Relevant bibliographies by topics / Cyclooxygenase

Academic literature on the topic 'Cyclooxygenase'

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Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Cyclooxygenase"

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Zhang, Xinping, Scott G. Morham, Robert Langenbach, and Donald A. Young. "Malignant Transformation and Antineoplastic Actions of Nonsteroidal Antiinflammatory Drugs (Nsaids) on Cyclooxygenase-Null Embryo Fibroblasts." Journal of Experimental Medicine 190, no. 4 (August 16, 1999): 451–60. http://dx.doi.org/10.1084/jem.190.4.451.

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In this study, we use primary embryonic fibroblasts derived from cyclooxygenase-deficient transgenic embryos to further investigate the role of the two cyclooxygenases, cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2), in the process of neoplastic transformation. Cells with either, neither, or both of the cyclooxygenases were transformed by Ha-ras and/or SV40. Our results show that when a cyclooxygenase enzyme is present, the transformed cells have marked increases in COX-2 and/or COX-1 expression. Nevertheless, each type of cell, deficient in either or both cyclooxygenases, can be readily transformed at almost equal efficiency. Different nonsteroidal antiinflammatory drugs (NSAIDs) were used to examine their possible antineoplastic effects on the transformed cells, which have various levels of expression of COX-1 or COX-2. Our results show that NSAIDs suppress the colony formation in soft agar in a dosage-dependent manner in the absence of the cyclooxygenase(s). Thymidine incorporation and apoptosis analyses further demonstrate that the NSAIDs are effective in the cyclooxygenase-null cells. Our findings with cyclooxygenase knockout cells confirm recent reports that some of the antiproliferative and antineoplastic effects of NSAIDs are independent of the inhibition of either COX-1 or COX-2. They also show that transformation is independent of the status of cyclooxygenase expression, suggesting that the involvement of the cyclooxygenases in tumorigenesis may occur at later steps.
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Dolan, Sharron, James G. Kelly, Marie Huan, and Andrea M. Nolan. "Transient Up-regulation of Spinal Cyclooxygenase-2 and Neuronal Nitric Oxide Synthase following Surgical Inflammation." Anesthesiology 98, no. 1 (January 1, 2003): 170–80. http://dx.doi.org/10.1097/00000542-200301000-00027.

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Background Surgery induces pain and hyperalgesia postoperatively. The products of cyclooxygenases and nitric oxide synthase (NOS) have been implicated in the development of inflammatory pain and hyperalgesia experimentally, and the use of drugs clinically that modify cyclooxygenase activity has been advocated in the management of perioperative pain. However, regulation of these enzymes following surgery has not been studied. Methods Adult female sheep (n = 12) undergoing a midline laparotomy for collection of ova were used in this study. Lumbar and cervical spinal cord tissue was collected from animals euthanized 1 day and 6 or 7 days after surgery and processed for cyclooxygenase (cyclooxygenase-1 and cyclooxygenase-2), neuronal NOS mRNA expression using reverse-transcription polymerase chain reaction and hybridization. Tissues were also processed for NADPH-diaphorase staining and cyclooxygenase-1 and cyclooxygenase-2 protein expression by immunohistochemistry and Western blotting. Results No alteration in cyclooxygenase-1 or cyclooxygenase-2 mRNA or protein concentrations were detected in spinal cord by reverse-transcription polymerase chain reaction and Western blotting, respectively, at 1 day or 6 or 7 days after surgery. However, using techniques that localize mRNA and protein expression ( hybridization and immunohistochemistry, respectively), increases in cyclooxygenase-2 were identified in lamina V dorsal horn neurons in lumbar spinal cord 1 day after surgery. A significant increase in neuronal NOS mRNA was observed in lumbar spinal cord 1 day after surgery, localized to laminae I-II and lamina V neurons, which returned to baseline concentrations by 6 to 7 days. NADPH-diaphorase staining was significantly increased in laminae I-II in lumbar spinal cord 1 day after surgery but not after 6 to 7 days. Conclusions Spinal cyclooxygenase and neuronal NOS pathways are differentially altered following surgical inflammation. The early and transient nature of these changes suggests that these enzymes are implicated in postoperative pain and hypersensitivity.
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YAMAMOTO, KEI. "Cyclooxygenase - 1 and cyclooxygenase - 2." Japanese Journal of Clinical Immunology 19, no. 6 (1996): 564–67. http://dx.doi.org/10.2177/jsci.19.564.

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Stockton, Rebecca A., and Bruce S. Jacobson. "Modulation of Cell-Substrate Adhesion by Arachidonic Acid: Lipoxygenase Regulates Cell Spreading and ERK1/2-inducible Cyclooxygenase Regulates Cell Migration in NIH-3T3 Fibroblasts." Molecular Biology of the Cell 12, no. 7 (July 2001): 1937–56. http://dx.doi.org/10.1091/mbc.12.7.1937.

