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Journal articles on the topic 'TXA2'

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Published: 4 June 2021

Last updated: 7 February 2022

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1

Chueh, Tsung-Hung, Yu-Hsiuan Cheng, Kuo-Hsin Chen, and Chiang-Ting Chien. "Thromboxane A2 Synthase and Thromboxane Receptor Deletion Reduces Ischaemia/Reperfusion-Evoked Inflammation, Apoptosis, Autophagy and Pyroptosis." Thrombosis and Haemostasis 120, no. 02 (2019): 329–43. http://dx.doi.org/10.1055/s-0039-3400304.

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Abstract Aim Enhancement of thromboxane A2 (TXA2) synthase (TXAS) activity, TXA2 release, and thromboxane prostanoid (TP) receptor activation leads to vasoconstriction and oxidative injury. We explored whether genetic deletion of TXAS/TXA2/TP signalling may reduce renal ischaemia/reperfusion (I/R) injury in mice. Materials and Methods Renal haemodynamics and function were evaluated in TXAS+/+TP+/+ (wild-type, WT), TXAS−/− (TXS−/−), TP−/− and TXAS−/−TP−/− (double knockout, dKO) mice in response to intravenous TXA2 mimetic-U46619 and 45-minute renal ischaemia and 4-hour reperfusion injury. We ex

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Chiang, Chih-Yao, Chen-Yen Chien, Wei-Yin Qiou, et al. "Genetic Depletion of Thromboxane A2/Thromboxane-Prostanoid Receptor Signalling Prevents Microvascular Dysfunction in Ischaemia/Reperfusion Injury." Thrombosis and Haemostasis 118, no. 11 (2018): 1982–96. http://dx.doi.org/10.1055/s-0038-1672206.

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Objective Activation of thromboxane A2 synthase (TXAS)/thromboxane A2 (TXA2)/thromboxane prostanoid (TP) receptor leads to arterial constriction, platelet aggregation and vascular injury. We attempted to characterize the microvascular dysfunction in ischaemia/reperfusion injury using genetically modified TXAS−/−, TP−/− and TXAS−/−TP−/− mice. Approach and Results The cardiac micro-circulation and electrocardiograms were evaluated from B6, TXAS−/−, TP−/− and TXAS−/−TP−/− mice in response to intravenous saline, endothelin-1, U46619 (a TXA2 agonist) and myocardial ischaemia/reperfusion injury. Car

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Hadiyanti, Nur, Didik Hasmono, and Mohammad Saiful Islam. "Analysis of Differences of Serum Thromboxane B2 Level after Taking Acetosal in Acute Thrombotic Stroke with Diabetes Mellitus and Non-Diabetes Mellitus." Folia Medica Indonesiana 54, no. 1 (2018): 53. http://dx.doi.org/10.20473/fmi.v54i1.8053.

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Endothelial dysfunction and vascular injuries are the early processes in thrombogenesis leading to thrombotic stroke. These processes trigger platelet activation characterized by synthesis of Thromboxane A2, potent agonist in platelet aggregation. Acetosal (ASA) 100 mg usually given to thrombotic stroke patients exerts its pharmacological effect by inhibition of TxA2 synthesis, thus could prevent thrombus formation. Diabetes mellitus (DM) as risk factor of thrombotic stroke exhibits an increase in TxA2 synthesis. It is not known whether ASA 100 mg could inhibit TxA2 adequately in diabetic pati

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Weber, C., J. R. Beetens, F. Tegtmeier, et al. "Ridogrel Inhibits Systemic and Renal Formation of Thromboxane A2 and Antagonizes Platelet Thromboxane A2/Prostaglandin Endoperoxide Receptors upon Chronic Administration to Man." Thrombosis and Haemostasis 68, no. 02 (1992): 214–20. http://dx.doi.org/10.1055/s-0038-1656351.

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SummaryThe effects of ridogrel, a dual thromboxane A2 (TXA2) synthase inhibitor and TXA2/prostaglandin (PG) endoperoxide receptor antagonist, on systemic and renal production of prostaglandins and on platelet TXA2/PG endoperoxide receptors was evaluated upon chronic administration (300 mg b. i. d. orally, for 8 and 29 days) to man. Such a medication with ridogrel inhibits the systemic as well as the renal production of TXA2 as measured by the urinary excretion of 2,3-dinor-TXB2 and TXB2 respectively without inducing significant changes in systemic or renal PGI2 production. Simultaneously with

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Cudd, T. A., and C. E. Wood. "Does thromboxane mediate the fetal ACTH response to acidemia?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 3 (1996): R594—R598. http://dx.doi.org/10.1152/ajpregu.1996.270.3.r594.

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Intravenous mineral acid infusions into fetal sheep stimulate increases in plasma adrenocorticotropic hormone (ACTH) and cortisol concentrations that correlate to the induced changes in arterial pH (pHa). We have recently demonstrated that ACTH and cortisol responses to mineral acid infusion in adult sheep are mediated by thromboxane A2 (TxA2). We designed the present experiments to test the hypothesis that fetal ACTH and cortisol responses are also mediated by TxA2. We infused chronically instrumented fetal sheep with 1 N HCl (0.5 ml/min i.v.) for 60 min, with or without pretreatment with the

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6

Cong, Ping, Zuo-Liang Xiao, Piero Biancani, and Jose Behar. "Prostaglandins mediate tonic contraction of the guinea pig and human gallbladder." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 1 (2007): G409—G418. http://dx.doi.org/10.1152/ajpgi.00091.2006.

