Journal articles: 'Prostaglandines – Synthèse'

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Yang, Ling, Xu Han, Leying Zhang, Ning Li, Zimo Zhao, and Jiachen Bai. "Changes in expression of prostaglandin synthase in ovine liver during early pregnancy." Canadian Journal of Animal Science 100, no. 3 (September 1, 2020): 432–39. http://dx.doi.org/10.1139/cjas-2019-0171.

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Liver can function as part of the innate and adaptive immune systems. We hypothesize that prostaglandins participate in the regulation of hepatic immune function during early pregnancy in sheep. The objective of this study was to elucidate expression of prostaglandin synthase in ovine liver during early pregnancy. Ovine livers were sampled on day 16 of the estrous cycle, and days 13, 16, and 25 of pregnancy, and the expression of prostaglandin synthases, including prostaglandin-endoperoxide synthase 1 (PTGS1), PTGS2, prostaglandin E synthase (PTGES), and aldo-keto reductase family 1, member B1, a prostaglandin F synthase (PGFS), were detected by quantitative real-time polymerase chain reaction, Western blot, and immunohistochemistry analysis. There were increases in the expression of mRNA and the proteins of PTGS2, PTGES, and PGFS in the livers during early pregnancy, but PTGS1 was decreased in the pregnant ewes. The PGFS protein was limited to the hepatocytes and the endothelial cells of the proper hepatic arteries and hepatic portal veins. In summary, the upregulation of PTGS2, PTGES, and PGFS and downregulation of PTGS1 may be involved in the maternal hepatic immune adjustment during early pregnancy in sheep.

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Berthou, F., F. Ceppo, M. Cormont, and J. F. Tanti. "P2096 Implication de la kinase Tpl2 dans l’expression de COX-2 et la synthèse des prostaglandines induites par les cytokines inflammatoires dans les adipocytes." Diabetes & Metabolism 39 (March 2013): A90—A91. http://dx.doi.org/10.1016/s1262-3636(13)72006-8.

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Tsuchida, Keiichiro, Takae Ibuki, and Kiyoshi Matsumura. "Bromoenol Lactone, an Inhibitor of Calcium-Independent Phospholipase A2, Suppresses Carrageenan-Induced Prostaglandin Production and Hyperalgesia in Rat Hind Paw." Mediators of Inflammation 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/605727.

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Prostaglandin (PG) E2and PGI2are essential to hyperalgesia in inflammatory tissues. These prostaglandins are produced from arachidonic acid, which is cleaved from membrane phospholipids by the action of phospholipase A2(PLA2). Which isozyme of PLA2is responsible for the cleavage of arachidonic acid and the production of prostaglandins essential to inflammation-induced hyperalgesia is not clear. In this study, we examined the effects of two PLA2isozyme-specific inhibitors on carrageenan-induced production of PGE2and PGI2in rat hind paw and behavioral nociceptive response to radiant heat. Local administration of bromoenol lactone (BEL), an inhibitor of calcium-independent PLA2(iPLA2), significantly reduced carrageenan-induced elevation of prostaglandins in the inflamed foot pad 3 h after injection. It also ameliorated the hyperalgesic response between 1 h and 3 h after carrageenan injection. On the other hand, AACOCF3, an inhibitor of cytosolic PLA2, suppressed neither prostaglandin production nor the hyperalgesic response. BEL did not suppress the mRNA levels of iPLA2β, iPLA2γ, cyclooxygenase-2, microsomal prostaglandin E synthase, prostaglandin I synthase, or proinflammatory cytokines in the inflamed foot pad, indicating that BEL did not suppress inflammation itself. These results suggest that iPLA2is involved in the production of prostaglandins and hyperalgesia at the inflammatory loci.

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Gómez-Foix, A. M., J. E. Rodriguez-Gil, J. J. Guinovart, and F. Bosch. "Prostaglandins E2 and F2α affect glycogen synthase and phosphorylase in isolated hepatocytes." Biochemical Journal 261, no. 1 (July 1, 1989): 93–97. http://dx.doi.org/10.1042/bj2610093.

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Prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) inactivated glycogen synthase and activated glycogen phosphorylase in rat hepatocytes in a dose- and time-dependent manner. These effects were dependent on the presence of Ca2+ in the incubation medium. When glycogen synthase was immunoprecipitated from cells incubated with [32P]Pi and then treated with PGE2 or PGF2 alpha, there was increased phosphorylation of the 88 kDa subunit of the enzyme. This phosphorylation affected two CNBr fragments of the glycogen synthase, CB-1 and CB-2, the same fragments that are phosphorylated by different glycogenolytic hormones. No phosphorylation of glycogen synthase by prostaglandins was observed in the absence of Ca2+. Thus the effect of PGE2 and PGF2 alpha on these glycogen-metabolizing enzymes supports a role for regulation by prostaglandins of glucose metabolism in parenchymal liver cells.

