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

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

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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12

Cho, Sun-Ah, and Su-Jun Lee. "Increased expression and catalytic activity of prostacyclin synthase after simvastatin application to human umbilical vein endothelial cells." Archives of Biological Sciences 72, no. 4 (2020): 567–74. http://dx.doi.org/10.2298/abs201028050c.

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In addition to lowering blood cholesterol levels, statins are known to exert antiplatelet effects. One of the key factors contributing to the antiplatelet effects of statins includes the upregulation of prostacyclin (PGI2) level. The present study was undertaken to determine the effects of statins on prostacyclin synthase (PGIS, CYP8A1) and PGI2 synthesis at the molecular level. Human umbilical vein endothelial cells (HUVEC) were exposed to five structurally different statins (atorvastatin, simvastatin, pravastatin, lovastatin, and rosuvastatin) and changes in CYP8A1 expression levels and the

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13

ZOU, Ming-Hui, Thomas KLEIN, Jean-Paul PASQUET та Volker ULLRICH. "Interleukin 1β decreases prostacyclin synthase activity in rat mesangial cells via endogenous peroxynitrite formation". Biochemical Journal 336, № 2 (1998): 507–12. http://dx.doi.org/10.1042/bj3360507.

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We have reported that peroxynitrite (PON) selectively inactivated prostacyclin synthase (PGIS) by a mechanism of tyrosine nitration at the active site [Zou, Martin and Ullrich (1997) Biol. Chem. Hoppe–Seyler 378, 707–713]. We have now extended our studies on rat mesangial cells (RMC) and show that nitration can occur under the influence of cytokines. Pretreatment of RMC with interleukin 1β (IL-1β), which up-regulated cyclo-oxygenase 2 and inducible nitric oxide synthase (NOS-2), significantly attenuated the conversion of [14C]prostaglandin H2 (PGH2) into the stable prostacyclin (PGI2) metaboli

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14

Gurgul-Convey, Ewa, Katarzyna Hanzelka, and Sigurd Lenzen. "Mechanism of Prostacyclin-Induced Potentiation of Glucose-Induced Insulin Secretion." Endocrinology 153, no. 6 (2012): 2612–22. http://dx.doi.org/10.1210/en.2011-2027.

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Arachidonic acid metabolites are crucial mediators of inflammation in diabetes. Although eicosanoids are established modulators of pancreatic β-cell function, the role of prostacyclin (prostaglandin I2) is unknown. Therefore, this study aimed to analyze the role of prostacyclin in β-cell function. Prostacyclin synthase (PGIS) was weakly expressed in rat islet cells but nevertheless significantly increased by incubation with 30 mM glucose, especially in non-β-cells. PGIS was overexpressed in INS1E cells, and the regulation of insulin secretion was analyzed. PGIS overexpression strongly potentia

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15

Ruan, Diana T., Nanhong Tang, Hironari Akasaka, Renzhong Lu, and Ke-He Ruan. "Engineering ‘Enzymelink’ for screening lead compounds to inhibit mPGES-1 while maintaining prostacyclin synthase activity." Future Medicinal Chemistry 13, no. 13 (2021): 1091–103. http://dx.doi.org/10.4155/fmc-2021-0056.

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Aim: This study investigated our Enzymelinks, COX-2-10aa-mPGES-1 and COX-2-10aa-PGIS, as cellular cross-screening targets for quick identification of lead compounds to inhibit inflammatory PGE2 biosynthesis while maintaining prostacyclin synthesis. Methods: We integrated virtual and wet cross-screening using Enzymelinks to rapidly identify lead compounds from a large compound library. Results: From 380,000 compounds virtually cross-screened with the Enzymelinks, 1576 compounds were identified and used for wet cross-screening using HEK293 cells that overexpressed individual Enzymelinks as targe

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16

Lim, Hyunjung, and Sudhansu K. Dey. "Minireview: A Novel Pathway of Prostacyclin Signaling—Hanging Out with Nuclear Receptors." Endocrinology 143, no. 9 (2002): 3207–10. http://dx.doi.org/10.1210/en.2002-220159.