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Adhesion of cells to an extracellular matrix is characterized by several discrete morphological and functional stages beginning with cell-substrate attachment, followed by cell spreading, migration, and immobilization. We find that although arachidonic acid release is rate-limiting in the overall process of adhesion, its oxidation by lipoxygenase and cyclooxygenases regulates, respectively, the cell spreading and cell migration stages. During the adhesion of NIH-3T3 cells to fibronectin, two functionally and kinetically distinct phases of arachidonic acid release take place. An initial transient arachidonate release occurs during cell attachment to fibronectin, and is sufficient to signal the cell spreading stage after its oxidation by 5-lipoxygenase to leukotrienes. A later sustained arachidonate release occurs during and after spreading, and signals the subsequent migration stage through its oxidation to prostaglandins by newly synthesized cyclooxygenase-2. In signaling migration, constitutively expressed cyclooxygenase-1 appears to contribute ∼25% of prostaglandins synthesized compared with the inducible cyclooxygenase-2. Both the second sustained arachidonate release, and cyclooxygenase-2 protein induction and synthesis, appear to be regulated by the mitogen-activated protein kinase extracellular signal-regulated kinase (ERK)1/2. The initial cell attachment-induced transient arachidonic acid release that signals spreading through lipoxygenase oxidation is not sensitive to ERK1/2 inhibition by PD98059, whereas PD98059 produces both a reduction in the larger second arachidonate release and a blockade of induced cyclooxygenase-2 protein expression with concomitant reduction of prostaglandin synthesis. The second arachidonate release, and cyclooxygenase-2 expression and activity, both appear to be required for cell migration but not for the preceding stages of attachment and spreading. These data suggest a bifurcation in the arachidonic acid adhesion-signaling pathway, wherein lipoxygenase oxidation generates leukotriene metabolites regulating the spreading stage of cell adhesion, whereas ERK 1/2-induced cyclooxygenase synthesis results in oxidation of a later release, generating prostaglandin metabolites regulating the later migration stage.
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Tegeder, Irmgard, Josef Pfeilschifter, and Gerd Geisslinger. "Cyclooxygenase‐independent actions of cyclooxygenase inhibitors." FASEB Journal 15, no. 12 (October 2001): 2057–72. http://dx.doi.org/10.1096/fj.01-0390rev.

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Kutil, Zsofia, Veronika Temml, David Maghradze, Marie Pribylova, Marcela Dvorakova, Daniela Schuster, Tomas Vanek, and Premysl Landa. "Impact of Wines and Wine Constituents on Cyclooxygenase-1, Cyclooxygenase-2, and 5-Lipoxygenase Catalytic Activity." Mediators of Inflammation 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/178931.

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Cyclooxygenases and lipoxygenases are proinflammatory enzymes; the former affects platelet aggregation, vasoconstriction, vasodilatation and later the development of atherosclerosis. Red wines from Georgia and central and western Europe inhibited cyclooxygenase-1 (COX-1) activity in the range of 63–94%, cyclooxygenase-2 (COX-2) activity in the range of 20–44% (tested at a concentration of 5 mL/L), and 5-lipoxygenase (5-LOX) activity in the range of 72–84% (at a concentration of 18.87 mL/L). White wines inhibited 5-LOX in the range of 41–68% at a concentration of 18.87 mL/L and did not inhibit COX-1 and COX-2. Piceatannol (IC50= 0.76 μM) was identified as a strong inhibitor of 5-LOX followed by luteolin (IC50= 2.25 μM), quercetin (IC50= 3.29 μM), and myricetin (IC50= 4.02 μM).trans-Resveratrol was identified as an inhibitor of COX-1 (IC50= 2.27 μM) and COX-2 (IC50= 3.40 μM). Red wine as a complex mixture is a powerful inhibitor of COX-1, COX-2, and 5-LOX, the enzymes involved in eicosanoid biosynthetic pathway.
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Sladek, Krzysztof, and James R. Sheller. "Cyclooxygenase Mediators." Immunology and Allergy Clinics of North America 10, no. 2 (May 1990): 409–18. http://dx.doi.org/10.1016/s0889-8561(22)00279-x.

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Mao, Yumeng, Isabel Poschke, and Rolf Kiessling. "Cyclooxygenase-2." OncoImmunology 2, no. 8 (August 2013): e25157. http://dx.doi.org/10.4161/onci.25157.

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Marnett, Lawrence J. "Cyclooxygenase mechanisms." Current Opinion in Chemical Biology 4, no. 5 (October 2000): 545–52. http://dx.doi.org/10.1016/s1367-5931(00)00130-7.

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Breyer, Matthew D. "Beyond cyclooxygenase." Kidney International 62, no. 5 (November 2002): 1898–99. http://dx.doi.org/10.1046/j.1523-1755.2002.00645.x.

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Dissertations / Theses on the topic "Cyclooxygenase"

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Gilroy, Derek William. "Cyclooxygenase 2 inflammation." Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265077.

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Chen, Suzi Su-Hsin, and suzi chen@med monash edu au. "Cyclooxygenase Expression in Human Diabetes." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080206.121439.