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Laurent, Fabrice, Martin F. Kagnoff, Tor C. Savidge, Muriel Naciri, and Lars Eckmann. "Human Intestinal Epithelial Cells Respond toCryptosporidium parvum Infection with Increased Prostaglandin H Synthase 2 Expression and Prostaglandin E2and F2α Production." Infection and Immunity 66, no. 4 (April 1, 1998): 1787–90. http://dx.doi.org/10.1128/iai.66.4.1787-1790.1998.

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ABSTRACT Cryptosporidium parvum is an important cause of diarrhea in humans and several animal species. Prostaglandins play a central role in regulating intestinal fluid secretion in animal models of cryptosporidiosis, but their cellular sources and mechanisms of induction are unclear. Here, we show that C. parvuminfection directly activates prostaglandin H synthase 2 expression and prostaglandin E2 and F2α production in human intestinal epithelial cells.

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Mitchell, MD, RJ Romero, SS Edwin, and MS Trautman. "Prostaglandins and parturition." Reproduction, Fertility and Development 7, no. 3 (1995): 623. http://dx.doi.org/10.1071/rd9950623.

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It seems likely that prostaglandins play a significant part in the mechanisms of parturition both at term and preterm. Concentrations of prostaglandins are increased in the blood, urine and amniotic fluid during labour. There are differences in the concentrations of prostaglandins in amniotic fluid from the forebag and hindbag. Nevertheless, if liquor is sampled only from the hindbag a highly significant increase in prostaglandin concentrations occurs throughout labour. Furthermore, we now have evidence that prostaglandin concentrations in amniotic fluid increase before the onset of labour. Prostaglandins are synthesized by uterine tissues and increased rates of production occur during labour. The amnion, chorion and decidua all contain mRNA for the newly-discovered inducible form of prostaglandin H synthase (PGHS-2) as well as mRNA for the constitutive form (PGHS-1). Using the reverse transcription polymerase chain reaction (RT-PCR) both mRNAs can be detected during late pregnancy whether women are in labour or not. PGHS-2 protein is detected by Western blot analysis in cells derived from all three tissues. There is regulation of PGHS-2 protein amounts by cytokines, phorbol esters and growth factors. For example, in amnion cells interleukin-1 beta induces a rapid increase in PGHS-2 mRNA levels followed by a decrease to undetectable levels within 4 h of treatment; PGHS-2 protein amounts are also elevated by this treatment. Administration of prostaglandins will induce labour and delivery, whereas inhibition of prostaglandin biosynthesis will delay labour and delivery. Hence, increased prostaglandin production is likely to be a key determinant of the onset and progression of the parturient process.

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Tang, Eva H. C., and Paul M. Vanhoutte. "Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension." Physiological Genomics 32, no. 3 (February 2008): 409–18. http://dx.doi.org/10.1152/physiolgenomics.00136.2007.

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The present study was designed to assess whether or not changes in genomic expression of cyclooxygenases (COX-1, COX-2), endothelial nitric oxide synthase (eNOS), and prostanoid synthases in the endothelium and of prostanoid receptors in vascular smooth muscle contribute to the occurrence of endothelium-dependent contractions during aging and hypertension. Gene expression was quantified by real-time PCR using isolated endothelial cells and smooth muscle cells (SMC) from the aorta of Wistar-Kyoto and spontaneously hypertensive rats. Genes for all known prostanoid synthases and receptors were present in endothelial cells and SMC, respectively. Aging caused overexpression of eNOS, COX-1, COX-2, thromboxane synthase, hematopoietic-type prostaglandin D synthase, membrane prostaglandin E synthase-2, and prostaglandin F synthase in endothelial cells and COX-1 and prostaglandin E2 (EP)4 receptors in SMC. Hypertension augmented the expression of COX-1, prostacyclin synthase, thromboxane synthase, and hematopoietic-type prostaglandin D synthase in endothelial cells and prostaglandin D2 (DP), EP3, and EP4 receptors in SMC. The increase in genomic expression of endothelial COX-1 explains why in aging and hypertension the endothelium has greater propensity to release cyclooxygenase-derived vasoconstrictive prostanoids. The expression of prostacyclin synthase was by far the most abundant, explaining why the majority of the COX-1-derived endoperoxides are transformed into prostacyclin, substantiating the role of prostacyclin as an endothelium-derived contracting factor. The expression of thromboxane synthase was increased in the cells of aging or hypertensive rats, explaining why the prostanoid can contribute to endothelium-dependent contractions. It is uncertain whether the gene modifications caused by aging and hypertension directly contribute to endothelium-dependent contractions or rather to vascular aging and the vascular complications of the hypertensive process.

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Chopra, Sahil, Paolo Giovanelli, Perla Abigail Alvarado-Vazquez, Sara Alonso, Minkyung Song, Tito A. Sandoval, Chang-Suk Chae, et al. "IRE1α–XBP1 signaling in leukocytes controls prostaglandin biosynthesis and pain." Science 365, no. 6450 (July 18, 2019): eaau6499. http://dx.doi.org/10.1126/science.aau6499.