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The gallbladder (GB) maintains tonic contraction modulated by neurohormonal inputs but generated by myogenic mechanisms. The aim of these studies was to examine the role of prostaglandins in the genesis of GB myogenic tension. Muscle strips and cells were treated with prostaglandin agonists, antagonists, cyclooxygenase (COX) inhibitors, and small interference RNA (siRNA). The results show that PGE2, thromboxane A2 (TxA2), and PGF2α cause a dose-dependent contraction of muscle strips and cells. However, only TxA2 and PGE2 (E prostanoid 1 receptor type) antagonists induced a dose-dependent decre

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Giubilato, Simona, Andrea Leo, Nicola Cosentino, et al. "Predictors of thromboxane levels in patients with non-ST-elevation acute coronary syndromes on chronic aspirin therapy." Thrombosis and Haemostasis 108, no. 07 (2012): 133–39. http://dx.doi.org/10.1160/th11-09-0635.

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SummaryHigh levels of thromboxane A2 (TxA2), a key mediator of platelet activation and aggregation, are associated with an increased risk of cardiovascular events. We aimed at assessing the predictors of higher plasma levels of TxB2, the stable metabolite of TxA2, in consecutive patients presenting with non-ST-elevation acute coronary syndrome (NSTE-ACS) on previous aspirin (ASA) treatment undergoing coronary angiography. Ninety-eight consecutive patients (age 61 ± 11, 75% males) with NSTE-ACS, on previous chronic ASA treatment, were prospectively enrolled in this study. Coronary disease exten

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Yokoyama, Yukihiro, Hongzhi Xu, Nicole Kresge, et al. "Role of thromboxane A2 in early BDL-induced portal hypertension." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 3 (2003): G453—G460. http://dx.doi.org/10.1152/ajpgi.00315.2002.

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Although the mechanisms of cirrhosis-induced portal hypertension have been studied extensively, the role of thromboxane A2 (TXA2) in the development of portal hypertension has never been explicitly explored. In the present study, we sought to determine the role of TXA2 in bile duct ligation (BDL)-induced portal hypertension in Sprague-Dawley rats. After 1 wk of BDL or sham operation, the liver was isolated and perfused with Krebs-Henseleit bicarbonate buffer at a constant flow rate. After 30 min of nonrecirculating perfusion, the buffer was recirculated in a total volume of 100 ml. The perfusa

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Xu, Hongzhi, Katarzyna Korneszczuk, Amel Karaa, Tian Lin, Mark G. Clemens, and Jian X. Zhang. "Thromboxane A2 from Kupffer cells contributes to the hyperresponsiveness of hepatic portal circulation to endothelin-1 in endotoxemic rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 2 (2005): G277—G283. http://dx.doi.org/10.1152/ajpgi.00256.2004.

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We examined the role of thromboxane A2 (TXA2) in LPS-induced hyperresponsiveness of hepatic portal circulation to endothelins (ETs) and whether Kupffer cells are the primary source of TXA2 release in response to ET-1 in endotoxemia. After 6 h of LPS (1 mg/kg body wt ip) or saline (control), liver was isolated and perfused with recirculating Krebs-Henseleit bicarbonate buffer at a constant flow rate (100 ml·min−1·kg body wt−1). ET-1 (10 pmol/min) was infused for 10 min. Portal pressure (PP) was continuously monitored during perfusion. Perfusate was sampled for enzyme immunoassay of thromboxane

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Grone, H. J., R. S. Grippo, W. J. Arendshorst, and M. J. Dunn. "Role of thromboxane in control of arterial pressure and renal function in young spontaneously hypertensive rats." American Journal of Physiology-Renal Physiology 250, no. 3 (1986): F488—F496. http://dx.doi.org/10.1152/ajprenal.1986.250.3.f488.

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As platelet and renal thromboxane (TX)A2 synthesis are increased in spontaneously hypertensive rats (SHR), we tested the hypothesis that increased renal TXA2 synthesis may cause the reduction in glomerular filtration rate (GFR), renal plasma flow (RPF), and the increase in arterial pressure in SHR of the Okamoto-Aoki strain. A selective inhibitor of TXA2 synthetase (UK 38485) was given acutely, with or without a TXA2 receptor antagonist (EP-092), to 6- to 8-wk-old SHR and age-matched Wistar-Kyoto rats (WKY) and chronically for 5.5 wk to 3.5-wk-old SHR. Inhibition of TXA2, measured by the stabl

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Fuse, I., M. Mito, A. Hattori, et al. "Defective signal transduction induced by thromboxane A2 in a patient with a mild bleeding disorder: impaired phospholipase C activation despite normal phospholipase A2 activation." Blood 81, no. 4 (1993): 994–1000. http://dx.doi.org/10.1182/blood.v81.4.994.994.

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Abstract A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A2 (TXA2) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in shape change, aggregation, and release reaction in response to synthetic TXA2 mimetic (STA2). When the platelet TXA2 receptor was examined with both a 125I-labeled derivative of a TXA2 receptor antagonist ([125I]-PTAOH) and [3H]-labeled TXA2 agonist ([3H]U-46619), the equilibrium dissociation rate constants (kd) and the maximal concentrations of binding sites (Bmax) of the platelets to

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Fuse, I., M. Mito, A. Hattori, et al. "Defective signal transduction induced by thromboxane A2 in a patient with a mild bleeding disorder: impaired phospholipase C activation despite normal phospholipase A2 activation." Blood 81, no. 4 (1993): 994–1000. http://dx.doi.org/10.1182/blood.v81.4.994.bloodjournal814994.

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A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A2 (TXA2) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in shape change, aggregation, and release reaction in response to synthetic TXA2 mimetic (STA2). When the platelet TXA2 receptor was examined with both a 125I-labeled derivative of a TXA2 receptor antagonist ([125I]-PTAOH) and [3H]-labeled TXA2 agonist ([3H]U-46619), the equilibrium dissociation rate constants (kd) and the maximal concentrations of binding sites (Bmax) of the platelets to both lig

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Packham, M. A., N. L. Bryant, M. A. Guccione, R. L. Kinlough-Rathbone, and J. F. Mustard. "Effect of the Concentration of Ca2+ in the Suspending Medium on the Responses of Human and Rabbit Platelets to Aggregating Agents." Thrombosis and Haemostasis 62, no. 03 (1989): 968–76. http://dx.doi.org/10.1055/s-0038-1651037.