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Abstract Prostacylin (PGI2), one of the major prostaglandins, is derived from arachidonic acid by the action of the cyclooxygenase (COX) system coupled to PGI2 synthase (PGIS). The presence of the COX-2/PGIS at the nuclear and endoplasmic reticular membrane suggests differential signaling pathways of PGI2 actions involving both cell surface and nuclear receptors. Although the signaling of PGI2 via its cell surface receptor, prostacyclin receptor (IP), is well documented in vascular biology, its action via nuclear receptors in other physiological responses is gradually being more appreciated. P

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17

Fike, Candice D., Sandra L. Pfister, James C. Slaughter, et al. "Protein complex formation with heat shock protein 90 in chronic hypoxia-induced pulmonary hypertension in newborn piglets." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 4 (2010): H1190—H1204. http://dx.doi.org/10.1152/ajpheart.01207.2009.

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Aberrant interactions between heat shock protein (Hsp)90 and its client proteins could contribute to pulmonary hypertension. We tested the hypotheses that 1) the interaction between Hsp90 and its known client protein, endothelial nitric oxide synthase (eNOS), is impaired in pulmonary resistance arteries (PRAs) from piglets with pulmonary hypertension caused by exposure to 3 or 10 days of hypoxia and 2) Hsp90 interacts with the prostanoid pathway proteins prostacyclin synthase (PGIS) and/or thromboxane synthase (TXAS). We also determined whether Hsp90 antagonism with geldanamycin alters the ago

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18

Cong, Jing, Hong-Lu Diao, Yue-Chao Zhao, Hua Ni, Yun-Qin Yan, and Zeng-Ming Yang. "Differential expression and regulation of cylooxygenases, prostaglandin E synthases and prostacyclin synthase in rat uterus during the peri-implantation period." Reproduction 131, no. 1 (2006): 139–51. http://dx.doi.org/10.1530/rep.1.00861.

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It has been shown that both prostaglandin I2 (PGI2) and PGE2 are essential for mouse implantation, whereas only PGE2 is required for hamster implantation. To date, the expression and regulation of cyclooxygenase (COX) and prostaglandin E synthase (PGES), which are responsible for PGE2 production, have not been reported in the rat. The aim of this study was to examine the expression pattern and regulation of COX-1, COX-2, membrane-associated PGES-1 (mPGES-1), mPGES-2 and cytosolic PGES (cPGES) in rat uterus during early pregnancy and pseudopregnancy, and under delayed implantation. At implantat

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19

Battersby, S., H. O. D. Critchley, A. J. de Brum-Fernandes, and H. N. Jabbour. "Temporal expression and signalling of prostacyclin receptor in the human endometrium across the menstrual cycle." Reproduction 127, no. 1 (2004): 79–86. http://dx.doi.org/10.1530/rep.1.00038.

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Prostacyclin (PGI2) synthesis and function in the human uterus has been implicated in the regulation of the process of normal and dysfunctional menstruation. PGI2synthesis is elevated during normal menstruation and is also associated with blood loss in women who suffer from heavy menses. This study was designed to outline further the role of PGI2in menstruation by investigating the temporal pattern and site of expression of prostaglandin I synthase (PGIS) and the prostacyclin receptor (IP receptor) in the non-pregnant human endometrium across the menstrual cycle. Quantitative RT-PCR demonstrat

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Cathcart, M., K. Gatley, E. Kay, G. P. Pidgeon, and K. J. O’ Byrne. "Altered expression of prostaglandin synthases in NSCLC: Therapeutic strategies and targets for intervention." Journal of Clinical Oncology 25, no. 18_suppl (2007): 18083. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.18083.

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18083 Background: Prostacyclin Synthase (PGIS) and Thromboxane synthase (TXS) metabolize PGH(2) into prostacyclin and thromboxane respectively. PGIS over-expression inhibits cancer growth in a mouse model, while over-expression of TXS caused opposite effects. TXS is expressed in a variety of tumours, associated with poor prognosis and increased metastasis. The aim of this study was to examine the expression of PGIS and TXS in NSCLC, the effect of targeted TXS inhibition, and the mechanisms regulating these effects. Methods: A panel of resected human lung tumours were stained for PGIS and TXS e

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Dorris, Stacy L., and R. Stokes Peebles. "PGI2as a Regulator of Inflammatory Diseases." Mediators of Inflammation 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/926968.