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Inositol-requiring enzyme 1[α] (IRE1[α])–X-box binding protein spliced (XBP1) signaling maintains endoplasmic reticulum (ER) homeostasis while controlling immunometabolic processes. Yet, the physiological consequences of IRE1α–XBP1 activation in leukocytes remain unexplored. We found that induction of prostaglandin-endoperoxide synthase 2 (Ptgs2/Cox-2) and prostaglandin E synthase (Ptges/mPGES-1) was compromised in IRE1α-deficient myeloid cells undergoing ER stress or stimulated through pattern recognition receptors. Inducible biosynthesis of prostaglandins, including the pro-algesic mediator prostaglandin E2 (PGE2), was decreased in myeloid cells that lack IRE1α or XBP1 but not other ER stress sensors. Functional XBP1 transactivated the human PTGS2 and PTGES genes to enable optimal PGE2 production. Mice that lack IRE1α–XBP1 in leukocytes, or that were treated with IRE1α inhibitors, demonstrated reduced pain behaviors in PGE2-dependent models of pain. Thus, IRE1α–XBP1 is a mediator of prostaglandin biosynthesis and a potential target to control pain.

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9

Rice, G. E., M. H. Wong, and G. D. Thorburn. "Gestational changes in prostaglandin synthase activity of ovine cotyledonary microsomes." Journal of Endocrinology 118, no. 2 (August 1988): 265–70. http://dx.doi.org/10.1677/joe.0.1180265.

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ABSTRACT The capacity of cotyledonary microsomes, prepared from pregnant ewes (20–145 days of gestation), to metabolize exogenous arachidonic acid was quantified using a radiolabel technique. During gestation, the capacity of microsomes to metabolize arachidonic acid increased 25-fold, from 0·36±0·06μmol arachidonic acid/incubation (n = 8) at <100 days of gestation to 9·06±1 ·02μmol arachidonic acid/incubation at 130–145 days of gestation (n = 5; P<0·05). Arachidonic acid was metabolized to prostaglandin E2 and F2α, as determined by thin-layer chromatography and reverse-phase high performance liquid chromatography. The profile of prostaglandins synthesized by cotyledonary microsomes did not change throughout gestation. These data suggest that the increase in cotyledonary prostaglandin synthesis that occurs during late gestation and at term may reflect an increase in the tissue content of prostaglandin H2 synthase. J. Endocr. (1988) 118, 265–270

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Li, Ke, Jing Zhao, Mingxuan Wang, Lingzhi Niu, Yuanping Wang, Yanxia Li, and Yajuan Zheng. "The Roles of Various Prostaglandins in Fibrosis: A Review." Biomolecules 11, no. 6 (May 24, 2021): 789. http://dx.doi.org/10.3390/biom11060789.

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Organ fibrosis is a common pathological result of various chronic diseases with multiple causes. Fibrosis is characterized by the excessive deposition of extracellular matrix and eventually leads to the destruction of the tissue structure and impaired organ function. Prostaglandins are produced by arachidonic acid through cyclooxygenases and various prostaglandin-specific synthases. Prostaglandins bind to homologous receptors on adjacent tissue cells in an autocrine or paracrine manner and participate in the regulation of a series of physiological or pathological processes, including fibrosis. This review summarizes the properties, synthesis, and degradation of various prostaglandins, as well as the roles of these prostaglandins and their receptors in fibrosis in multiple models to reveal the clinical significance of prostaglandins and their receptors in the treatment of fibrosis.

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11

Williams, C. S., and R. N. DuBois. "Prostaglandin endoperoxide synthase: why two isoforms?" American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 3 (March 1, 1996): G393—G400. http://dx.doi.org/10.1152/ajpgi.1996.270.3.g393.

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Prostaglandin endoperoxide synthase-1 [prostaglandin G/H synthase-1 (PGHS-1)] and PGHS-2 are key enzymes in the conversion of arachidonic acid to prostaglandins and other eicosanoids. We refer to these isoforms as cyclooxygenase-1 (COX-1) and COX-2 in this review. This brief review focuses on recent developments in the study of these enzymes. Alterations in the expression levels of COX-2 result in distinct phenotypic changes in intestinal epithelial cells. Overexpression of COX-2 in intestinal epithelial cells results in increased adhesion to extracellular matrix proteins and inhibition of apoptosis. Disruption of the COX-2 gene in mice results in renal dysplasia, cardiac fibrosis, and defects in the ovary. Interestingly, disruption of the COX-1 gene results in distinct phenotypic changes different from those observed for COX-2. COX-1 null mice survive well, have no gastric pathology, and show less indomethacin-induced gastric ulceration than wild-type mice. These two closely related enzymes must have distinct functions in the organisms, since lack of their expression causes distinct phenotypic changes for each respective isoform.