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SummaryThe effect of the concentration of Ca2+ in the suspending medium of human and rabbit platelets on aggregation, release of 14C-serotonin, and TXB2 formation in response to ADP, thrombin, l-0-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (PAF), collagen and arachidonic acid was studied in either platelet-rich plasma anticoagulated with D-phenylalanyl-prolyl-arginyl chloromethylketone (PPACK) or citrate, or suspensions of washed platelets in modified Tyrode-albumin solutions containing 1 mM Mg2+ and concentrations of added Ca2+ ranging from 0 to 5 mM. In response to ADP, thrombin, or PAF,

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Sobrino, Agua, Pilar J. Oviedo, Susana Novella та ін. "Estradiol selectively stimulates endothelial prostacyclin production through estrogen receptor-α". Journal of Molecular Endocrinology 44, № 4 (2010): 237–46. http://dx.doi.org/10.1677/jme-09-0112.

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Estradiol (E2) acts on the endothelium to promote vasodilatation through the release of several compounds, including prostanoids, which are products of arachidonic acid metabolism. Among these, prostacyclin (PGI2) and thromboxane A2 (TXA2) exert opposite effects on vascular tone. The role of different estrogen receptors (ERs) in the PGI2/TXA2 balance, however, has not been fully elucidated. Our study sought to uncover whether E2 enhances basal production of PGI2 or TXA2 in cultured human umbilical vein endothelial cells (HUVECs), to analyze the enzymatic mechanisms involved, and to evaluate th

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Coceani, F., J. Lees, and I. Bishai. "Further evidence implicating prostaglandin E2 in the genesis of pyrogen fever." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 3 (1988): R463—R469. http://dx.doi.org/10.1152/ajpregu.1988.254.3.r463.

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Conscious cats were used to study the effects of endotoxin and interleukin 1 (IL 1) on levels of prostaglandin (PG) E2 and thromboxane (TX) B2 (the stable TXA2 byproduct) in cerebrospinal fluid (CSF) from the third ventricle. Pyrogens were given intravenously or intraventricularly and prostanoids were measured by radioimmunoassay. PGE2 was normally less abundant than TXB2 (mean, 37 vs. 528 pg/ml), and its level increased severalfold during the sustained fever following intravenous endotoxin (bolus) or IL 1 (bolus plus infusion). PGE2 elevation preceded the fever and was maintained thereafter.

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Patrignani, Paola, Concetta Di Febbo, Stefania Tacconelli, et al. "Reduced thromboxane biosynthesis in carriers of toll-like receptor 4 polymorphisms in vivo." Blood 107, no. 9 (2006): 3572–74. http://dx.doi.org/10.1182/blood-2005-12-4811.

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The recent demonstration that platelets express a functional toll-like receptor 4 (TLR4) prompted us to explore the influence of TLR4 polymorphisms (Asp299Gly alone or in combination with Thr399Ile) on thromboxane A2 (TXA2) biosynthesis in vivo. In 17 subjects with TLR4 polymorphisms versus 17 wild type (untreated with aspirin, matched for age, sex, and cardiovascular risk factors), intima-media thickness in the common carotid arteries was significantly lower. Average urinary excretion of 11-dehydro-TXB2, an index of systemic biosynthesis of TX, was significantly reduced by 65%. The urinary ex

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Moscardó, Antonio, María Paz Fuset, Miguel Ruano, María Teresa Santos, and Juana Vallés. "Residual cyclooxygenase-1 activity and epinephrine reduce the antiplatelet effect of aspirin in patients with acute myocardial infarction." Thrombosis and Haemostasis 105, no. 04 (2011): 663–69. http://dx.doi.org/10.1160/th10-08-0550.

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SummaryAspirin treatment is essential in patients with acute myocardial infarction (AMI) to block platelet thromboxane (TXA)2 synthesis. Epinephrine is known to enhance platelet reactivity induced by other agonists and to be elevated in patients with AMI due to stress. Our objective was to study the influence of epinephrine on platelet TXA2 synthesis in patients treated with aspirin for AMI at early onset (within 48 hours) and the potential biochemical mechanisms involved in the functional response. Washed platelets from 45 patients with AMI and 10 aspirin-free controls were stimulated with ar

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Hirakata, Hideo, Fumitaka Ushikubi, Hiroshi Toda, et al. "Sevoflurane Inhibits Human Platelet Aggregation and Thromboxane A2Formation, Possibly by Suppression of Cyclooxygenase Activity." Anesthesiology 85, no. 6 (1996): 1447–53. http://dx.doi.org/10.1097/00000542-199612000-00027.

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Background Halothane increases bleeding time and suppresses platelet aggregation in vivo and in vitro. A previous study by the authors suggests that halothane inhibits platelet aggregation by reducing thromboxane (TX) A2 receptor-binding affinity. However, no studies of the effects of sevoflurane on platelet aggregation have been published. Methods The effects of sevoflurane, halothane, and isoflurane were examined at doses of 0.13-1.4 mM. Human platelet aggregation was induced by adenosine diphosphate, epinephrine, arachidonic acid, prostaglandin G2, and a TXA2 agonist ([+]-9, 11-epithia-11,

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Jiang, Jihong, Linda Tran, Harish Vasudevan, Zhengyuan Xia, Violet G. Yuen, and John H. McNeill. "Endothelin-1 blockade prevents COX2 induction and TXA2 production in the fructose hypertensive ratThis paper is one of a selection of papers published in this Special Issue, entitled The Cellular and Molecular Basis of Cardiovascular Dysfunction, Dhalla 70th Birthday Tribute." Canadian Journal of Physiology and Pharmacology 85, no. 3-4 (2007): 422–29. http://dx.doi.org/10.1139/y06-088.