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Prostacyclin, or PGI2, is an end product derived from the sequential metabolism of arachidonic acid via cyclooxygenase and PGI synthase (PGIS). The receptor for PGI2, IP, can be found on a variety of cell types and signaling through this receptor exhibits broad physiological effects. Historically, PGI2has been understood to play a role in cardiovascular health, specifically having powerful vasodilatory effects via relaxation of smooth muscle and inhibiting of platelet aggregation. For these reasons, PGI2has a long history of use for the treatment of pulmonary arterial hypertension (PAH). Only

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22

Ghosh, Mallika, Haibin Wang, Youxi Ai та ін. "COX-2 suppresses tissue factor expression via endocannabinoid-directed PPARδ activation". Journal of Experimental Medicine 204, № 9 (2007): 2053–61. http://dx.doi.org/10.1084/jem.20070828.

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Although cyclooxygenase (COX)-2 inhibitors (coxibs) are effective in controlling inflammation, pain, and tumorigenesis, their use is limited by the recent revelation of increased adverse cardiovascular events. The mechanistic basis of this side effect is not well understood. We show that the metabolism of endocannabinoids by the endothelial cell COX-2 coupled to the prostacyclin (PGI2) synthase (PGIS) activates the nuclear receptor peroxisomal proliferator–activated receptor (PPAR) δ, which negatively regulates the expression of tissue factor (TF), the primary initiator of blood coagulation. C

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23

Parker, Thomas A., Sam Afshar, John P. Kinsella, et al. "Effects of chronic estrogen-receptor blockade on ovine perinatal pulmonary circulation." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 3 (2001): H1005—H1014. http://dx.doi.org/10.1152/ajpheart.2001.281.3.h1005.

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Prolonged infusions of 17β-estradiol reduce fetal pulmonary vascular resistance (PVR), but the effects of endogenous estrogens in the fetal pulmonary circulation are unknown. To test the hypothesis that endogenous estrogen promotes pulmonary vasodilation at birth, we studied the hemodynamic effects of prolonged estrogen-receptor blockade during late gestation and at birth in fetal lambs. We treated chronically prepared fetal lambs with ICI-182,780 (ICI, a specific estrogen-receptor blocker, n = 5) or 1% DMSO (CTRL, n = 5) for 7 days and then measured pulmonary hemodynamic responses to ventilat

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24

Bird, Ian M., Lubo Zhang, and Ronald R. Magness. "Possible mechanisms underlying pregnancy-induced changes in uterine artery endothelial function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 2 (2003): R245—R258. http://dx.doi.org/10.1152/ajpregu.00108.2002.

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The last 10 years has seen a dramatic increase in our understanding of the mechanisms underlying the pregnancy-specific adaptation in cardiovascular function in general and the dramatic changes that occur in uterine artery endothelium in particular to support the growing fetus. The importance of these changes is clear from a number of studies linking restriction of uterine blood flow (UBF) and/or endothelial dysfunction and clinical conditions such as intrauterine growth retardation (IUGR) and/or preeclampsia in both humans and animal models; these topics are covered only briefly here. The rec

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25

Sanduja, S. K., A. L. Tsai, N. Matijevic-Aleksic, and K. K. Wu. "Kinetics of prostacyclin synthesis in PGHS-1-overexpressed endothelial cells." American Journal of Physiology-Cell Physiology 267, no. 5 (1994): C1459—C1466. http://dx.doi.org/10.1152/ajpcell.1994.267.5.c1459.

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The availability of a human endothelial cell overexpressed with prostaglandin H synthase-1 (PGHS-1) by retrovirus-mediated gene transfer made it possible to quantify the kinetics of prostacyclin [prostaglandin (PG)I2] synthesis and PGHS-1 turnover. Prostacyclin synthesis in response to arachidonate (AA) and ionophore A-23187 fit a single exponential kinetics. The rate constants for AA- and ionophore-treated cells were 0.064 min-1 [half-life (t1/2) of 11 min] and 0.032 min-1 (t1/2 = 22 min), respectively. The rate constant of PGI2 synthesis from PGH2 was 0.13 min-1. Using kinetic analysis coupl

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26

Ruan, Ke-He. "High resolution nuclear magnetic resonance spectroscopy-guided mutagenesis for characterization of membrane-bound proteins: Experimental designs and applications." Spectroscopy 18, no. 1 (2004): 13–29. http://dx.doi.org/10.1155/2004/802728.