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Roberto da Costa, Rosário P., Ana S. Costa, Anna J. Korzekwa, Rafal Platek, Marta Siemieniuch, António Galvão, Dale A. Redmer, José Robalo Silva, Dariusz J. Skarzynski, and Graça Ferreira-Dias. "Actions of a nitric oxide donor on prostaglandin production and angiogenic activity in the equine endometrium." Reproduction, Fertility and Development 20, no. 6 (2008): 674. http://dx.doi.org/10.1071/rd08015.

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Nitric oxide (NO) plays an important role in prostaglandin secretion and angiogenesis in the reproductive system. In the present study, the roles of the NO donor spermine NONOate and tumour necrosis factor-α (TNF; as a positive control) in prostaglandin production and angiogenic activity of equine endometria during the oestrous cycle were evaluated. In addition, the correlation between NO production and the expression of key prostaglandin synthase proteins was determined. The protein expression of prostaglandin F synthase (PGFS) increased in early and mid-luteal stages, whereas that of prostaglandin E synthase (PGES) was increased in the early luteal stage. The in vitro release of NO was highest after ovulation. There was a high correlation between NO production and PGES expression, as well as NO release and PGFS expression. There were no differences detected in prostaglandin H synthase 2 (PTGS-2) throughout the oestrous cycle and there was no correlation between PTGS-2 expression and NO. In TNF- or spermine-treated endometria, the expression of prostaglandin (PG) E2 increased in the early and mid-luteal phases, whereas that of PGF2α increased in the follicular and late luteal phases. Bovine aortic endothelial cell (BAEC) proliferation was stimulated in TNF-treated follicular-phase endometria. However, in spermine-treated endometria, NO delivered from its donor had no effect, or even an inhibitory effect, on BAEC proliferation. In conclusion, despite no change in PTGS-2 expression throughout the oestrous cycle in equine endometrial tissue, there were changes observed in the expression of PGES and PGFS, as well as in the production of PGE2 and PGF2α. In the mare, NO is involved in the secretory function of the endometrium, modulating PGE2 and PGF2α production. Even though TNF caused an increase in the production of angiogenic factors and prostaglandins, its complex action in mare uterus should be elucidated.

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Gaffney, RC, GE Rice, and SP Brennecke. "Is human labour triggered by an increase in the rate of synthesis of prostaglandin G/H synthase?" Reproduction, Fertility and Development 2, no. 5 (1990): 603. http://dx.doi.org/10.1071/rd9900603.

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The increase in the synthesis of prostaglandins by intrauterine tissues which occurs at the time of parturition may be the consequence of periparturient changes in several regulatory pathways. The aim of this study was to determine whether changes in the rate of synthesis of prostaglandin G/H synthase (PGHS) contribute to the labour-associated increase in prostaglandin synthesis by human chorioamnion and placenta. The rate of recovery of prostaglandin E2 (PGE2) synthesis following inhibition of PGHS by aspirin was used as an estimation of PGHS resynthesis. In tissues obtained following spontaneous delivery, the half-time recovery of PGE2 synthesis was 3.5 to 6.0-fold less (P less than 0.001; n = 5) than the half-time recovery observed in tissues obtained before the onset of labour. These data suggest that a periparturient increase in the rate of synthesis of PGHS contributes to enhanced prostaglandin synthesis at term.

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O'Reilly, Katherine M. A., Richard P. Phipps, Thomas H. Thatcher, Beth A. Graf, John Van Kirk, and Patricia J. Sime. "Crystalline and amorphous silica differentially regulate the cyclooxygenase-prostaglandin pathway in pulmonary fibroblasts: implications for pulmonary fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 6 (June 2005): L1010—L1016. http://dx.doi.org/10.1152/ajplung.00024.2004.

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Inhalation of crystalline (CS) and amorphous silica (AS) results in human pulmonary inflammation. However, silicosis develops only following CS exposure, and the pathogenic mechanisms are poorly understood. This report describes the differential abilities of CS and AS to directly upregulate the early inflammatory mediator COX-2, the recently identified prostaglandin E (PGE) synthase and the downstream mediator PGE2 in primary human lung fibroblasts. Increased cyclooxygenase (COX)-2 gene transcription and protein production were demonstrated by ribonuclease protection assay, Western blot analysis, and immunocytochemistry. In each case the ability of AS to induce COX-2 exceeded that of CS. Similarly, downstream of COX-2, production of the antifibrotic prostaglandin PGE2 was induced in a dose-dependent fashion, but AS was significantly more potent (maximal production: CS = 4,710 pg/ml and AS = 7,651 pg/ml). These increases in COX-2 and PGE2 were preceded by induction of the PGE2 synthase protein, demonstrating the potential role of this novel molecule in silica-mediated inflammation. There was specificity of induction of prostaglandins, as PGF2α, but not PGD2, was induced. Using specific COX-2 inhibitors, we showed increased PG production to be dependent on the COX-2 enzyme. Furthermore, stimulation of fibroblasts was particle specific, as silica but not carbon black resulted in fibroblast activation. These results demonstrate that silica can directly stimulate human lung fibroblasts to produce key inflammatory enzymes and prostaglandins. Moreover, they suggest a mechanism to explain the differing fibrogenic potential of CS and AS. The molecules COX-2, PGE synthase, and PGE2 are identified as effectors in silicosis.