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Feeding rats with a high fructose diet results in insulin resistance and hypertension. Fructose-hypertensive rats (FHR) have increased vascular levels of endothelin-1 (ET-1) and thromboxane (TXA2). We have previously shown that chronic treatment with either the dual endothelin receptor blocker, bosentan, or the thromboxane synthase inhibitor, dazmegrel, prevented fructose-induced increases in blood pressure, suggesting that both ET-1 and TXA2 play important roles in the development of hyperinsulinemia/insulin resistance-associated hypertension. In this study, we investigated the potential inte

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Cudd, T. A., and C. E. Wood. "Thromboxane A2 receptor antagonism prevents hormonal and cardiovascular responses to mineral acid infusion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 5 (1994): R1235—R1240. http://dx.doi.org/10.1152/ajpregu.1994.267.5.r1235.

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Small infusions of strong acid create large elevations in heart rate (HR), mean arterial pressure (MAP), adrenocorticotropic hormone (ACTH), cortisol, and thromboxane A2 (TxA2). We hypothesized that TxA2 is responsible for these hormonal and hemodynamic responses. Conscious sheep received HCl (1 N, 1 ml/min for 30 min) with or without receiving SQ-29548 [a TxA2/prostaglandin (PG) H2 receptor antagonist]. HCl increased TxB2 from 133 +/- 44 to 1,213 +/- 531 (SE) pg/ml while SQ-29548 + HCl increased TxB2 from 141 +/- 41 to 1,051 +/- 518 pg/ml. HCl decreased pH (7.464 +/- 0.015 to 7.413 +/- 0.011)

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Johnson, Gerhard J., Linda A. Leis, and Richard A. King. "Thromboxane Responsiveness of Dog Platelets Is Inherited as an Autosomal Recessive Trait." Thrombosis and Haemostasis 65, no. 05 (1991): 578–80. http://dx.doi.org/10.1055/s-0038-1648193.

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SummaryMost mongrel dogs have platelets that form thromboxane A2 (TXA2) from exogenous arachidonate, but they fail to aggregate or secrete in response to it. In contrast to these TXA2 insensitive (TXA2-) platelets, some dogs have TXA2 sensitive (TXA2+) platelets that aggregate and secrete when stirred with arachidonate. To evaluate the possible genetic basis for this difference, we carried out seven matings of mongrel dogs that yielded 48 viable offspring. Four matings of dogs with TXA2- platelets (presumed genotype TT) including 2 back-crosses, produced 32 pups with TXA2- (TT) platelets and 0

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Ćavar, Ivan, Tomislav Kelava, Danijel Pravdić, and Filip Čulo. "Anti-thromboxane B2 antibodies protect against acetaminophen-induced liver injury in mice." Journal of Xenobiotics 1, no. 1 (2011): 8. http://dx.doi.org/10.4081/xeno.2011.e8.

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Prostanoids are lipid compounds that mediate a variety of physiological and pathological functions in almost all body tissues and organs. Thromboxane (TX) A2 is a powerful inducer of platelet aggregation and vasoconstriction and it has ulcerogenic activity in the gastrointestinal tract. Overdose or chronic use of a high dose of acetaminophen (N-acetyl-paminophenol, APAP) is a major cause of acute liver failure in the Western world. We investigated whether TXA2 plays a role in host response to toxic effect of APAP. CBA/H Zg mice of both sexes were intoxicated with a single lethal or high sublet

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Mederle, Katharina, Manuel Meurer, Hayo Castrop, and Klaus Höcherl. "Inhibition of COX-1 attenuates the formation of thromboxane A2 and ameliorates the acute decrease in glomerular filtration rate in endotoxemic mice." American Journal of Physiology-Renal Physiology 309, no. 4 (2015): F332—F340. http://dx.doi.org/10.1152/ajprenal.00567.2014.

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Thromboxane (Tx) A2 has been suggested to be involved in the development of sepsis-induced acute kidney injury (AKI). Therefore, we investigated the impact of cyclooxygenase (COX)-1 and COX-2 activity on lipopolysaccharide (LPS)-induced renal TxA2 formation, and on endotoxemia-induced AKI in mice. Injection of LPS (3 mg/kg ip) decreased glomerular filtration rate (GFR) and the amount of thrombocytes to ∼50% of basal values after 4 h. Plasma and renocortical tissue levels of TxB2 were increased ∼10- and 1.7-fold in response to LPS, respectively. The COX-1 inhibitor SC-560 attenuated the LPS-ind

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Papanicolaou, N., E. L. Gkika, G. Gkikas, and J. Bariety. "Selective Inhibition of Renal Thromboxane Biosynthesis Increased Sodium Excretion Rate in Normal and Saline-Loaded Rats." Clinical Science 68, no. 1 (1985): 79–82. http://dx.doi.org/10.1042/cs0680079.

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1. The excretion rates of renal thromboxane B2 (TXB2) and 6-ketoPGF1α, the stable chemical metabolites of thromboxane A2(TXA2) and prostaglandin I2 (PGI2) respectively, PGE2 and sodium were determined in normal and saline-loaded rats treated with the thromboxane synthetase inhibitor imidazole. 2. In normal rats the administration of imidazole in doses which did not affect renal 6-keto-PGF1α and PGE2 excretion but selectively inhibited renal TXB2 excretion, significantly increased the sodium excretion rate. 3. Volume expansion with saline increased renal PGE2 and 6-ketoPGF1α excretion but did n

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Deng, Qing-Ping, Mao-Jie Wang, Xing Zeng, George Gong Chen, and Run-Yue Huang. "Effects of Glycyrrhizin in a Mouse Model of Lung Adenocarcinoma." Cellular Physiology and Biochemistry 41, no. 4 (2017): 1383–92. http://dx.doi.org/10.1159/000467897.