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High resolution Nuclear Magnetic Resonance (NMR) spectroscopy is a powerful tool for determining the solution structures of peptides and small proteins, and their ligand binding functions. Molecular biology mutagenesis is a widely used and powerful approach for identification of the protein functions. We have developed a strategy integrating NMR experiments with mutagenesis studies to advance and extend the approaches used for structure/function relationship studies of proteins, especially for membrane-bound proteins, which play important roles in physiopathological processes. The procedures i

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Gillio-Meina, Carolina, Sen Han Phang, James P. Mather, Brian S. Knight, and Thomas G. Kennedy. "Expression patterns and role of prostaglandin-endoperoxide synthases, prostaglandin E synthases, prostacyclin synthase, prostacyclin receptor, peroxisome proliferator-activated receptor delta and retinoid x receptor alpha in rat endometrium during artificially-induced decidualization." REPRODUCTION 137, no. 3 (2009): 537–52. http://dx.doi.org/10.1530/rep-08-0294.

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To determine if changes in endometrial expression of the enzymes and receptors involved in prostaglandin (PG) synthesis and action might provide insights into the PGs involved in the initiation of decidualization, ovariectomized steroid-treated rats at the equivalent of day 5 of pseudopregnancy were given a deciduogenic stimulus and killed at various times up to 32 h thereafter. The expression of PG-endoperoxide synthases (PTGS1 and PTGS2), microsomal PGE synthases (PTGES and PTGES2), cytosolic PGE synthase (PTGES3), prostacyclin synthase (PTGIS), prostacyclin receptor, peroxisome proliferator

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Cooke, Christy-Lynn M., та Sandra T. Davidge. "Peroxynitrite increases iNOS through NF-κB and decreases prostacyclin synthase in endothelial cells". American Journal of Physiology-Cell Physiology 282, № 2 (2002): C395—C402. http://dx.doi.org/10.1152/ajpcell.00295.2001.

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Peroxynitrite, a marker of oxidative stress, is elevated in conditions associated with vascular endothelial cell dysfunction, such as atherosclerosis, preeclampsia, and diabetes. However, the effects of peroxynitrite on endothelial cell function are not clear. The endothelium-derived enzymes nitric oxide synthase (NOS) and prostaglandin H synthase (PGHS) mediate vascular reactivity and contain oxidant-sensitive isoforms (iNOS and PGHS-2) that can be induced by nuclear factor (NF)-κB activation. We investigated the effect(s) of peroxynitrite on NOS and PGHS pathways in endothelial cells. We hyp

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Zou, Ming-Hui, and Markus Bachschmid. "Hypoxia–Reoxygenation Triggers Coronary Vasospasm in Isolated Bovine Coronary Arteries via Tyrosine Nitration of Prostacyclin Synthase." Journal of Experimental Medicine 190, no. 1 (1999): 135–40. http://dx.doi.org/10.1084/jem.190.1.135.

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The role of peroxynitrite in hypoxia–reoxygenation-induced coronary vasospasm was investigated in isolated bovine coronary arteries. Hypoxia–reoxygenation selectively blunted prostacyclin (PGI2)-dependent vasorelaxation and elicited a sustained vasoconstriction that was blocked by a cyclooxygenase inhibitor, indomethacin, and SQ29548, a thromboxane (Tx)A2/prostaglandin H2 receptor antagonist, but not by CGS13080, a TxA2 synthase blocker. The inactivation of PGI2 synthase, as evidenced by suppressed 6-keto-PGF1α release and a decreased conversion of 14C-prostaglandin H2 into 6-keto-PGF1α, was p

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Gubler, David B., Chad R. Ahlstrom, Lihua Liu, Jin-Feng Zhou, Charles J. Parker, and George M. Rodgers. "Procoagulant Albumin Increases Vascular Endothelial Cell Prostacyclin Secretion." Thrombosis and Haemostasis 74, no. 06 (1995): 1573–77. http://dx.doi.org/10.1055/s-0038-1649984.

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SummaryVascular endothelium regulates multiple aspects of platelet function through secretion of a variety of substances, including von Willebrand factor, nitric oxide, and prostacyclin (PGI2). The objective of this study was to determine whether procoagulant albumin (P-AI), a modified form of albumin present in normal human plasma could modulate endothelial cell secretion of these substances. P-AI did not affect constitutive secretion of von Willebrand factor or nitric oxide, but did increase PGI2 secretion in a time- and concentration-dependent manner. Pretreatment of endothelial cells with

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31

Wessels, D. A., and S. L. Hempel. "Ibuprofen protects human endothelial cell prostaglandin H synthase from hydrogen peroxide." American Journal of Physiology-Cell Physiology 271, no. 6 (1996): C1879—C1886. http://dx.doi.org/10.1152/ajpcell.1996.271.6.c1879.