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Cyclooxygenase (COX) is the rate limiting enzyme that catalyses the production of prostanoids, which are crucial to vascular homeostasis. Evidence suggests that endothelial dysfunction and inflammation play a role in vascular complications in aging and diabetes. Previous animal studies by our laboratory at RMIT University reported enhanced COX expression with aging in rat aortas, platelets and monocytes. Potentially, alteration in COX expression may result in an imbalanced prostanoid production favoring the synthesis of vasoconstrictors and hence increase the risk of cardiovascular events in the aging population. The regulation of altered COX expression in aging, however, is not clear. It has been suggested that histone hyperacetylation may be an important mechanism that regulates COX levels during the aging process as increased histone acetylation has been shown to occur with aging. Thus, we hypothesized that COX expression is modulated by histone hyperacetylati on. This was investigated by measuring COX expression in histone hyperacetylated cultured endothelial cells. In the case of diabetes, studies have reported that the development of diabetes and its complications is associated with persistent inflammatory activity, evident with increased inflammatory markers in the circulation. COX-mediated pathways may be involved in this inflammatory process in diabetes. Furthermore, the formation of advanced glycation end products (AGEs) is accelerated in diabetes. AGEs can bind to receptors for AGEs (RAGE), which has also been suggested to play a role in inflammation in diabetes. We hypothesized that COX- and RAGE-mediated pathways contribute to increased inflammation in diabetes and potentiate the development of diabetic vascular complications. This was investigated by measuring changes in COX-mediated pathways in both rat and human diabetic models. The current thesis reports: 1) in cultured endothelial cells, histone hyperacetylation was associated with increased COX expression; 2) an overall increase in inflammation was observed in diabetes involving COX- and RAGE-mediated pathways. This was supported by increased platelet COX-1 and monocyte COX-2 levels in Zucker rats, increased monocyte COX-2 in human Type 1 diabetes and elevated plasma TXB2 and PGE2 levels in both human Type 1 and Type 2 diabetic subjects. Up-regulation of RAGE expression was further found in platelets and monocytes in both human diabetes types. When treated with NSAIDs, plasma prostanoid levels, COX and RAGE expression were reduced significantly in both platelets and monocytes in human diabetic subjects. 3) It is unclear how COX and RAGE expression was regulated, but histone modifications may be one of the mechanisms. Data from cultured cells indicated that increased COX expression was associated with increased histone acetylation levels induced by TSA. Concurrent increases in histone acetylation and COX-2 levels were also observed in human Type 1 diabetes, but similar findings were not observed in human Type 2 diabetes. In addition, we failed to find an age-dependent increase in monocyte histone H4 acetylation in human Type 2 diabetes despite an age-dependent increase in monocyte COX-2 expression. Thus, whether histone hyperacetylation modulates COX expression and in what conditions require further investigation.
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Cahlin, Christian. "Cyclooxygenase activity and tumor progression /." Göteborg : Departments of Surgery and Transplantation, Institute of Clinical Sciences at Sahlgrenska Academy, University of Gothenburg, 2008. http://hdl.handle.net/2077/18198.

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Xu, Yibing. "Studies on Cyclooxygenase-1, its Structure and Splice Variants, and Modulation of Cyclooxygenase-2 by Inducible Nitric Oxide Synthase and Novel Phytochemicals." BYU ScholarsArchive, 2006. https://scholarsarchive.byu.edu/etd/6208.

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Cyclooxygenases (COXs) are of important therapeutic value as they are the target site of aspirin-like drugs. Here I report nine new COX-1 splice variants in chapter 1, which I characterized with regard to heme-binding and other properties. Inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) are co-inducible in many tissues following mitogenic and proinflammatory stimulation. In chapter 2, I investigate the physical and enzymatic properties of human COX-2 and iNOS and demonstrate that, despite reports to the contrary by another laboratory, they do not interact. The only reported COX-1 splice variant to exhibit cyclooxygenase activity has been isolated from dog brain and is termed COX-3. It contains an in-frame insertion of intron 1. However the existence of human COX-3 remains questionable since intron 1 is out of frame. Two putative in-frame human COX-3 isozymes, COX-1b2 and COX-1b3, (herein designated as COX-3-72 and COX-3-50) have been reported in the literature, but only one of them, COX-3-72, has been characterized. In chapter 3, COX-3-50 and COX-3-72 are reported to be over-expressed and determined to be active cyclooxygenases. COX-3-72 and, to a greater extent, COX-3-50, were stimulated by rofecoxib at physiological concentrations. A similar rofecoxib-stimulated COX activity is observed in quiescent A549 cells. Immunoblot and immunoprecipitation analysis suggest that human platelet and potentially A549 cells, contain a COX-3-50 like protein. Lonicera japonica is used as an anti-inflammatory treatment in traditional Chinese medicine. Its working mechanism is not well known. In chapter 4, I report that extracts from this herb inhibit COX-2 by three mechanisms: direct inhibition, transcriptional and post-transcriptional down regulation. COX-1 and COX-2 are similar to each other in their crystallographic structures. One of the most striking differences is that there are eight amino acids immediately following the signal peptide in COX-1 which are not found in COX-2. The function of this sequence is unknown. In chapter 5, I found that deletion of these amino acids decreased COX-1 Vmax by approximately 4-fold, but had little effect on other properties of the enzyme. Selecting bacteria transformed with recombinant plasmids is a laborious step in gene cloning experiments. This selection process is even more tedious when large numbers of clones need to be screened. In appendix I, I describe an ultra fast plasmid screening method. This new method was frequently used in the experiments performed in chapters 2-6.
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Müller, Berit Maria. "Expression der Cyclooxygenase-2 im Mammakarzinom." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=974951161.