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Background: Currently, there is a global attempt to identify potential anti-cancer agents with low toxicity. Previous studies have found that glycyrrhizin exerts anti-cancer action with low toxicity through suppressing thromboxane A2 (TxA2) in lung cancer cell lines. However, these effects have not yet been determined in animal models of lung cancer. Methods: Human lung adenocarcinoma xenografts were established in nude mice by the introduction of A549 cells with stable transfection of the TxA2 receptor (TPα). The animal model was confirmed by the hematoxylin and eosin (H&E) method. Tumor-

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Xiang, Anbo, Yoshiyuki Uchida, Akihiro Nomura, et al. "Involvement of thromboxane A2 in airway mucous cells in asthma-related cough." Journal of Applied Physiology 92, no. 2 (2002): 763–70. http://dx.doi.org/10.1152/jappl.2002.92.2.763.

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The aim of this study was to elucidate the role of thromboxane A2 (TxA2) on asthma-related cough in guinea pigs. Animals were immunosensitized and repeatedly challenged with ovalbumin as an antigen. Coughs were induced by the inhalation of 10−5 M capsaicin solution for 10 min. Thromboxane synthetase (TxS) inhibitor OKY-046 and thromboxane-receptor antagonist AA-2414 significantly inhibited cough responses in repeatedly challenged animals. Inhalation of TxA2 mimic STA-2- potentiated cough responses in normal and immunosensitized animals but not in repeatedly challenged ones. Moreover, STA-2-pot

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Yokoyama, Yukihiro, Balazs Toth, William C. Kitchens, Martin G. Schwacha, Kirby I. Bland, and Irshad H. Chaudry. "Role of thromboxane in producing portal hypertension following trauma-hemorrhage." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 6 (2003): G1293—G1299. http://dx.doi.org/10.1152/ajpgi.00268.2003.

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Thromboxane A2 (TXA2) and endothelin-1 (ET-1) have been proposed as the important vasoconstrictors that increase portal venous resistance in paracrine or autocrine fashion. We hypothesized that the hepatic damage following trauma-hemorrhage (T-H) is induced by the impaired hepatic circulation due to the increased production of vasoconstrictors such as ET-1 and TXA2 by the liver. To test this, male Sprague-Dawley rats ( n = 6/group) were subjected to trauma (i.e., midline laparotomy) and hemorrhage (35-40 mmHg for 90 min followed by fluid resuscitation) or sham operation. At 2 or 5 h after the

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Patel, Pravin, Meghna U. Naik, and Ulhas Naik. "Apoptosis Signal-Regulating Kinase (ASK1) Regulates Thrombosis in Part By Regulating cPLA2 phosphorylation-Dependent TxA2 Generation." Blood 128, no. 22 (2016): 3719. http://dx.doi.org/10.1182/blood.v128.22.3719.3719.

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Abstract When vascular endothelium is injured, circulating platelets are activated by primary agonists. Activation causes platelets to change shape, aggregate, and release secondary agonists which reinforce initial platelet activation as well as help recruit additional platelets to the site of vascular injury. MAP kinases have been shown to be important regulators of platelet function and secondary agonist production. One important secondary agonist released by activated platelets is TxA2. TxA2 is generated by metabolism of Arachidonic acid (AA). AA is released from platelet membrane phospholi

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Spurney, R. F., J. J. Onorato, F. J. Albers, and T. M. Coffman. "Thromboxane binding and signal transduction in rat glomerular mesangial cells." American Journal of Physiology-Renal Physiology 264, no. 2 (1993): F292—F299. http://dx.doi.org/10.1152/ajprenal.1993.264.2.f292.

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Thromboxane A2 (TxA2) stimulates contraction of glomerular mesangial cells. However, mesangial cell TxA2 receptors have not been previously characterized. We therefore investigated TxA2 binding and TxA2-associated signal transduction pathways in rat glomerular mesangial cells using the specific thromboxane receptor agonist (1S-[1 alpha,2 beta(5Z),3 alpha-(1E,3S)4 alpha])-7-(3-[3-hydroxy-4-(p- iodophenoxy)-1-butenyl]7-oxabicyclo[2.2.1]hept-2-yl)-5-heptenoic acid (IBOP). In these cells, [125I]BOP binding was saturable, displaceable, and of high affinity. Scatchard analysis revealed a single clas

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Ding, Yu-An, D. Euan MacIntyre, Christopher J. Kenyon, and Peter F. Semple. "Potentiation of Adrenaline-Induced Platelet Aggregation by Angiotensin II." Thrombosis and Haemostasis 54, no. 03 (1985): 717–20. http://dx.doi.org/10.1055/s-0038-1660105.

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SummaryThe effects of angiotensin II (ANG II) alone and in combination with other agonists on human platelet aggregation, thromboxane B2 (TxB2) and cytosolic [Ca2+]i were investigated. ANG II (10™11 - 10™7 M) alone had no direct effect on aggregation, TxB2 production or [Ca2+]i after short- (<2 min) or longterm (30 min) incubation. In contrast, low concentrations of ANG II (10™11 M) enhanced adrenaline-induced platelet aggregation but high concentrations (10™7 M) had an inhibitory effect. Moreover, ANG II (10™11 - 10™7 M) augmented platelet responses to the TxA2 mimetic, U44069. Pretreatmen

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31

Tomiyama, Yoshiaki, Shigenori Honda, Kayoko Senzaki та ін. "Difference of [Ca2+]i Movements in Platelets Stimulated by Thrombin and TRAP: the Involvement of αIIbβ3-Mediated TXA2 Synthesis". Thrombosis and Haemostasis 79, № 06 (1998): 1184–90. http://dx.doi.org/10.1055/s-0037-1615038.