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Human endothelial cells exposed to H2O2 demonstrate decreased prostacyclin (PGI2) synthesis due to decreased prostaglandin H synthase (PGH synthase) activity. We tested the hypothesis that PGH synthase activity could be protected from H2O2 by a reversible nonsteroidal anti-inflammatory drug. Experiments demonstrate that ibuprofen if present during H2O2 exposure, protects endothelial cell PGH synthase against the decrease in prostaglandin formation caused by H2O2. Additional studies demonstrated that decreasing arachidonic acid release from cell phospholipids during H2O2 exposure did not protec

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Cammas, L., P. Reinaud, N. Bordas, O. Dubois, G. Germain, and G. Charpigny. "Developmental regulation of prostacyclin synthase and prostacyclin receptors in the ovine uterus and conceptus during the peri-implantation period." Reproduction 131, no. 5 (2006): 917–27. http://dx.doi.org/10.1530/rep.1.00799.

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This study documents the expression of prostacyclin (PGI2) synthase (PTGIS) and PGI2 receptors in the trophoblast and uterus of the ewe at the time of maternal recognition of pregnancy (i.e. days 7, 9, 12, 14 and 17). The membrane receptor for PGI2 (PTGIR) and the nuclear receptors, i.e. peroxisome proliferator-activated receptors (PPAR) and their heterodimer partners the retinoid X receptors (RXR), were analysed. In the endometrium, PTGIS transcript and protein were expressed at day 9 of pregnancy and levels declined from days 12 to 17. Immunohistochemistry andin situhybridization indicated t

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Hempel, S. L., D. A. Wessels, and A. A. Spector. "Effect of glutathione on endothelial prostacyclin synthesis after anoxia." American Journal of Physiology-Cell Physiology 264, no. 6 (1993): C1448—C1457. http://dx.doi.org/10.1152/ajpcell.1993.264.6.c1448.

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We previously observed decreased prostacyclin (PGI2) formation after reoxygenation of anoxic endothelium. In the present study, the effects of glutathione on endothelial prostaglandin (PG) H synthase activity after reoxygenation were explored. Intracellular glutathione content decreased 70% after 24 h of anoxia; reoxygenation did not produce any additional decrease in glutathione content. Intracellular glutathione was maintained in the reduced state by the endothelium even during the oxidant stress caused by reoxygenation or the addition of peroxide. Glutathione depletion produced by DL-buthio

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Goltsov, Alexey, Maciej Swat, Kirill Peskov, and Yuri Kosinsky. "Cycle Network Model of Prostaglandin H Synthase-1." Pharmaceuticals 13, no. 10 (2020): 265. http://dx.doi.org/10.3390/ph13100265.

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The kinetic model of Prostaglandin H Synthase-1 (PGHS-1) was developed to investigate its complex network kinetics and non-steroidal anti-inflammatory drugs (NSAIDs) efficacy in different in vitro and in vivo conditions. To correctly describe the complex mechanism of PGHS-1 catalysis, we developed a microscopic approach to modelling of intricate network dynamics of 35 intraenzyme reactions among 24 intermediate states of the enzyme. The developed model quantitatively describes interconnection between cyclooxygenase and peroxidase enzyme activities; substrate (arachidonic acid, AA) and reducing

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Hempel, S. L., D. L. Haycraft, J. C. Hoak, and A. A. Spector. "Reduced prostacyclin formation after reoxygenation of anoxic endothelium." American Journal of Physiology-Cell Physiology 259, no. 5 (1990): C738—C745. http://dx.doi.org/10.1152/ajpcell.1990.259.5.c738.

