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Relevant bibliographies by topics / Prostacyclin synthase (PGIS)

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Academic literature on the topic 'Prostacyclin synthase (PGIS)'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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Journal articles on the topic "Prostacyclin synthase (PGIS)"

1

Fang, Yao-Ching, Jui-Sheng Wu, Jean-Ju Chen, et al. "Induction of Prostacyclin/PGI2 Synthase Expression After Cerebral Ischemia–Reperfusion." Journal of Cerebral Blood Flow & Metabolism 26, no. 4 (2005): 491–501. http://dx.doi.org/10.1038/sj.jcbfm.9600205.

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Prostacyclin (PGI2), a potent vasodilator and inhibitor of platelet aggregation and leukocyte activation, is crucial in vascular diseases such as stroke. Prostacyclin synthase (PGIS) is the key enzyme for PGI2 synthesis. Although expression of PGIS was noted in the brain, its role in ischemic insult remains unclear. Here we reported the temporal and spatial expression of PGIS mRNA and protein after 60-min transient ischemia. Northern blot and in situ hybridization revealed a delayed increase of PGIS mRNA in the ischemic cortex at 24- to 72-h after ischemia; PGIS was detected mainly in the ipsi

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Kengni, Junie Hurette Chansi, Isabelle St-Louis, Sophie Parent, Valérie Leblanc, Carl Shooner, and Eric Asselin. "Regulation of prostaglandin D synthase and prostacyclin synthase in the endometrium of cyclic, pregnant, and pseudopregnant rats and their regulation by sex steroids." Journal of Endocrinology 195, no. 2 (2007): 301–11. http://dx.doi.org/10.1677/joe-07-0353.

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Prostaglandins (PGs) are critical regulators of a number of reproductive processes. To date, the presence and regulation of PGS in the rat endometrium have not yet been described. The objective of the present study was to investigate the expression of PGD synthase (PGDS) and prostacyclin synthase (PGIS) in the endometrium. Endometrial proteins and tissues were collected from cyclic non-pregnant, pregnant, and steroid-induced pseudopregnant rats. PGIS and PGDS were detected in the endometrium of cyclic, pregnant, and pseudopregnant rats but were not influenced by the estrous cycle. During early

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Siegle, Isabel, Thomas Klein, Ming-Hui Zou, Peter Fritz, and Martin Kömhoff. "Distribution and Cellular Localization of Prostacyclin Synthase in Human Brain." Journal of Histochemistry & Cytochemistry 48, no. 5 (2000): 631–41. http://dx.doi.org/10.1177/002215540004800507.

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SUMMARY Prostacyclin (PGI2) is a labile, lipid-derived metabolite of arachidonic acid synthesized through the sequential action of cyclo-oxygenase (COX) and prostacyclin synthase (PGIS). In addition to its well-characterized vasodilatory and thrombolytic effects, an increasing number of studies report an important role of PGI2 in nociception in various animal species. In this study we investigated the regional distribution of PGIS in human brain by immunohistochemistry and in situ hybridization. PGIS-immunoreactive (ir) protein was localized to blood vessels throughout the brain. Neuronal cell

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Nakalekha, Chalida, Chieko Yokoyama, Hiroyuki Miura, et al. "Increased bone mass in adult prostacyclin-deficient mice." Journal of Endocrinology 204, no. 2 (2009): 125–33. http://dx.doi.org/10.1677/joe-09-0376.

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Prostaglandins (PGs) are key regulatory factors that affect bone metabolism. Prostaglandin E2 (PGE2) regulates bone resorption and bone formation. Prostacyclin (PGI2) is one of the major products derived from arachidonic acid by the action of cyclooxygenase and PGI2 synthase (PGIS). Unlike PGE2, there are few reports about the role of PGI2 in bone regulation. Therefore, we investigated the potential effect of PGI2 on bone metabolism. We used PGIS knockout (PGIS−/−), PGIS heterozygous (PGIS+/−), and wild-type mice to investigate the role of PGI2. Notably, PGIS−/− mice gradually displayed an inc

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Klein, Thomas, Günther Klaus, and Martin Kömhoff. "Prostacyclin Synthase: Upregulation during Renal Development and in Glomerular Disease as well as Its Constitutive Expression in Cultured Human Mesangial Cells." Mediators of Inflammation 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/654151.

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Prostacyclin (PGI2) plays a critical role in nephrogenesis and renal physiology. However, our understanding of how prostacyclin release in the kidney is regulated remains poorly defined. We studied expression of prostacyclin synthase (PGIS) in developing and adult human kidneys, and also in selected pediatric renal diseases. We also examined PGI2formation in human mesangial cellsin vitro. We observed abundant expression of PGIS in the nephrogenic cortex in humans andin situhybridization revealed an identical pattern in mice. In the normal adult kidney, PGIS-immunoreactive protein and mRNA appe

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Wang, Wei, Einath Zolty, Sandor Falk, et al. "Prostacyclin in endotoxemia-induced acute kidney injury: cyclooxygenase inhibition and renal prostacyclin synthase transgenic mice." American Journal of Physiology-Renal Physiology 293, no. 4 (2007): F1131—F1136. http://dx.doi.org/10.1152/ajprenal.00212.2007.