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SummaryThis study investigated the difference of [Ca2+]i movement in platelets in response to thrombin and TRAP. The involvement of αIIbβ3 in this signaling was also studied. Stimulation of platelets with thrombin at 0.03 U/ml caused platelet aggregation and a two-peak increase in [Ca2+]i. The second peak of [Ca2+]i, but not the first peak was abolished by the inhibition of platelet aggregation with αIIbβ3 antagonists or by scavenging endogenous ADP with apyrase. A cyclooxygenase inhibitor, aspirin, and a TXA2 receptor antagonist, BM13505, also abolished the second peak of [Ca2+]i but not the

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32

de Castellarnau, C., C. Cullare, S. Lopez, et al. "Prostacyclin and Thromboxane Production by Autogenous Femoral Veins Grafted into the Arterial Circulation of the Dog." Thrombosis and Haemostasis 61, no. 02 (1989): 279–85. http://dx.doi.org/10.1055/s-0038-1646576.

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SummaryVascular prostacyclin (PGI2) production is different in the arteries and veins of the dog. Experiments were performed to determine whether chronic grafting of the femoral vein into the arterial circulation would alter the normal PGI2 and thromboxane (TxA2) synthesis of the “arterialized” veins. Spontaneous and arachidonic acid (AA) stimulated PGI2 and TxA2 production (measured by radioimmunoassay of 6-keto PGF1α and TxB2 respectively) were analysed in full thickness punch biopsies of the middle part of the grafts after 3 and 16 months and compared with unoperated veins and arteries. PGI

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Fukushima, M., and T. Kobayashi. "Effects of thromboxane synthase inhibition on air emboli lung injury in sheep." Journal of Applied Physiology 60, no. 6 (1986): 1828–33. http://dx.doi.org/10.1152/jappl.1986.60.6.1828.

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We tested the effects of OKY-046, a thromboxane synthase inhibitor, on lung injury induced by 2 h of pulmonary air infusion (1.23 ml/min) in the pulmonary artery of unanesthetized sheep with chronic lung lymph fistula so as to assess the role of thromboxane A2 (TxA2) in the lung injury. We measured pulmonary hemodynamic parameters and the lung fluid balance. The concentrations of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) in plasma and lung lymph were determined by radioimmunoassay. Air infusion caused sustained pulmonary hypertension and an increase in pulmonar

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34

Perico, N., A. Benigni, C. Zoja, F. Delaini, and G. Remuzzi. "Functional significance of exaggerated renal thromboxane A2 synthesis induced by cyclosporin A." American Journal of Physiology-Renal Physiology 251, no. 4 (1986): F581—F587. http://dx.doi.org/10.1152/ajprenal.1986.251.4.f581.

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Animals and humans undergoing a chronic treatment with cyclosporin A (CyA) show a reduction in glomerular filtration rate (GFR). The cause of this abnormality has not been established. Since CyA interferes with arachidonic acid (AA) metabolism in various cells, we wished to determine whether alterations in renal AA metabolites contribute to deteriorating renal function in rats on CyA. We show that chronic CyA treatment induces a progressive increase in the renal synthesis of thromboxane (TX) A2. This is a selective abnormality in that CyA does not influence the renal synthesis of prostaglandin

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35

Zahavi, J., and M. Zahavi. "Enhanced Platelet Release Reaction, Shortened Platelet Survival Time and Increased Platelet Aggregation and Plasma Thromboxane B2 in Chronic Obstructive Arterial Disease." Thrombosis and Haemostasis 53, no. 01 (1985): 105–9. http://dx.doi.org/10.1055/s-0038-1661246.

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SummaryPlasma β-thromboglobulin (βTG) and thromboxane B2 (TXB2) level, platelet aggregation (PA) in platelet rich plasma, platelet survival time using luIndium radiolabelled platelets and platelet sensitivity to prostacyclin (PGI2) were measured in chronic obstructive arterial disease (COAD) patients. Severity of the disease was assessed by the ankle pressure index using Doppler auscultation.Platelet survival time was shorter, plasma βTG and TXB2 and the rate and extent of PA induced by ADP or 1-epinephrine (but not collagen) were greater in the patients than in controls. βTG was inversly corr

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36

Spurney, R. F., J. P. Middleton, J. R. Raymond, and T. M. Coffman. "Modulation of thromboxane receptor activation in rat glomerular mesangial cells." American Journal of Physiology-Renal Physiology 267, no. 3 (1994): F467—F478. http://dx.doi.org/10.1152/ajprenal.1994.267.3.f467.

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Rat glomerular mesangial cells were used to investigate mechanisms of thromboxane A2 (TxA2) receptor regulation in the kidney. Exposure of mesangial cells to the TxA2 agonist U-46619 for 10 min reduced subsequent TxA2-induced increases in inositol phosphates and intracellular Ca2+ levels by approximately 70%. This loss of receptor responsiveness could be blocked by the TxA2 receptor antagonist SQ-29548 and was reversible after removal of agonist from the incubation medium. Radioligand binding studies using the TxA2 agonist [125I]BOP suggested that exposure of mesangial cells to U-46619 for 10

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37

Eldor, A., F. Lellouche, A. Goldfarb, EA Rachmilewitz, and J. Maclouf. "In vivo platelet activation in beta-thalassemia major reflected by increased platelet-thromboxane urinary metabolites." Blood 77, no. 8 (1991): 1749–53. http://dx.doi.org/10.1182/blood.v77.8.1749.1749.

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Abstract Increased frequency of thromboembolic events has been recently observed in patients with beta-thalassemia major (TM). Platelet function anomalies including impaired aggregation, increased circulating aggregates, and our finding of shortened platelet survival indicate that platelets may be involved in the hypercoagulability in thalassemia. Consequently, we used a technique based on thin layer chromatography purification and enzyme immunoassay to measure urinary metabolites of thromboxane A2 (TXA2) and prostacyclin (PGI2) in nine splenectomized patients with beta-TM regularly transfused

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38

Eldor, A., F. Lellouche, A. Goldfarb, EA Rachmilewitz, and J. Maclouf. "In vivo platelet activation in beta-thalassemia major reflected by increased platelet-thromboxane urinary metabolites." Blood 77, no. 8 (1991): 1749–53. http://dx.doi.org/10.1182/blood.v77.8.1749.bloodjournal7781749.

