 exhibited lower values of serum thromboxane B2 compared with those with myocardial blush

192 looxygenase metabolites prostaglandin E2 and thromboxane B2 differed at baseline.

193 assay for the clopidogrel response and serum thromboxane B2 for the aspirin response) and aggregation

194 serum hemolytic activity and increase plasma thromboxane B2 levels in rats.

195 VerifyNow Aspirin assays and serum thromboxane B2 measurements were performed.

196 pe of psoriasis, including activation of the thromboxane B2 pathway, which should be considered a bio

197 nary biomarker evidence of activation of the thromboxane B2 pathway.

198 ted arachidonic acid-induced aggregation and thromboxane B2 production by > or = 99% (P<0.0001).

199 Serum thromboxane B2 significantly increased after 120 minutes

200 din E2, 11-hydroxyeicosatetraenoic acid, and thromboxane B2 were identified as differentiating metabo

201 creases in concentrations of prostaglandins, thromboxane B2, 15-HETE and 11-HETE in cerebellar sample

202 We analyzed whether serum thromboxane B2, a stable metabolite of thromboxane A2, m

203 flammatory leukotriene B4 and procoagulating thromboxane B2, as well as lower specialized proresolvin

204 , M1 and M2 phenotypes were distinguished by thromboxane B2, prostaglandin (PG) E2, and PGD2 producti

205 Serum levels of thromboxane B2, reperfusion indexes (corrected Thromboly

206 537 on leukotriene, HETE, prostaglandin, and thromboxane biosynthesis in stimulated whole blood.

207 nted PGI(2) expression, and had no effect on thromboxane biosynthesis in vivo.

208 rin 100 mg/day seems insufficient to inhibit thromboxane biosynthesis.

209 Inhibition of urinary thromboxane excretion and platelet activation in pathway

210 ast, inhibition of connexins, P2Y12, P2Y1 or thromboxane formation had no effect on synchrony or ball

211 ion can be explained by a greater release of thromboxane from PVAT from female animals and greater se

212 The rate and extent of serum thromboxane generation and aspirin pharmacokinetics were

213 which inhibits cyclooxygenase-1 activity and thromboxane generation in platelets, reduces early SVG o

214 Aspirin-insensitive thromboxane generation measured by UTXB(2) and shear-dep

215 ad no affect on ADP-induced aggregation when thromboxane generation was blocked.

216 nPKCeta positively regulates agonist-induced thromboxane generation with no effects on platelet aggre

217 ted to increased MAPK pathway activation and thromboxane generation.

218 lphaIIbbeta3 signaling, which contributes to thromboxane generation.

219 inhibitor of nPKCeta, inhibited ADP-induced thromboxane generation.

220 ts, through inhibition of ERK activation and thromboxane generation.

221 X-V, integrin alpha(IIb)beta(3,) P2Y(12), or thromboxane generation.

222 OX-2-derived PGI2 and COX-1-derived platelet thromboxane is misplaced.

223 anoids such as prostaglandins, leukotrienes, thromboxanes, isoprostanes, resolvins, hydroxides, hydro

224 ic acid-derived eicosanoids (prostaglandins, thromboxanes, leukotrienes, and other oxidized derivativ

225 D prostanoid receptor 1 (DP(1)) or the thromboxane-like prostanoid (TP) receptor did not play a

226 duction induced by PGD2, while the selective thromboxane-like prostanoid receptor antagonist SQ29548

227 Ramatroban, a dual CRTH2/thromboxane-like prostanoid receptor antagonist, markedl

228 /- 0.8 pmol/mg creatinine [Cr], P < .05) and thromboxane metabolite (TX-M; 1.4 +/- 0.3 vs 0.9 +/- 0.1

229 Urinary prostaglandin D(2) and thromboxane metabolites decreased in both groups.

230 ,15-EET, the opioid antagonist naloxone, the thromboxane mimetic U46619, or the cannabinoid antagonis

231 h an H2S donor, after preconstriction with a thromboxane mimetic, resulted in dose-dependent vasorela

232 elet factor 4, beta-thromboglobulin, RANTES, thromboxane, or serotonin) in the pathogenesis of allerg

233 e sensitive at characterizing defects in the thromboxane pathway, which presented with normal respons

234 improved graft survival and decreased plasma thromboxane, platelet factor 4 (CXCL4), and IFN-gamma.

235 when activated, which then induces platelet thromboxane production by signaling through platelet-exp

236 olished VWF-induced platelet aggregation and thromboxane production in non-aspirin-treated washed pla

237 mg/d are adequate to fully inhibit platelet thromboxane production, dosages as high as 1300 mg/d are

238 dium arachidonate or ADP; 3) agonist-induced thromboxane production; and 4) NO production, cGMP synth

239 l concentrations of ADP, collagen, thrombin, thromboxane, prostacyclin, and nitric oxide.

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

241 iscovered a robust voltage dependence of the thromboxane receptor (TP receptor) on the receptor level

242 effect of 8-iso-PGF2alpha was mimicked by a thromboxane receptor (TP) agonist (U46619) and blocked b

243 aglandin E(2) receptor subtype 4 (EP(4)) and thromboxane receptor (TP).