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Human umbilical vein endothelial cells subjected to 24 h of anoxia followed by reoxygenation released less prostacyclin (PGI2) in response to thrombin, calcium ionophore A23187, or arachidonic acid. This was associated with a substantial increase in stimulated platelet adherence. Increased lactate dehydrogenase and 51Cr release occurred after 1 h of reoxygenation, but the high rate of release did not persist during the subsequent 23 h of reoxygenation. The changes in platelet adherence and PGI2 release partially resolved over 24 h. PGI2 formation from prostaglandin H2 was not reduced, suggesti

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Morio, H., A. Hirai, T. Terano, Y. Tamura, and S. Yoshida. "Effect of the Infusion of OKY-046, a Thromboxane A2 Synthase Inhibitor, on Urinary Metabolites of Prostacyclin and Thromboxane A2 in Healthy Human Subjects." Thrombosis and Haemostasis 69, no. 03 (1993): 276–81. http://dx.doi.org/10.1055/s-0038-1651595.

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SummaryThe influence of OKY-046, a selective thromboxane synthase inhibitor, on prostanoid formation in healthy human subjects was studied. Vehicle (5% glucose solution) or OKY-046 in 5% glucose solution at 15 μg kg−1 min−1 was intravenously administered to five male healthy volunteers for 6 h. Platelet aggregation and thromboxane B2 (TXB2) formation induced by collagen and arachidonic acid were suppressed by the infusion of OKY-046, while both were not affected by the infusion of vehicle. Urinary excretion of 11-dehydro-thromboxane B2, one of major urinary metabolites of thromboxane A2 (TXA2)

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Hempel, S. L., and D. A. Wessels. "Prostaglandin E2 synthesis after oxidant stress is dependent on cell glutathione content." American Journal of Physiology-Cell Physiology 266, no. 5 (1994): C1392—C1399. http://dx.doi.org/10.1152/ajpcell.1994.266.5.c1392.

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The role of glutathione in protecting prostaglandin (PG) generation after exposure of fibroblasts to oxidant stress was investigated. Exposure of 3T3 fibroblasts to H2O2, followed by washing and then 20 microM arachidonic acid, caused a dose-dependent decrease in PG synthesis as assessed by radioimmunoassay. PGE2 production decreased from 3.7 +/- 1.1 to 0.15 +/- 0.04 pmol/microgram protein, and prostacyclin (PGI2) formation decreased from 0.56 +/- 0.03 to 0.06 +/- 0.03 pmol/microgram protein after exposure to 200 microM H2O2. Decreasing intracellular glutathione with 50 micrograms/ml 1,3-bis(c

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Spisni, Enzo, Cristiana Griffoni, Spartaco Santi, et al. "Colocalization Prostacyclin (PGI2) Synthase–Caveolin-1 in Endothelial Cells and New Roles for PGI2 in Angiogenesis." Experimental Cell Research 266, no. 1 (2001): 31–43. http://dx.doi.org/10.1006/excr.2001.5198.

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Spisni, Enzo, Giovanna Bartolini, Marina Orlandi, Barbara Belletti, Spartaco Santi, and Vittorio Tomasi. "Prostacyclin (PGI2) Synthase Is a Constitutively Expressed Enzyme in Human Endothelial Cells." Experimental Cell Research 219, no. 2 (1995): 507–13. http://dx.doi.org/10.1006/excr.1995.1259.

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Gluais, Pascale, Jerôme Paysant, Cécile Badier-Commander, Tony Verbeuren, Paul M. Vanhoutte, and Michel Félétou. "In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A2 as endothelium-derived contracting factors." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 5 (2006): H2255—H2264. http://dx.doi.org/10.1152/ajpheart.01115.2005.

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In mature spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), acetylcholine and the calcium ionophore A-23187 release endothelium-derived contracting factors (EDCFs), cyclooxygenase derivatives that activate thromboxane-endoperoxide (TP) receptors on vascular smooth muscle. The EDCFs released by acetylcholine are most likely prostacyclin and prostaglandin (PG)H2, whereas those released by A-23187 remain to be identified. Isometric tension and the release of PGs were measured in rings of isolated aortas of WKY and SHR. A-23187 evoked the endothelium-dependent release of prostacyc

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Liu, Bin, Yingzhan Zhang, Ningxia Zhu, Hui Li, Wenhong Luo, and Yingbi Zhou. "A vasoconstrictor role for cyclooxygenase-1-mediated prostacyclin synthesis in mouse renal arteries." American Journal of Physiology-Renal Physiology 305, no. 9 (2013): F1315—F1322. http://dx.doi.org/10.1152/ajprenal.00332.2013.