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Faluyi, Olusola Olusesan. "Cyclooxygenase 2 expression in intestinal tumorigenesis." Thesis, University of Leeds, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275680.

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Acton, Stephen Justin. "Post-transcriptional control of cyclooxygenase-2." Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29531.

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Cyclooxygenase-2 is an early response gene that is rapidly and transiently induced by a variety of extracellular ligands in many cell types, including macrophages and mesangial cells. The 3' untranslated region (UTR) of cox-2 mRNA plays a vital role in its post-transcriptional control by regulating mRNA stability and translation. The proximal 60-nucleotides of the 3' UTR contain highly conserved Adenosine-uridine Rich Elements (AREs)---AUUUA, which are known to regulate mRNA stability and translation.;Insertion of the 1--60 sequence was sufficient to cause a marked decrease (>65%) in expression of a luciferase reporter-gene, in both rat mesangial and RAW 264.7 cells. Although reporter-gene constructs proved unresponsive to stimulation with IL1beta in the rat mesangial cells, a response was seen with LPS in the RAW 264.7 cells, which was dependent on the proximal 20 nucleotides of the 1--60 sequence.;Electromobility shift assays revealed that multiple RNA binding proteins, including HuR, TIA-1, TIAR, hnRNP U and AUF1, interacted with this region of the cyclooxygenaase-2 3' TR, with some noticeable differences occurring following removal of the LPS responsive sequence.;These studies provide further evidence of the role played by the 3 ' UTR in the post-transcriptional control of cyclooxygenase-2, as well as identifying several RNA binding proteins likely to be involved in this process.
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Müller, Berit Maria. "Expression der Cyclooxygenase-2 im Mammakarzinom." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/15245.

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Cyclooxygenasen regulieren die Produktion von Prostaglandinen und spielen eine Rolle bei der Entstehung und Progression maligner Tumore. Versuche mit COX Inhibitoren (NSAIDs) zeigten im Tiermodell eine deutliche Reduktion von Inzidenz und Größe der Tumoren in einer dosisabhängigen Weise. Das Ziel der vorliegenden Arbeit war, das Expressionsmuster der induzierbaren Isoform COX-2 und der konstitutiven Isoform COX-1 im Mammakarzinom zu untersuchen. Die Grundlage der Untersuchung bildeten Tumorproben von 221 Patientinnen mit primärem Mammakarzinom. Diese wurden mittels immunhistochemischer Methoden auf beide COX-Isoenzyme untersucht. Eine erhöhte COX-2 Expression wurde in 36% der untersuchten Mammakarzinome festgestellt. Sie korrelierte signifikant mit verschiedenen klinisch-pathologischen Parametern, insbesondere mit einem positiven Lymphknotenstatus, einer geringen Differenzierung und einer Tumorgröße >20 mm. Eine erhöhte COX-1 Expression wurde in 45% der untersuchten Tumoren gefunden und korrelierte signifikant mit kleineren und nicht in regionäre Lymphknoten metastasierten Karzinomen. In der univariaten Überlebensanalyse stellte sich eine positive COX-2 Expression im Gegensatz zur COX-1 sowohl im rezidivfreien Überleben als auch im Gesamtüberleben als prognostisch relevant heraus. In der multivariaten Analyse erreichte eine erhöhte COX-2 Expression eine grenzwertige statistische Signifikanz als unabhängiger Parameter innerhalb des rezidivfreien Überlebens. Eine erhöhte COX-1 Expression erreichte keinen statistisch signifikanten Einfluß auf die Prognose. Aufgrund dieser Ergebnisse ist somit eine erhöhte COX-2 Expression im Mammakarzinom mit prognostisch ungünstigen Faktoren assoziiert. Inwieweit selektive COX-2 Inhibitoren als Therapeutika geeignet sind, werden die Ergebnisse weiterer Studien zeigen.
Cyclooxygenases regulate the production of prostaglandins and play a role in tumor development and progression. COX-inhibitors (NSAIDs) showed a significant reduction of tumor incidence and tumor size in rodent models. In this study, we investigated the prognostic impact of expression of both COX-isoforms as well as the association of COX expression and other clinicopathological parameters in primary breast cancer. The expression of COX-1 and –2 was determined by immunohistochemistry retrospectivly in a cohort of 221 women. An elevated expression of COX-2 as the inducible form of the cyclooxygenases was detected in 36% of tumors and was significantly associated with several clinicopathological parameters, for example positive nodal status, poor differentiation and larger tumor size. In contrast, an increased expression of COX-1 was detected in 45% of breast carcinomas and was associated with smaller tumor size and negative nodal status. In univariate survival analysis a significant association between an increased expression of COX-2 and a decreased disease-free survival as well as decreased overall survival was found. An elevated expression of COX-1 had no significant influence on patient prognosis. The data of this study show a prognostic role of COX-2 expression. Further studies on selective COX-2 inhibitors will investigate their role in treatment of patients with breast cancer.
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Tarantino, E. "THE ROLE OF CYCLOOXYGENASE-1 (COX-1) AND CYCLOOXYGENASE-2 (COX-2) IN A VENOUS THROMBOSIS MOUSE MODEL." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/353697.