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Deenarn, Pacharawan, Punsa Tobwor, Vanicha Vichai, Suwanchai Phomklad, Panomkorn Chaitongsakul, Rungnapa Leelatanawit, and Wananit Wimuttisuk. "Polychaete consumption increased prostaglandin biosynthesis in female Penaeus monodon." Reproduction 160, no. 6 (December 2020): 873–85. http://dx.doi.org/10.1530/rep-20-0217.

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The polychaete Perinereis nuntia is preferred over commercial feed pellets for boosting ovarian maturation of the female black tiger shrimp Penaeus monodon. High levels of prostaglandins in polychaetes are believed to enhance shrimp ovarian development. However, the impact of polychaete feeding on shrimp prostaglandin biosynthesis and fatty acid regulatory pathways have yet to be investigated. As polychaetes contain higher levels of arachidonic acid (ARA), eicosapentaenoic acid (EPA), prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) than feed pellets, we examined the effects of polychaete feeding alone and in combination with eyestalk ablation on shrimp hepatopancreases and ovaries. Shrimp fed with polychaetes contained higher levels of EPA, PGE2 and PGF2α in hepatopancreases than those of pellet-fed shrimp. Similarly, higher levels of ARA and higher transcription levels of cyclooxygenase (COX) and prostaglandin F synthase (PGFS) were detected in ovaries of polychaete-fed shrimp compared to those of pellet-fed shrimp. The combination of polychaete-feeding and eyestalk ablation, commonly practiced to induce ovarian development, increased levels of ARA and EPA and transcription levels of COX in hepatopancreases and ovaries of polychaete-fed shrimp compared to those of pellet-fed shrimp. In ovaries, prostaglandin biosynthesis gene transcripts were induced by polychaete feeding while transcriptional levels of fatty acid regulatory genes were regulated by shrimp feed and eyestalk ablation. Our findings not only elucidate the effects of polychaete consumption on shrimp prostaglandin biosynthesis and fatty acid regulatory pathways during larvae production, but also suggests that high levels of dietary ARA, EPA and prostaglandins are essential during P. monodon ovarian development.

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Yang, Chin-Yuh, Ching-Liang Meng, and Patrick Y. K. Wong. "Human parathyroid hormone fragment stimulates thede novosynthesis of prostaglandin endoperoxide synthase in chick calvaria." Mediators of Inflammation 2, no. 2 (1993): 143–47. http://dx.doi.org/10.1155/s0962935193000213.

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The human parathyroid hormone N-terminal fragment [hPTH-(1–34)] increases the conversion of exogenous unsaturated fatty acids to prostaglandins (PGs) in calvarial homogenates. Enzyme activities were completely blocked by indomethacin (5 × 10−7M), a PG synthase inhibitor, and actinomycin D (5 μM), an inhibitor of transcription, by binding to DNA. In addition, a potent inhibitor of protein synthesis, cycloheximide (10 μM), totally inhibited the stimulating effect of hPTH-(1–34) on prostaglandin endoperoxide synthase (PG synthase, EC 1.14.99.1). The stimulatory effect of hPTH-(1–34) on PG synthase was also reduced by the addition of stannous chloride. However, epidermal growth factor (EGF), platelet-derived activating factor (PDGF), and ionophore A23187 did not show the same stimulating effect as hPTH-(1–34) on PG synthase in calvaria. The results further demonstrated that PG synthase is a membrane-bound enzyme in chick calvaria. In this communication, evidence is presented that hPTH-(1–34) stimulates thede novosynthesis of PG synthase as demonstrated by the increased activity in calvarial homogenates and microsomes.

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Jabbour, H. N. "007. INFLAMMATORY PATHWAYS IN ENDOMETRIAL CANCER." Reproduction, Fertility and Development 21, no. 9 (2009): 5. http://dx.doi.org/10.1071/srb09abs007.