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This study was to determine whether prostacyclin [prostaglandin I2 (PGI2)] evokes mouse renal vasoconstriction and, if so, the underlying mechanism(s) and how its synthesis via cyclooxygenase-1 (COX-1) influences local vasomotor reaction. Experiments were performed on vessels from C57BL/6 mice and/or those with COX-1 deficiency (COX-1−/−). Results showed that in renal arteries PGI2 evoked contraction more potently than in carotid arteries, where COX-1 is suggested to mediate prominent endothelium-dependent contraction. A similar result was observed with the thromboxane-prostanoid (TP) receptor

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Myers, S., C. T. Evans, L. Bartula, B. Kalley-Taylor, A. R. Habeeb, and T. Goka. "Increased gall-bladder prostanoid synthesis after bile-duct ligation in the rabbit is secondary to new enzyme formation." Biochemical Journal 288, no. 2 (1992): 585–90. http://dx.doi.org/10.1042/bj2880585.

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Ligation of the common bile duct (BDL) in the male rabbit resulted in increased gall-bladder microsomal total cyclo-oxygenase activity with prostaglandin E2 (PGE2) and 6-oxoprostaglandin F1 alpha [6-oxo-PGF1 alpha, stable metabolite of prostaglandin I2 (PGI2; prostacyclin)] as the major prostanoids synthesized after 24 and 72 h. Kinetic analysis of gallbladder microsomal membrane fractions incubated with increasing levels of [14C]arachidonic acid indicated that BDL for 24 and 72 h did not change substrate affinity (apparent Km) but markedly increased the rate of conversion (apparent Vmax.) sug

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Goodwill, Adam G., Milinda E. James, and Jefferson C. Frisbee. "Increased vascular thromboxane generation impairs dilation of skeletal muscle arterioles of obese Zucker rats with reduced oxygen tension." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (2008): H1522—H1528. http://dx.doi.org/10.1152/ajpheart.00596.2008.

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This study determined if altered vascular prostacyclin (PGI2) and/or thromboxane A2 (TxA2) production with reduced Po2 contributes to impaired hypoxic dilation of skeletal muscle resistance arterioles of obese Zucker rats (OZRs) versus lean Zucker rats (LZRs). Mechanical responses were assessed in isolated gracilis muscle arterioles following reductions in Po2 under control conditions and following pharmacological interventions inhibiting arachidonic acid metabolism and nitric oxide synthase and alleviating elevated vascular oxidant stress. The production of arachidonic acid metabolites was as

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Liou, Jun-Yang, Song-Kun Shyue, May-Jywan Tsai, Chia-Lin Chung, Kuan-Yu Chu, and Kenneth K. Wu. "Colocalization of Prostacyclin Synthase with Prostaglandin H Synthase-1 (PGHS-1) but Not Phorbol Ester-induced PGHS-2 in Cultured Endothelial Cells." Journal of Biological Chemistry 275, no. 20 (2000): 15314–20. http://dx.doi.org/10.1074/jbc.275.20.15314.

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Liu, Bin, Wenhong Luo, Yingzhan Zhang, et al. "Role of cyclooxygenase-1-mediated prostacyclin synthesis in endothelium-dependent vasoconstrictor activity of porcine interlobular renal arteries." American Journal of Physiology-Renal Physiology 302, no. 9 (2012): F1133—F1140. http://dx.doi.org/10.1152/ajprenal.00604.2011.

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This study aimed to determine whether PGI2 would be evoked by the endogenous endothelial B2 receptor agonist bradykinin (BK) in the porcine interlobular renal artery and, if so, to determine how it would influence the vasomotor reaction, and the specific cyclooxygenase (COX) isoform(s) involved in its synthesis. The production of the PGI2 metabolite 6-keto-PGF1α was analyzed with HPLC-mass spectroscopy, while vasomotor reaction to PGI2 or BK was determined with isometric force measurement. Results showed that BK evoked an increase in the production of 6-keto-PGF1α, which was abolished by endot

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Pan, Xue-yin, Ling Wang, Hong-mei You, et al. "Alternative activation of macrophages by prostacyclin synthase ameliorates alcohol induced liver injury." Laboratory Investigation 101, no. 9 (2021): 1210–24. http://dx.doi.org/10.1038/s41374-021-00531-7.