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Background: Deep vein thrombosis (DVT) is a serious national health problem, and pulmonary thromboembolism (PE) represents the life-threatening most common complication. Venous thromboembolism (VTE), including both these conditions, is traditionally treated with anticoagulant drugs. In particular, vitamin K antagonists and heparins are usually used in the reduction of thrombus development and in secondary prevention. However, the use of these drugs has several limitations: wide variability dose/response relationship between patients and in the same patient, multiple interactions with other drugs/foods, variability of daily doses, need of periodic withdrawals of blood during therapy, problems of overdosing. Then, the discovery of new drugs for VTE needs. The cyclooxygenase isoenzymes, COX-1 and COX-2, catalyse the formation of prostaglandins and, thromboxane from arachidonic acid, and play a critical role in thrombosis. Recent meta-analysis suggests that low-dose aspirin (ASA) reduces the rate of VTE recurrence. In contrast, the clinical use of COX-2 inhibitors seems associated with increased risk of venous thrombosis. However, the role of COX-1 and COX-2 in venous thrombosis remain unclear. Aim: We investigated the impact of COX-1 and COX-2 enzymes in venous thrombosis in order to identify the molecular mechanisms responsible for this effect and develop new therapeutic strategies to prevent venous thrombosis. In particular, we focused on the impact of inhibition of COX-pathway on leukocyte activation, important regulators of formation and propagation of venous thrombus. Methods and Results: Using in vivo and in vitro approaches, we provide evidence that: a) thromboxane, produced by platelets, triggers activation of leukocytes, with consequent development and propagation of venous thrombus induced by inferior vena cava ligation. In particular, we showed that ASA, by inhibiting irreversibly platelet COX-1, prevents platelet thromboxane production resulting in decreased venous thrombosis. b) COX-2 deletion induces platelet hyper-activity and hyper-coagulation state, associated with a reduced fibrinolysis and formation of bigger thrombi. In this scenario, the high levels of tissue factor observed in leukocytes of COX-2KO mouse may explain the positive association observed between administration of COX-2 inhibitors and VTE. Thanking advantage of an accurate, and clinically relevant, technique such as ultrasonography, we are setting a method helpful to monitor thrombus growing and to better understand the pathophysiology of venous thromboembolism. Conclusion: In conclusion, data obtained show that the inhibition of COX-1 and COX-2 in a venous thrombosis mouse model could lead to opposite effect on the thrombus development, stabilization and resolution. In particular, COX-1 inhibition is responsible of an impairment development and growth of venous thrombus, with a mechanism most likely dependent of TXA2/TP pathway. In contrast, COX-2 inhibition caused an increased in thrombus development, growing accompanied with reduction in the thrombus resolution. All data obtained support evidences that both COX-1 and COX-2 play a key role in DVT, opening the way to novel therapeutic approaches.
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Bräutigam, Lutz. "Analytik und pharmakologische Effekte selektiver Cyclooxygenase-Inhibitoren." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=970822464.

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Books on the topic "Cyclooxygenase"

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Cyclooxygenases: Methods and protocols. New York, N.Y: Humana Press, 2010.

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Meunier, Andreas. Cyclooxygenase-2 inhibitors and knee prosthesis surgery. Linköping: Department of Clinical and Experimental Medicine, Linköping University, 2008.

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US-Italy Symposium on Cyclooxygenase and Lipoxygenase Modulators in Lung Reactivity (1984 Milan). Cyclooxygenase and lipoxgenase modulators in lung reactivity: US-Italy Symposium on Cyclooxygenase and Lipoxygenase Modulators in Lung Reactivity. Edited by Berti F, Hurd S, and Hegyeli R. J. 1931-. Basel: Karger, 1985.

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R, Vane John, Botting Regina M, William Harvey Research Conference (1997 : Phuket, Thailand), and William Harvey Research Conference (1998 : Boston, Mass.), eds. Clinical significance and potential of selective COX-2 inhibitors: The combined proceedings of the William Harvey Conferences held in Phuket, Thailand, on 18-19 September, 1997 and in Boston, USA, on 23-24 April, 1998, supported by an educational grant from Boehringer Ingelheim. London: William Harvey Press, 1998.