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Endometrial cancer is the most common gynaecological malignancy and accounts for 5% of cancers in women (http://info.cancerresearchuk.org/cancerstats/). The majority of endometrial cancers occur in post-menopausal women and 80% of patients are diagnosed when the tumour is confined to the uterus (stage 1 disease). Many of the risk factors for developing endometrial cancer are associated with excess exposure to oestrogen unopposed by progesterone. It is well established that local inflammatory pathways contribute to the initiation and progression of endometrial cancers via the release of local mediators to facilitate immune cell recruitment, angiogenesis and neoplastic cell proliferation and metastasis. Prostaglandins are one class of molecules that are important mediators of these processes. Prostaglandins are bioactive lipids produced from arachidonic acid by cyclooxygenase (COX) enzymes and specific terminal prostanoid synthase enzymes. Following biosynthesis, prostaglandins are rapidly transported outside the cell and exert an autocrine/paracrine function by coupling to specific prostanoid G protein-coupled receptors (GPCR). Expression of COX enzyme, synthesis of prostaglandins and expression of various prostaglandin receptors are elevated in pathologies of the endometrium including cancer. Using genome wide array analysis, we have identified target genes that are regulated by prostaglandins such as PGF2α via interaction with its GPCR - FP receptor. Gene ontology analysis have highlighted significant elevation in expression of genes involved in inflammatory and vascular processes which are central to endometrial function. Moreover, using an array of cellular and molecular techniques and in vivo models we have established an important role for PGF2α-FP interaction in regulating inflammatory and vascular functions. To-date, suppression of the activity of prostaglandins in pathology has focussed on using inhibitors of cyclooxygenase enzymes, which are key enzymes in the pathway to prostaglandin synthesis. However, this has been associated with serious cardiovascular side effects. Development of novel drugs that target specific receptors may provide better therapeutic alternatives.

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Janowski, Tomasz, Wojciech Barański, Karolina Łukasik, Dariusz Skarżyński, Sławomir Zduńczyk, and Katarzyna Malinowska. "Endometrial mRNA expression of prostaglandin synthase enzymes PTGS 2, PTGFS and mPTGES 1 in repeat-breeding cows with cytologically determined endometritis." Acta Veterinaria Hungarica 65, no. 1 (March 2017): 96–104. http://dx.doi.org/10.1556/004.2017.010.

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Little is known about the inflammatory response of the endometrium in repeat-breeding cows with subclinical endometritis (SE). The objective of this study was to evaluate the mRNA expression of prostaglandin-endoperoxide synthase 2 (PTGS 2), prostaglandin F2α synthase (PTGFS) and prostaglandin E2 microsomal synthase 1 (mPTGES 1) in the endometrium of repeat-breeding cows with and without SE. SE was diagnosed cytologically using the cytobrush method, with the threshold being set at 5% polymorphonuclear neutrophils. Biopsy samples were obtained from the endometrium of repeat-breeding cows with SE (n = 10) and without SE (n = 10). The mRNA expression of the synthases was evaluated using qRT-PCR. Significantly higher (P < 0.05) expression of the PTGS 2 gene was detected in the repeat breeders with SE, whereas there was no significant difference in the expression of PTGFS and mPTGES 1 mRNAs between repeatbreeding cows with SE and those without it (P > 0.05). Our study confirms that increased endometrial expression of the PTGS 2 gene is involved in the inflammatory response in repeat breeders.

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Reimsnider, SK, and CE Wood. "Co-localisation of prostaglandin endoperoxide synthase and immunoreactive adrenocorticotrophic hormone in ovine foetal pituitary." Journal of Endocrinology 180, no. 2 (February 1, 2004): 303–10. http://dx.doi.org/10.1677/joe.0.1800303.

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Previous studies have shown that both an intact hypothalamic-pituitary-adrenal axis and prostaglandin E(2) (PGE(2)) are involved in the timing of parturition in sheep. PGE(2) is known to be synthesised by the placenta but has also been found in the foetal brain and pituitary. We propose that the enzymes necessary for production of PGE(2) are found in the ovine foetal pituitary and may be able to exert an autocrine and/or paracrine influence on corticotropes, resulting in an increased secretion of immunoreactive adrenocorticotrophin (irACTH). Pituitary tissues from foetal sheep, of gestational ages 119-126 days, were examined by immunohistochemistry. Primary antibodies for prostaglandin H synthase-1 and -2 (PGHS-1 and PGHS-2), microsomal prostaglandin endoperoxide synthase (mPGES) and irACTH were used to probe expressed proteins and Alexa-Fluor red- and green-fluorescent secondary antibodies were used to visualise the bound primary antibody. Staining for PGHS-1, PGHS-2 and mPGES was found throughout the foetal anterior pituitary. PGHS-1 and mPGES were widely distributed, including but not restricted to corticotropes. PGHS-2 was less widely distributed but occasionally was found in cells adjacent to corticotropes. The results indicate that locally produced prostaglandins may have an influence on the secretion of ACTH, independent of placental PGE(2).

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Pilbeam, Carol C., Lawrence G. Raisz, Olga Voznesensky, Cynthia B. Alander, Bradley N. Delman, and Hiroshi Kawaguchi. "Autoregulation of inducible prostaglandin G/H synthase in osteoblastic cells by prostaglandins." Journal of Bone and Mineral Research 10, no. 3 (December 3, 2009): 406–14. http://dx.doi.org/10.1002/jbmr.5650100311.