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AbstractAlcoholic liver disease (ALD) is a major cause of chronic liver disease worldwide. Macrophages exhibit different functional states and are classified as classically activated (M1) and alternatively activated (M2) macrophages. However, the mechanisms that govern M1/M2 polarization in chronic ALD remain to be elucidated. Prostacyclin (PGI2) synthase (PTGIS) is an enzyme of the prostaglandin pathway which catalyzes the conversion of Prostaglandin H2 (PGH2) to PGI2. PTGIS has anti-inflammatory properties. However, the function of PTGIS in ALD has not yet been determined. In this study, we

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Song, Bong-Seok, Ji-Su Kim, Cheol-Hee Kim, et al. "Prostacyclin stimulates embryonic development via regulation of the cAMP response element-binding protein - cyclo-oxygenase-2 signalling pathway in cattle." Reproduction, Fertility and Development 21, no. 3 (2009): 400. http://dx.doi.org/10.1071/rd08180.

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Prostacyclin (PGI2) in oviducal fluid is synthesised from arachidonic acid by cyclo-oxygenase (COX) and prostacyclin synthetase and enhances the implantation and live birth potential of mouse embryos. In the present study, we investigated the developmental competence of bovine embryos by examining the effects of the PGI2 analogue iloprost on blastocyst development, quality and COX-2 expression during IVF and somatic cell nuclear transfer (SCNT). Bovine IVF and SCNT embryos were cultured in CR1-aa medium supplemented with 0.3% bovine serum albumin in either the presence or absence of 1 μm ilopr

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Zenge, Jeanne P., Robyn L. Rairigh, Theresa R. Grover, et al. "NO and prostaglandin interactions during hemodynamic stress in the fetal ovine pulmonary circulation." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 5 (2001): L1157—L1163. http://dx.doi.org/10.1152/ajplung.2001.281.5.l1157.

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Nitric oxide (NO) and prostacyclin (PGI2) are potent fetal pulmonary vasodilators, but their relative roles and interactions in the regulation of the perinatal pulmonary circulation are poorly understood. We compared the separate and combined effects of nitric oxide synthase (NOS) and cyclooxygenase (COX) inhibition during acute hemodynamic stress caused by brief mechanical compression of the ductus arteriosus (DA) in chronically prepared fetal lambs. Nitro-l-arginine (l-NNA; NOS antagonist), meclofenamate (Mec; COX inhibitor), combined drugs (l-NNA-Mec), or saline (control) was infused into t

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Isobe, Hirotaka, Kenji Okajima, Mitsuhiro Uchiba, Naoaki Harada, and Hiroaki Okabe. "Antithrombin prevents endotoxin-induced hypotension by inhibiting the induction of nitric oxide synthase in rats." Blood 99, no. 5 (2002): 1638–45. http://dx.doi.org/10.1182/blood.v99.5.1638.

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Antithrombin (AT) prevents Escherichia coli–induced hypotension in animal models of sepsis, and it further reduces the mortality of patients with septic shock. In the present study, we examined whether AT may prevent the endotoxin (ET)-induced hypotension by promoting the endothelial release of prostacyclin (PGI2) in rats. Intravenous administration of AT (250 U/kg) prevented both hypotension and the increases in plasma levels of NO2−/NO3− in rats given ET. Lung expression of messenger RNA (mRNA) for tumor necrosis factor-α (TNF-α) was transiently increased after ET administration, followed by

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Liu, Dongling, Bin Liu, Wenhong Luo, Hui Li, Yingzhan Zhang, and Yingbi Zhou. "A vasoconstrictor response to COX-1-mediated prostacyclin synthesis in young rat renal arteries that increases in prehypertensive conditions." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 5 (2015): H804—H811. http://dx.doi.org/10.1152/ajpheart.00150.2015.

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This study aimed to determine whether prostacyclin (PGI2) functions as an endothelium-derived contracting factor (EDCF) in young rat renal arteries, and, if so, we wanted to examine the underlying mechanism(s) and how it changes in prehypertensive conditions. Vessels from Wistar-Kyoto (WKY) and prehypertensive spontaneously hypertensive rats (SHRs) of 25–28 days of age were isolated for functional and biochemical analyses. Result showed that following NO synthase (NOS) inhibition PGI2 and the thromboxane-prostanoid (TP) receptor agonist U-46619 evoked contractions in young WKY renal arteries t

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