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Ayoub, Samir S., Roderick J. Flower, and Michael P. Seed, eds. Cyclooxygenases. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-364-6.

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Bandali, Karim Sadrudin. The role of the cyclooxygenase pathway in the cardiovascular and renal sympathoinhibitory effects of atrial natriuretic factor. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Masline, Shelagh Ryan. Celebrex: Cox-2 inhibitors--the amazing new pain fighters. New York: Avon Books, 1999.

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Maetzel, Andreas. The cost-effectiveness of celecoxib and rofecoxib in patients with osteoarthritis or rheumatoid arthritis. Ottawa, Ont: Canadian Coordinating Office for Health Technology Assessment, 2002.

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H, Vandenburgh Herman, and United States. National Aeronautics and Space Administration., eds. Mechanical stimulation of skeletal muscle increases prostaglandin F[́alpha] synthesis and cyclooxygenase activity by a pertussis toxin sensitive mechanism. Providence, RI: Dept. of Pathology and Laboratory Medicine, Brown University School of Medicine and the Miriam Hospital, 1992.

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The Cox-2 connection: Natural breakthrough treatment for arthritis, Alzheimer's, and cancer. Rochester, Vt: Healing Arts Press, 2001.

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Book chapters on the topic "Cyclooxygenase"

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Schwab, Manfred. "Cyclooxygenase." In Encyclopedia of Cancer, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_1433-2.

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Flower, Roderick J. "Cyclooxygenase Inhibitors." In Prostaglandins, Leukotrienes, and Lipoxins, 583–91. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4946-4_56.

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Kort, Will J., Lorette O. M. Hulsman, Pieter E. Zondervan, and Dick L. Westbroek. "Cyclooxygenase Inhibitors." In Prostaglandins, Leukotrienes, and Lipoxins, 619–25. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4946-4_59.

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Waldvogel, Herman Hans. "Cyclooxygenase-Isoformen." In Analgetika Antinozizeptiva Adjuvanzien, 377–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56710-0_51.

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Park, John M., Jürgen B. Schnermann, and Josephine P. Briggs. "Cyclooxygenase-2." In Advances in Experimental Medicine and Biology, 171–81. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4737-2_13.

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Kamp, Marc Willem. "Cyclooxygenase – Computational Studies." In Encyclopedia of Biophysics, 414–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_243.

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Staten, Nicholas R., and Beverly A. Reitz. "Cloning and Expression of Cyclooxygenase-1 and Cyclooxygenase-2." In Methods in Molecular Biology, 31–43. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-364-6_4.

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Morham, S. G., and R. Langenbach. "Characteristics of cyclooxygenase-1 and cyclooxygenase-2-deficient mice." In New Targets in Inflammation, 63–70. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-5386-7_7.

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Glaser, K. B. "Cyclooxygenase Selectivity and NSAIDs: Cyclooxygenase-2 Selectivity of Etodolac (Lodine)." In Side Effects of Anti-Inflammatory Drugs IV, 211–21. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5394-2_22.

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Tsujii, Masahiko, Shingo Tsuji, and Sunao Kawano. "Cyclooxygenase and Colon Cancer." In Trends in Gastroenterology and Hepatology, 263–66. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-67895-3_49.

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Conference papers on the topic "Cyclooxygenase"

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Arnaud, Claire, Elodie Gautier, Jean-Louis Pepin, Jean-Philippe Baguet, Renaud Tamisier, Patrick A. Levy, and Françoise Stanke-Labesque. "Cyclooxygenase Pathway Activation In Sleep Apnea Syndrome." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2173.

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Rao, Gautam G., Tyler Kochel, Namita Kundu, Jocelyn Reader, and Amy Fulton. "Abstract 524: Cyclooxygenase pathway in ovarian cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-524.

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Cordova, C., F. Violi, D. Praticò, A. Ghiselli, C. Alessandri, and F. Balsano. "CYCLOOXYGENASE INDIPENDENT PLATELET AGGREGATION:RELATION WITH ASPI RIN CONCENTRATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644828.