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Sepsis-related acute kidney injury (AKI) is the leading cause of AKI in intensive care units. Endotoxin is a primary initiator of inflammatory and hemodynamic consequences of sepsis and is associated with experimental AKI. The present study was undertaken to further examine the role of the endothelium, specifically prostacyclin (PGI2), in the pathogenesis of endotoxemia-related AKI. A low dose of endotoxin (LPS, 1 mg/kg) in wild-type (WT) mice was associated with stable glomerular filtration rate (GFR) (164.0 ± 16.7 vs. 173.3 ± 6.7 μl/min, P = not significant) as urinary excretion of 6-keto-PG

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Gnedenko, O. V., E. O. Yablokov, P. V. Ershov, et al. "Interaction of prostacyclin synthase with cytochromes P450." Biomeditsinskaya Khimiya 65, no. 1 (2019): 63–66. http://dx.doi.org/10.18097/pbmc20196501063.

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Biosensor experiments on investigation of interaction between prostacyclin synthase (PGIS) and different proteins of the cytochrome P450 monooxygenase systems were perfomed. Interaction of PGIS with microsomal (CYP21A2, CYP2E1) and mitochondrial (CYP27A1, CYP11B1, CYP11B2, CYP11A1) cytochrome P450s was detected. Kinetic and equilibrium parameters of protein complexes formation were determined. Data obtained suggest an essential role of these hemoproteins interaction in regulation of prostacyclin and thromboxane A2 biosynthesis.

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Tsai, May-Jywan, Ching-Feng Weng, Nien-Chu Yu, et al. "Enhanced Prostacyclin Synthesis by Adenoviral Gene Transfer Reduced Glial Activation and Ameliorated Dopaminergic Dysfunction in Hemiparkinsonian Rats." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/649809.

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Prostacyclin (PGI2), a potent vasodilator and platelet antiaggregatory eicosanoid, is cytoprotective in cerebral circulation. It is synthesized from arachidonic acid (AA) by the sequential action of cyclooxygenase- (COX-) 1 or 2 and prostacyclin synthase (PGIS). Because prostacyclin is unstablein vivo, PGI2analogs have been developed and demonstrated to protect against brain ischemia. This work attempts to selectively augment PGI2synthesis in mixed glial culture or in a model of Parkinson’s disease (PD) by direct adenoviral gene transfer of prostacyclin biosynthetic enzymes and examines whethe

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Klein, Thomas, Jens Benders, Friederike Roth, Monika Baudler, Isabel Siegle, and Martin Kömhoff. "Expression of Prostacyclin-Synthase in Human Breast Cancer: Negative Prognostic Factor and Protection against Cell DeathIn Vitro." Mediators of Inflammation 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/864136.

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Endogenously formed prostacyclin (PGI2) and synthetic PGI2analogues have recently been shown to regulate cell survival in various cell lines. To elucidate the significance of PGI2in human breast cancer, we performed immunohistochemistry to analyze expression of prostacyclin-synthase (PGIS) in 248 human breast cancer specimens obtained from surgical pathology files. We examined patients’ 10-year survival retrospectively by sending a questionnaire to their general practitioners and performed univariate analysis to determine whether PGIS expression correlated with patient survival. Lastly, the ef

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DENG, Hui, Aimin HUANG, Shui-Ping SO, Yue-Zhen LIN, and Ke-He RUAN. "Substrate access channel topology in membrane-bound prostacyclin synthase." Biochemical Journal 362, no. 3 (2002): 545–51. http://dx.doi.org/10.1042/bj3620545.

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Results from our molecular-modelling and site-directed-mutagenesis studies of prostaglandin I2 synthase (PGIS) have suggested that the large PGIS cytoplasmic domain is anchored to the endoplasmic reticulum (ER) membrane by the N-terminal segment in a way that orients the substrate access channel opening to face the membrane. To test this hypothesis we have explored the accessibility of the PGIS substrate channel opening to site-specific antibodies. The working three-dimensional PGIS model constructed by protein homology modelling was used to predict surface portions near the substrate access c

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Dissertations / Theses on the topic "Prostacyclin synthase (PGIS)"

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Chansi, Kengni Hurette Junie. "Régulation et expression de la prostaglandine D synthétase (PGDS) et de la prostacycline synthétase (PGIS) dans l'endomètre de rat gestant, non gestant et pseudogestant." Thèse, Université du Québec à Trois-Rivières, 2006. http://depot-e.uqtr.ca/1907/1/000134642.pdf.

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Palhares, de Miranda Ana Luisa. "Recherches sur les effecteurs de la biosynthèse de la prostacycline (PGI 2) de la thromboxane A 2 (TXA 2), et du facteur anti-thromboxane synthetase ("Fats")." Toulouse, INPT, 1986. http://www.theses.fr/1986INPT031G.