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Novaro, V., A. Jawerbaum, A. Faletti, M. A. F. Gimeno, and E. T. González. "Uterine nitric oxide and prostaglandin E during embryonic implantation in non-insulin-dependent diabetic rats." Reproduction, Fertility and Development 10, no. 3 (1998): 217. http://dx.doi.org/10.1071/r98027.

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In the process of embryo implantation in the rat, both nitric oxide and prostaglandins act as vascular and myometrial regulators. The aim of the present work was to evaluate the effect of diabetes on the synthesis of both agents during embryo implantation. In diabetic rats, uterine activity of the enzyme nitric oxide synthase and prostaglandin E production were increased during peri-implantation compared to the control group (P < 0·05 and P < 0·001, respectively). Both parameters showed a prolonged increase in temporal profile during peri-implantation days. Local production of nitric oxide and prostaglandin E in the implantation sites was higher in diabetic rats (P < 0·05), but the intersite : site ratio was similar to that of the control group. On the other hand, the implantation rate and the timing of the beginning of this process were not altered in the diabetic group. These results suggest that the vasoactive modulators of the implantation process, nitric oxide and prostaglandins, are increased in this diabetic pathology, and that this increase is probably functioning as a compensatory mechanism, so as to allow an unaltered rate of embryo implantation in this model. Extra keyword: diabetes mellitus.

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Kortenoeven, Marleen L. A., Horst Schweer, Rik Cox, Jack F. M. Wetzels, and Peter M. T. Deen. "Lithium reduces aquaporin-2 transcription independent of prostaglandins." American Journal of Physiology-Cell Physiology 302, no. 1 (January 2012): C131—C140. http://dx.doi.org/10.1152/ajpcell.00197.2011.

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Vasopressin (AVP)-stimulated translocation and transcription of aquaporin-2 (AQP2) water channels in renal principal cells is essential for urine concentration. Twenty percent of patients treated with lithium develop nephrogenic diabetes insipidus (NDI), a disorder in which the kidney is unable to concentrate urine. In vivo and in mouse collecting duct (mpkCCD) cells, lithium treatment coincides with decreased AQP2 abundance and inactivation of glycogen synthase kinase (Gsk) 3β. This is paralleled in vivo by an increased renal cyclooxygenase 2 (COX-2) expression and urinary prostaglandin PGE2 excretion. PGE2 reduces AVP-stimulated water reabsorption, but its precise role in lithium-induced downregulation of AQP2 is unclear. Using mpkCCD cells, we here investigated whether prostaglandins contribute to lithium-induced downregulation of AQP2. In these cells, lithium application reduced AQP2 abundance, which coincided with Gsk3β inactivation and increased COX-2 expression. Inhibition of COX by indomethacin, leading to reduced PGE2 and PGF2α levels, or dexamethasone-induced downregulation of COX-2 both increased AQP2 abundance, while PGE2 addition reduced AQP2 abundance. However, lithium did not change the prostaglandin levels, and indomethacin and dexamethasone did not prevent lithium-induced AQP2 downregulation. Further analysis revealed that lithium decreased AQP2 protein abundance, mRNA levels and transcription, while PGE2 reduced AQP2 abundance by increasing its lysosomal degradation, but not by reducing AQP2 gene transcription. In conclusion, our data reveal that in mpkCCD cells, prostaglandins decrease AQP2 protein stability by increasing its lysosomal degradation, indicating that in vivo paracrine-produced prostaglandins might have a role in lithium-induced NDI via this mechanism. However, lithium affects also AQP2 gene transcription, which is prostaglandin independent.

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23

Dong, Zhiheng, Nan Zhang, Wei Mao, Bo Liu, Na Huang, Peifeng Li, Changyou Li, and Jinshan Cao. "Kinetic effect of oestrogen on secretion of prostaglandins E2 and F2α in bovine oviduct epithelial cells." Reproduction, Fertility and Development 29, no. 3 (2017): 482. http://dx.doi.org/10.1071/rd15246.

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This study aimed to investigate the effect of oestrogen on prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) secretion in bovine oviduct epithelial cells. Bovine oviduct epithelial cells were obtained from the lumen of fresh bovine oviducts. Quantitative real-time polymerase chain reaction and in-cell western assays were used to measure PGE2 and PGF2α synthase activity and enzyme-linked immunosorbent assays were used to detect the concentrations of the two prostaglandins in extracellular fluid. We observed that oestradiol caused a short-term increase in cyclo-oxygenase-2 (COX-2), which stimulated PGE2 and PGF2α secretion, and that a subsequent decrease in COX-2 and an increase in cyclo-oxygenase-1 (COX-1) produced a high PGE2 : PGF2α ratio. These findings reflect the dynamic change in PGE2 and PGF2α levels under the influence of oestrogen, which may be essential for fertilisation.

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24

Watanabe, Kikuko, Kayoko Kurihara, Yoshimitsu Tokunaga, and Osamu Hayaishi. "Two Types of Microsomal Prostaglandin E Synthase: Glutathione-Dependent and -Independent Prostaglandin E Synthases." Biochemical and Biophysical Research Communications 235, no. 1 (June 1997): 148–52. http://dx.doi.org/10.1006/bbrc.1997.6708.