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Low doses of aspirin (20 mg/day) were previously reported to be uneffective in preventing platelet aggregation (PA) induced by pairs of aggregating agents such as PAF and adrenalin.This was in part attributed to the inability of such treatment to inhibit lipo oxygenase-dependent PA.The latter can be observed in vitro in"aspl rinated"platelets stimulated with high quantities of aggregating -agents.The aim of this study was to evaluate if the lipooxygenase-dependent PA was influenced by aspirin in a dose-dependent fashion. PA was studied in platelet rich plasma (PRP)(Born's method) by using threshold doses of aggregating agents (TDA) such as PAF(4-75 nM),epinephrine(0.6-2 μM) and collagen(2-4 μg/ml).PA performed in PRP pretrated with 100μM aspirin was fully prevented;in the same samples thromboxane (Tx) A2 evaluated by its metabolite Tx B2 was almost absent.Increasing amount of PAF(20 fold TDA),epinephrine(20 fold TDA) and collagen (36 fold TDA) do aggregate"aspirinated"pla telets;similarly"aspirinated"platelets aggregate when stimulated-with a pair of aggregating agents (TDA of PAF+epinephrine).This phenomenon was not detected if platelets were incubated with higher amounts of aspirin (250-500 μM).The study suggests that aspirin could influence lipooxygenase-dependent PA.This hypothesis is sup ported by a research showing the aspirin inhibits dose-dependently platelet HETE formation.A further study is now in progress to eva luate the influence of high doses of aspirin on cyclooxygenase-i"n dependent PA in vivo.
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Conner, Gregory E., Pedro Ivonnet, and Mathias Salathe. "Cyclooxygenase Mediates Hydrogen Peroxide Stimulation Of CFTR Activity." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6450.

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Wong, Kenneth, Konnie Urban, Angel Ang, Ning Zhang, Rajendra Singh, and Jae-Beom Kim. "Abstract 4292:In vivoandin vitroimaging of Cyclooxygenase-2 in tumor." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4292.

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Andrievskaya, Irina, Nataliya Ishutina, Inna Dovzhikova, and Nikolay Prihod'ko. "METHOD FOR ASSESSMENT THE IMPAIRMENT OF EMBRYO IMPLANTATION DURING PREGNANCY COMPLICATED BY CYTOMEGALOVIRAL INFECTION BY DETERMINING CYCLOOXYGENASE-2 IN HOMOGENATE OF VILLOUS CHORION." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c086109.30801383.

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A method for assessing the impairment of embryo implantation during pregnancy complicated by cytomegalovirus infection, based on the detection of cyclooxygenase 2 in the villous chorionic homogenate, is proposed
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Raji, Idris Olawale, Emily Janeira, Fatima Yadudu, Fathi Shaghayegh, James Kornacki, Milan Mrksich, and Adegboyega Oyelere. "Abstract 4534: Cyclooxygenase inhibitors as delivery vehicles for histone deacetylase inhibitors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4534.

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Trummlitz, G., and H. Wittneben. "SAT0080 Insight into the structural basis of selective cyclooxygenase-2 inhibition." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.455.

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Steinert, Bruce W., James M. Onoda, Bonnie F. Sloane, John D. Taylor, and Kenneth V. Honn. "CYCLOOXYGENASE AND LIPOXYGENASE PRODUCTS SYNERGISTICALLY MODULATE TUMOR CELL INDUCED PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644668.

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There has been considerable controversy surrounding the ability of inhibitors of arachidonic acid metabolism to concomitantly inhibit tumor cell induced platelet aggregation (TCIPA). Reconciliation of this controversy has been difficult due to the wide variability of experimental conditions (e.g., inhibitor concentration, strength of the inducing agonist).In the present study, we examined the effects of several cyclooxygenaseand lipoxygenase inhibitors on the induction of platelet aggregation by Walker 256 carcinosarcoma (W256) cells. We have previously demonstrated that aggregation of platelet rich plasma (PRP), induced by W256 cells, was initiated via a thrombin dependent mechanism. Platelet aggregation was induced by the addition of W256 cells (75,000-J500,000 cells/cuvette) to rat PRP preincubated with inhibitor(s) or diluent. The strength of the inducing stimulus affected both the degree of aggregation and the production of thromboxane A2 (TXA2) in a dose dependent manner. A weak stimulus (low concentration of W256 cells) produced only a low level of aggregation and low TXA2 production, whereas aggregation induced by a strong stimulus (high concentration of W256 cells) resulted in significant aggregation and increased TXA2 production. Preincubation (5 min., 37°C) of rat PRP with cyclooxygenase inhibitors (e.g., aspirin, indomethacin, ibuprofen) resulted in complete inhibition of platelet aggregation at low agonist concentration (75,000 W256 cells), whereas when a high agonist concentration (500,000 W256 cells) was used to induce aggregation, the inhibitors failed to inhibit TCIPA. The addition of fewer than 50,000W256 cells failed to induce any measurable platelet aggregation in the presence or absence of inhibitors. TCIPA was not affected by lipoxygenaseinhibitors (e.g.,quercetin) alone regardless of agonist concentration. Both cyclooxygenase and lipoxygenase inhibitors, however, were required to significantly inhibit TCIPA induced by high agonist concentration. Compounds which inhibited both the cycloogygenase and lipoxygenase pathways (e.g.,hydroquinone, BW755c) inhibited TCIPA at all agonist concentrations. Nafazatrom failed to inhibit TCIPA consistant with a lack of effect on platelet cyclooxygenase and lipoxygenase. Therefore, we conclude cyclooxygenase (e.g., TXA2) and lipoxygenase (e.g., 12-HETE) products of platelet arachidonic acid metabolism and the strength of the inducingagonist are important criteria in TCIPA. This study may help to clarify the current controversy regarding the inhibition of TCIPA by inhibitors of arachidonic acid metabolism.
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Lecomte, M., and J. M. Boeynaems. "COVALENT BINDING OF CYCLOOXYGENASE AND LIPOXYGENASE PRODUCTS TO HUMAN PLATELET PROTEINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643397.