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Effets de composes organiques de synthese et de produits biologiques sur la biosynthese du facteur antithromboxane synthetase par le coeur isole de lapin. Un derive amino pyridazinique inhibe la biosynthese de la thromboxane a2 et stimule celle de la prostacycline et du "fats". La nicotine inhibe la biosynthese de la prostacycline, alors que la cotinine la stimule. Cette possibilite de modifier la biosynthese du "fats" par des produits biologiques pourrait etre une recherche interessante en pharmacologie et en therapeutique

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Hétu, Pierre-Olivier. "Rôle de la cyclo-oxygénase-2 constitutive dans la synthèse des prostaglandines et caractérisation de ses relations avec les prostaglandines synthases terminales." Thèse, 2008. http://hdl.handle.net/1866/6587.

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Neagoe, Paul-Eduard. "La synthèse de prostacycline par le VEGF-A₁₆₅ requiert l'hétérodimérisation des récepteurs du VEGF." Thèse, 2005. http://hdl.handle.net/1866/15474.

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Book chapters on the topic "Prostacyclin synthase (PGIS)"

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Spisni, Enzo, Cristiana Griffoni, Spartaco Santi, Massimo Riccio, Roberta Marulli, and Vittorio Tomasi. "Co-Localization of Prostacyclin (PGI2)-Synthase and Caveolin-1 in Endothelial Cells Underscores New Roles of PGI2 in Angiogenesis." In Advances in Prostaglandin and Leukotriene Research. Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-015-9721-0_27.

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Conference papers on the topic "Prostacyclin synthase (PGIS)"

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Bordet, J. C., M. Guichardant, and M. Lagarde. "PEROXIDE STIMULATION OF PGI3 AND DIHOMO-PGI2 IN ENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643366.

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Human umbilical endothelial cell (EC) monolayers incubated with eicosapentaenoic acid (EPA) produce small amounts of prostaglandin E3 (PGI3). We have previously shown that this metabolite is markedly enhanced in EC supernatant by co-incubating EPA with arachidonic acid (AA) (BBRC 135, 403, 1986). Moreover we found that PGF3a and PGE3 were similarly enhanced, and we concluded that such a stimulation occured at the cyclooxygenase rather than at the prostacyclin synthase level. It is generally assumed that cyclooxygenase is a peroxide-dependent enzyme and the present study shows that the potentia

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Sheehan, S. J., A. B. Latif, S. R. Bibby, R. C. Kester, and S. M. Rajah. "THE RECOVERY OF ENDOTHELIAL CELL AND PLATELET PROSTAGLANDIN SYNTHESES AFTER ADMINISTRATION OF ASPIRIN AND INDOBUFEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643389.

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Suppression of endothelial prostacyclin (PGI2) by cyclooxygenase inhibition may contribute to the formation of neointimal hyperplasia. While aspirin (ASA) inhibits platelet function for several days, it returns to normal within 24 hours after indobufen (IDB), a reversible cyclooxygenase inhibitor, suggesting that prostacyclin may recover at an even faster rate. In a randomised, controlled study, recovery of platelet and endothelial cell prostaglandin synthesis was compared in 49 New Zealand white rabbits following indobufen (3.5 mg/kg) or aspirin (5 mg/kg). Prostacyclin in arterial incubates a

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Giannessi, D., R. De Caterina, G. Lazzerini, R. Sicari, and P. Gazzetti. "RELATIVE SENSITIVITY OF CARDIAC PROSTACYCLIN AND THROMBOXANE TO INHIBITION BY NON-STEROIDAL ANTIINFLAMMATORY DRUGS IN THE RAT HEART." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643390.

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We have previously shown that the isolated perfused rat Langendorff heart is able to synthesize detectable amounts of thromboxane (TX) A2, as well as prostacyclin (PGI2). Eicosanoid production in this system is increased during post-ischemic reperfusion, reflecting greater availability of substrate and net increase of synthesis. We assessed relative sensitivity of cyclooxygenases synthesizing TX and prostacyclin (probably located in different cell types) to aspirin (0.1, 0.5, 1 g/1), ibuprofen (1, 10, 80, 160, 320 mg/1) and diclofenac (0.01, 0.1, 0.5, 2.5, 5, 10, 25 mg/1), by radioimmunoassays

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Lumley, P., E. W. Collington, P. Hallett, et al. "THE EFFECTS OF GR32191, A NEW THROMBOXANE RECEPTOR BLOCKING DRUG,ON PLATELETS AND VASCULAR SMOOTH MUSCLE IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643754.

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The effect of a new thromboxane receptor blocking drug GR32191 ([1R-[1α(Z),2β,3β,5α]]-(+)-7-[5-[[(1,1"-biphenyl)-4-yl]methoxy] -3-hydroxy-2-(l-piperidinyl)cyclopentyl]-4-heptenoic acid,hydrochloride) has been examined upon platelets and vascular smooth muscle. In human platelet-rich plasma (PRP), aggregation to thromboxane(Tx) A2, PGH2, arachidonic acid, collagen andU-46619 was antagonised by GR32191 (IC50 range 2-36 nM).Primary aggregation (PRP treated with aspirin 10 pM) to ADP, 5-HT and adrenaline were unaffected by concentrations of GR32191 up to 10 pM. In human PRP, U-46619-induced aggreg

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