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Increased frequency of thromboembolic events has been recently observed in patients with beta-thalassemia major (TM). Platelet function anomalies including impaired aggregation, increased circulating aggregates, and our finding of shortened platelet survival indicate that platelets may be involved in the hypercoagulability in thalassemia. Consequently, we used a technique based on thin layer chromatography purification and enzyme immunoassay to measure urinary metabolites of thromboxane A2 (TXA2) and prostacyclin (PGI2) in nine splenectomized patients with beta-TM regularly transfused, five no

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39

Dragani, Alfredo, Silvia Pascale, Antonio Recchiuti, et al. "The contribution of cyclooxygenase-1 and -2 to persistent thromboxane biosynthesis in aspirin-treated essential thrombocythemia: implications for antiplatelet therapy." Blood 115, no. 5 (2010): 1054–61. http://dx.doi.org/10.1182/blood-2009-08-236679.

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Abstract We tested whether cyclooxygenase 2 (COX-2) expression and unacetylated COX-1 in newly formed platelets might contribute to persistent thromboxane (TX) biosynthesis in aspirin-treated essential thrombocythemia (ET). Forty-one patients on chronic aspirin (100 mg/day) and 24 healthy subjects were studied. Platelet COX-2 expression was significantly increased in patients and correlated with thiazole orange–positive platelets (r = 0.71, P < .001). The rate of TXA2 biosynthesis in vivo, as reflected by urinary 11-dehydro-TXB2 (TXM) excretion, and the maximal biosynthetic capacity of plat

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40

Dunlop, Patricia C., Linda A. Leis, and Gerhard J. Johnson. "Epinephrine correction of impaired platelet thromboxane receptor signaling." American Journal of Physiology-Cell Physiology 279, no. 6 (2000): C1760—C1771. http://dx.doi.org/10.1152/ajpcell.2000.279.6.c1760.

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This study evaluated the mechanism of epinephrine potentiation of platelet secretion induced by thromboxane A2(TXA2). Dog platelets that do not secrete in response to TXA2alone (TXA2−) were compared with dog platelets that do secrete (TXA2+) and with human platelets. TXA2− platelets had impaired TXA2receptor (TP receptor)-G protein coupling, indicated by 1) impaired stimulated GTPase activity, 2) elevated basal guanosine 5′- O-(3-thiotriphosphate) binding, and 3) elevated Gαqpalmitate turnover that was corrected by preexposure to epinephrine. Kinetic agonist binding studies revealed biphasic d

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Yong, E. C., E. Y. Chi, T. R. Fritsche, and W. R. Henderson. "Human platelet-mediated cytotoxicity against Toxoplasma gondii: role of thromboxane." Journal of Experimental Medicine 173, no. 1 (1991): 65–78. http://dx.doi.org/10.1084/jem.173.1.65.

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Human platelets, in the absence of antibody, are cytotoxic to tachyzoites of Toxoplasma gondii as determined by vital staining, transmission electron microscopy, and the failure of Toxoplasma to survive and replicate in mice after in vitro interaction of the organisms with platelets. Platelet to T. gondii ratios as low as 1:3 were toxic to the organisms with direct cell-cell contact essential for platelet-mediated cytotoxicity. Adherence of platelets to T. gondii and disruption of surface membranes and cytoplasmic contents of the organisms were observed ultrastructurally. Reactive oxygen speci

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Gonzales, Rayna J., Amir A. Ghaffari, Sue P. Duckles, and Diana N. Krause. "Testosterone treatment increases thromboxane function in rat cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 2 (2005): H578—H585. http://dx.doi.org/10.1152/ajpheart.00958.2004.

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We previously showed that testosterone, administered in vivo, increases the tone of cerebral arteries. A possible underlying mechanism is increased vasoconstriction through the thromboxane A2 (TxA2) pathway. Therefore, we investigated the effect of chronic testosterone treatment (4 wk) on TxA2 synthase levels and the contribution of TxA2 to vascular tone in rat middle cerebral arteries (MCAs). Using immunofluorescence and confocal microscopy, we demonstrated that TxA2 synthase is present in MCA segments in both smooth muscle and endothelial layers. Using Western blot analysis, we found that Tx

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Dorn, G. W. "Regulation of response to thromboxane A2 in CHRF-288 megakaryocytic cells." American Journal of Physiology-Cell Physiology 262, no. 4 (1992): C991—C999. http://dx.doi.org/10.1152/ajpcell.1992.262.4.c991.

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Thromboxane A2 (TxA2) is a potent platelet aggregating agent and a necessary intermediate for platelet stimulation by several other platelet agonists. A potentially important means whereby platelet responses to TxA2 could be modified in vivo is regulation of TxA2 receptors and/or effectors by platelet precursor megakaryocytes. We therefore investigated the mechanisms that regulate the response to TxA2 in CHRF-288, a cultured cell line derived from megakaryocytes. Incubation of CHRF-288 with the TxA2 agonist U-44069 resulted in a biexponential 75% decrease in subsequent TxA2 receptor-stimulated

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44

Toyofuku, T., T. Kobayashi, S. Koyama, and S. Kusama. "Pulmonary vascular response to platelet-activating factor in conscious sheep." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (1988): H434—H440. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h434.