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Several studies in acellular systems have shown a covalent binding of eicosanoids to proteins (1). We have therefore investigated whether eicosanoids bind covalently to proteins in intact platelets. After incubation of washed human platelets with 14C-arachidonic acid, ethanol precipitation followed by extractions, a small fraction of the radioactivity (0.3%) was tightly bound to the protein pellet. Four criteria suggest the covalent nature of this binding. The radioactivity remained bound after exhaustive extractions with solvents of various polarities, and was not removed by dialysis against SDS-buffer. 15 labelled protein bands could be separated by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). Finally, exhaustive enzymatic hydrolysis of platelet proteins by several proteases liberated an amphipathic radioactive material which had a chromatographic behaviour similar to that of a known peptidolipid, leuko-triene c4 This covalent binding involved products of both cyclooxygenase and lipoxygenase pathways : it was partially inhibited by indomethacin (±40%) and completely abolished by eicosatetraynoic acid. The covalent binding was increased five-fold by dazoxiben, suggesting attachment of prostaglandin endoperoxydes , and by diamide (a glutathione depleting agent) (2) suggesting the involvement of 12-hydro-peroxyeicosatetraenoic acid. Dazoxiben and diamide intensified selectively the labelling of distinct protein bands, separated by SDS-PAGE. Further studies will be needed to evaluate the possible physiological significance of this covalent modification.(1) Wilson, A.G.E. et al. Prostaglandins 18: 409-422, 1979.(2) Bryant, R.W. et al., J. Biol. Chem. 257: 14937-14943, 1982
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Reports on the topic "Cyclooxygenase"

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Wang, Congcong, Hongjuan Fu, Jun Wang, Fujun Huang, and Xuejun Cao. Preemptive analgesia using selective cyclooxygenase-2 inhibitors alleviates postoperative pain in patients undergoing total knee arthroplasty: A meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0101.

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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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Fields, Michael J., Mordechai Shemesh, and Anna-Riitta Fuchs. Significance of Oxytocin and Oxytocin Receptors in Bovine Pregnancy. United States Department of Agriculture, August 1994. http://dx.doi.org/10.32747/1994.7568790.bard.

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Oxytocin has multiple actions in bovine reproductive tract and it was our purpose to determine the nature of these actions and their significance for the physiology of bovine reproduction. The bovine oxytocin receptors (OTR) gene was cloned and its expression studied during the cycle and pregnancy. OTR mRNA changed in parallel with OTR with control occurring mainly at the transcriptional level. However, the endocrine regulation of OTR were found in endometrium and cervical mucosa at estrus and at parturition. In both tissues OTR were suppressed in the luteal phase and early pregnancy. Whereas cervical OTR remained suppressed throughout pregnancy, endometrial OTR began to increase soon after implantation and reached higher concentrations in midpregnancy than at estrus. OTR in caruncles did not increase until third trimester, and OTR in cervical mucosa, cotyledons and fetal membranes increased only at term. Myometrial OTR showed less variation and OTR were present throughout the cycle and pregnancy but increased significantly during mid- and late pregnancy. OTR were localized in endometrial epithelial cells and lumina epithelial cells of cervical mucosa as determined by immunohistochemistry. Endometrial OTR were functional throughout pregnancy and mediated PGF release from day 50 onwards in a receptor density related manner. OTR in cervical mucosa mediated PGE release both in vivo and in vitro, as shown in cyclic cows. The ontogeny of uterine OTR was studied from third trimester fetal stage until puberty. OTR were present in endometrium and cervical mucosa in high concentrations throughout this period; myometrial OTR began to increase somewhat later but also reached adult values by 6-mo of age. In the prepuberal heifers OT injections failed to initiate PGF2a, release. The influence of steroids on the effect of OT was examined. Ovariectomy and E2 were without effect, but P4 with or without E2 induced a massive PGF2a release in response to OT in spite of reduced OTR. Bovine cyclooxygenases (COX-1 and COX-2) were cloned and their expression studied in the endometrium of prepuberal heifers and pregnant cows. Untreated and E2 treated prepuberal heifers did not express COX-2 but P4 treated heifers did express the mRNA for COX-2, albeit weakly. During the second half of pregnancy COX-2 mRNA was strongly expressed in cotyledons and somewhat less in caruncles, whereas endometrium, myometrium and cervical mucosa showed only weak, if any, COX-2 mRNA under basal conditions. However, 2 h after OT injection significant increases in COX-2 mRNA were found in endometrial RNA. Thus OT is capable of inducing the expression of the inducible COX-2 gene, and hence the conversion of arachidonic acid to prostanoids. The results indicate that the functions of OT are numerous and probably essential for successful pregnancy and parturition.
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