244 L receptor-deficient mice) by activating the thromboxane receptor (TP).

245 TXA2 and isoprostanes) which act through the thromboxane receptor (TP).

246 The voltage-induced modulation of thromboxane receptor activity was observed on the level

247 ed human platelet aggregation induced by the thromboxane receptor agonist U46,619, and this effect wa

248 selectively blocked both ADP-stimulated and thromboxane receptor agonist U46619-stimulated platelet

249 amine, antioxidant treatment with Tempol and thromboxane receptor antagonism with SQ-29548) were show

250 oxygenase inhibitor, or SQ29548, a selective thromboxane receptor antagonist.

251 tease-activated receptor-1) antagonists, and thromboxane receptor antagonists.

252 with little further antagonism by additional thromboxane receptor blockade.

253 ipase A2, cyclooxygenase, or blockade of the thromboxane receptor markedly reduced the effects of H2S

254 n potential.(1) Their studies reveal a novel thromboxane receptor mutation (TP-V241G) in humans that

255 Inhibition of the thromboxane receptor or cyclooxygenase-2 dramatically at

256 nocytes and macrophages depends on autocrine thromboxane receptor signaling and that under normal con

257 d LDL-mediated PGIS nitration and associated thromboxane receptor stimulation might be important in t

258 cement by activating PGF(2alpha) receptor or thromboxane receptor, or approximately 15% enhancement b

259 ependent on a non-thromboxane agonist of the thromboxane receptor, whereas vasodilatory mechanisms of

260 h is mediated, in part, by activation of the thromboxane receptor.

261 ndertaken to determine the potential role of thromboxane receptors (TP) in bladder cancer.

262 and prostaglandin E(2) receptors as well as thromboxane receptors are activated upon depolarization,

263 menon by demonstrating that H1 histamine and thromboxane receptors utilize the same mechanism to augm

264 ion activated trapped platelets (assessed by thromboxane release).

265 ce of adenosine = 20-HETE > angiotensin II > thromboxane = superoxide > renal nerves > ATP.

266 Thromboxane synthase (TXAS) and thromboxane A(2) recepto

267 ntly, we reported prognostic significance of thromboxane synthase (TXAS) gene expression in invasive

268 Thromboxane synthase (TXAS) is one of the enzymes downst

269 xpression of nuclear factor-kappaB-dependent thromboxane synthase and microsomal PGE(2) synthase was

270 xane A(2) (TxA(2)) is a prostanoid formed by thromboxane synthase using the cyclooxygenase product pr

271 Previously, increased expression of thromboxane synthase was found in prostate tumors, and t

272 ell motility was attenuated by inhibitors of thromboxane synthase.

273 feres with the aspirin-induced inhibition of thromboxane synthesis and/or activation of the nitric ox

274 Blocking thromboxane synthesis reversed that finding and also nor

275 not modify the aspirin-induced inhibition of thromboxane synthesis, and inhibits the aspirin-induced

276 l role in the catalysis of prostaglandin and thromboxane synthesis.

277 d not modify the L-ASA-induced inhibition of thromboxane synthesis; and 3) prevented the L-ASA-induce

278 oxygenase pathway forming prostaglandins and thromboxanes, the lipoxygenase pathway generating leukot

279 plaque-like deposits, this was blocked by a thromboxane (TP) receptor antagonist, suggesting that TP

280 ation (EDH) is lost following stimulation of thromboxane (TP) receptors, an effect that may contribut

281 Platelet thromboxane (Tx) A(2) (P < 0.001) was inhibited in all a

282 Suppression of thromboxane (Tx) A(2) biosynthesis retards atherogenesis

283 pha1-adrenergic agonist phenylephrine or the thromboxane (TX) A2 analog U-46619 were similar between

284 In smokers, the biosynthesis of both thromboxane (Tx) A2 and prostacyclin is increased.

285 Thromboxane (TX) A2 is released from multiple cell types

286 aspirin leads to long-lasting suppression of thromboxane (TX) A2 production and TXA2-mediated platele

287 ro through the inhibition of COX-1-dependent thromboxane (TX) A2.

288 We investigated in vivo thromboxane (TX) and prostacyclin (PGI2) biosynthesis an

289 d human platelets, coincident with increased thromboxane (Tx) formation.

290 COX-1-mediated platelet thromboxane (TX) production has been proposed to promote

291 expression of both prostacyclin (PGI(2)) and thromboxane (Tx) synthases in endothelial cells, and VSM

292 This is coupled with enhanced levels of thromboxane (TX), an eicosanoid that facilitates platele

293 enase (COX)-1 activity and the production of thromboxane (Tx)A(2) , a pro-thrombotic eicosanoid.

294 omitant inhibition of platelet COX-1-derived thromboxane (Tx)A(2).

295 Generation of both thromboxane (Tx)A2 and the isoprostane, 8, 12 -iso iPF(2

296 the TP) for the cyclooxygenase (COX) product thromboxane (Tx)A2, retards atherogenesis in apolipoprot

297 Plasma thromboxane (TX)B2, an indicator of platelet reactivity,

298 extracellular-regulated kinase (ERK1/2) and thromboxane (TxA(2)) synthesis was dependent on both p11

299 en shown that ADP-, but not thrombin-induced thromboxane (TxA2) generation depends on integrin signal

300 olved in the synthesis of prostaglandins and thromboxanes, which are regulators of biologic processes