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Hemodynamic response to an intravenous infusion of platelet-activating factor (PAF; 1 microgram/kg) was studied in conscious sheep with lung lymph fistulas. PAF induced increases in pulmonary arterial pressure and decreases in left atrial and systemic arterial pressures and in cardiac output, together with transient increases in thromboxane (Tx) A2 (as TxB2) and prostacyclin (as 6-keto-PGF1 alpha) values in plasma and lung lymph. There were also transient decreases in circulating leukocytes and platelets. The second infusion of PAF induced a reduced response compared with the first one, but th

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45

Geske, F. Jon, Beth Hurley, Amy Whittier, Daniel Tew, Gordon Ens, and Luis Lopez. "A New and Rapid Immunoassay for the Detection of 11-Dehydro-Thromboxane B2." Blood 106, no. 11 (2005): 2641. http://dx.doi.org/10.1182/blood.v106.11.2641.2641.

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Abstract Aspirin inactivates cyclooxygenase, inhibiting synthesis of thromboxane A2 (TxA2) and other molecules relevant in the development of atherothrombotic vascular events. There is recent evidence suggesting that many individuals are resistant to aspirin’s effects, resulting in increased TxA2 levels. Current methods for detecting aspirin resistance include a number of blood-based assays that measure in vitro platelet aggregation. However, these methods are not quantitative and can be affected by factors that are unrelated to aspirin sensitivity. There is a quantitative commercial immunoass

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46

Clerck, F. De, J. Beetens, D. de Chaffoy de Courcelles, E. Freyne, and P. A. J. Janssen. "R 68 070: Thromboxane A2 Synthetase Inhibition and Thromboxane A2/Prostaglandin Endoperoxide Receptor Blockade Combined in One Molecule - I. Biochemical Profile In Vitro." Thrombosis and Haemostasis 61, no. 01 (1989): 035–42. http://dx.doi.org/10.1055/s-0038-1646523.

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SummaryR 68 070 or (E)-5-[[[(3-pyridinyl)[3-(trifluoromethyl)phenyl]- methylen]amino]oxy] pentanoic acid (Janssen Research Foundation, Belgium) combines specific thromboxane A2 (TXA2) synthetase inhibition with TXA2/prostaglandin endoperoxide receptor blockade in one molecule.In vitro, the compound specifically inhibits the production of TXB2 from [14C] arachidonic acid by washed human platelets (IC50 = 8.2 × 10-9 M) and by platelet microsomes (IC50 = 3.6 × 10-9 M), of MDA (IC50 = 1.91 × 10-8 M) and of TXB2 (IC50 = 1.47 × 10-8 M) by thrombin-coagulated human platelet-rich plasma (P.R.P.) and w

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47

Melki, T. S., M. L. Foegh, and P. W. Ramwell. "Implication of thromboxane in frusemide diuresis in rats." Clinical Science 71, no. 6 (1986): 647–50. http://dx.doi.org/10.1042/cs0710647.

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1. Administration of the thromboxane A2 (TXA2) synthase inhibitor OKY 1581 to rats significantly increased the urine output elicited by the loop diuretic frusemide. 2. The administration of the TXA2 receptor antagonist SQ 29548 significantly increased the diuretic effect of frusemide. 3. Another TXA2 receptor antagonist L-640,035 increased significantly the diuretic effect of frusemide. 4. Both the sodium excretion rate and urine osmolar excretion rate were significantly increased in rats treated with the TXA2 synthase inhibitor OKY 1581 and frusemide. 5. The data suggest that TXA2 is released

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48

Wurtz, M. M., A. H. Stephenson, R. S. Sprague, and A. J. Lonigro. "Enhanced microvascular permeability of PMA-induced acute lung injury is not mediated by cyclooxygenase products." Journal of Applied Physiology 73, no. 5 (1992): 2135–41. http://dx.doi.org/10.1152/jappl.1992.73.5.2135.

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Products of cyclooxygenase activity have been proposed to mediate the pulmonary hypertension and increased microvascular permeability associated with phorbol myristate acetate- (PMA) induced acute lung injury. Previously, we reported that thromboxane (Tx) does not mediate PMA-induced pulmonary hypertension in intact anesthetized dogs. In the present study, PMA was administered to isolated canine lungs perfused with autologous blood at constant flow to investigate a possible role for Tx in the PMA-induced increase in microvascular permeability. Changes in permeability were assessed by determini

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49

Ushikubi, Fumitaka, Minoru Okuma, Kenji Kanaji, et al. "Hemorrhagic Thrombocytopathy with Platelet Thromboxane A2 Receptor Abnormality: Defective Signal Transduction with Normal Binding Activity." Thrombosis and Haemostasis 57, no. 02 (1987): 158–64. http://dx.doi.org/10.1055/s-0038-1651086.

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SummarySubnormal platelet responses to thromboxane A2 (TXA2) were found in a patient with polycythemia vera, and the mechanism of this dysfunction was analyzed. The patient’s platelets showed defective aggregation and release reaction to arachidonic acid, enzymatically generated TXA2 and synthetic TXA2 mimetics (STA2, U-46619). In contrast, they showed normal responses to thrombin. When the platelet TXA2 receptor was examined with both a 125I-labelled derivative of a TXA2 receptor antagonist ([125I]-PTA-OH) and a 3H-labelled TXA2 agonist ([3H]U-46619), the equilibrium dissociation rate constan

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Ushikubi, F., Y. Aiba, K. Nakamura, et al. "Thromboxane A2 receptor is highly expressed in mouse immature thymocytes and mediates DNA fragmentation and apoptosis." Journal of Experimental Medicine 178, no. 5 (1993): 1825–30. http://dx.doi.org/10.1084/jem.178.5.1825.

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We have recently revealed that the thymus is the organ showing the highest expression of thromboxane (TX) A2 receptor in mice. In this study, thymic cell populations expressing the receptor were identified, and the effects of a TXA2 agonist on these cells were examined. Radioligand binding using a TXA2 receptor-specific radioligand revealed a single class of binding sites in the thymocytes with an affinity and specificity identical to those reported for the TXA2 receptor. The receptor density in these cells was comparable to that seen in blood platelets. This receptor is most highly expressed

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