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25

Beck, P. L., W. McKnight, S. S. Lee, and J. L. Wallace. "Prostaglandin modulation of the gastric vasculature and mucosal integrity in cirrhotic rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 3 (September 1, 1993): G453—G458. http://dx.doi.org/10.1152/ajpgi.1993.265.3.g453.

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Gastric bleeding is a frequent occurrence in cirrhotic patients and may be related to altered microcirculatory responses to luminal irritants and/or vasoactive mediators. Because gastric prostaglandin synthesis has been reported to be altered in cirrhosis, we have examined the role of prostaglandins in modulating gastric perfusion velocity and mucosal integrity in cirrhotic rats. Cirrhosis was induced by bile duct ligation. Gastric perfusion velocity was measured in an ex vivo gastric chamber preparation by laser-Doppler flowmetry. The responsiveness of the mucosa to topical application of 20% ethanol was assessed. Effects of pretreatment with indomethacin or misoprostol were also determined. Gastric and hepatic prostaglandin E2 syntheses were significantly depressed (by approximately 60%) in cirrhotic vs. normal rats. Administration of indomethacin (7.5 mg/kg) to normal rats did not significantly affect gastric perfusion velocity, but in cirrhotic rats it caused a 45% reduction (P < 0.05). Topically applied misoprostol produced significantly greater (2- to 5-fold) increases in gastric perfusion velocity in cirrhotics than in controls. Cirrhotic rats were significantly more susceptible to gastric injury induced by topically applied 20% ethanol than were controls. These results suggest that gastric perfusion velocity in cirrhotic rats is modulated by endogenous prostaglandins to a much greater degree than in controls. Gastric vascular hyperresponsiveness to misoprostol may be attributable to an adaptive response to depressed endogenous prostaglandin synthesis in the cirrhotic animals.

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26

Saydam, Okay, Carlos Abril, Bernd Vogt, Mathias Ackermann, and Martin Schwyzer. "Transactivator Protein BICP0 of Bovine Herpesvirus 1 (BHV-1) Is Blocked by Prostaglandin D2 (PGD2), Which Points to a Mechanism for PGD2-Mediated Inhibition of BHV-1 Replication." Journal of Virology 78, no. 8 (April 15, 2004): 3805–10. http://dx.doi.org/10.1128/jvi.78.8.3805-3810.2004.

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ABSTRACT The immediate-early protein, BICP0, of bovine herpesvirus 1 (BHV-1) transactivates a variety of viral and cellular genes. In a yeast two-hybrid cDNA library screening, we found that lipocalin-type prostaglandin D synthase, which catalyzes the production of prostaglandin D2 (PGD2), is a cellular target of BICP0. We observed that, during wild-type BHV-1 infection, PGD2 levels were increased intracellularly and decreased in the medium. These effects were absent upon infection with recombinant BHV-1 expressing β-galactosidase instead of BICP0 (A2G2). Transient-expression assays showed that BICP0 alone caused a significant increase in PGD2 levels in the cell. PGD2 repressed BHV-1 replication in cultured cells. Antiviral activities of prostaglandins have been documented long ago, but their mode of action remains to be clarified. Here we provide evidence that PGD2 impairs the transactivation ability of BICP0 that is necessary for efficient virus replication.

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27

Herschman, Harvey R., and Warren Hall. "Regulation of prostaglandin synthase-1 and prostaglandin synthase-2." Cancer and Metastasis Reviews 13, no. 3-4 (December 1994): 241–56. http://dx.doi.org/10.1007/bf00666095.

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28

Martinez, Javier, Teresa Sanchez, and Juan J. Moreno. "Role of prostaglandin H synthase-2-mediated conversion of arachidonic acid in controlling 3T6 fibroblast growth." American Journal of Physiology-Cell Physiology 273, no. 5 (November 1, 1997): C1466—C1471. http://dx.doi.org/10.1152/ajpcell.1997.273.5.c1466.

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The specific role(s) of arachidonic acid (AA) and its metabolites in the signaling pathways that regulated fibroblast growth was studied. A Western blot analysis demonstrated that prostaglandin H synthase-2 (PGHS-2) was expressed by 3T6 fibroblast cultures in RPMI 1640 supplemented with fetal calf serum (10%). Dexamethasone, which inhibits AA release and PGHS-2 expression, significantly reduced cell proliferation. Ketoprofen, a dual cyclooxygenase inhibitor, and CGP-28238, a specific PGHS-2 inhibitor, reduced fibroblast proliferation in a dose-dependent manner. These drugs also reduced [3H]thymidine incorporation into the DNA of fibroblasts. These effects were correlated with a decrease in prostaglandin (PG) E2 levels in the cell medium. However, piroxicam at doses that selectively inhibit PGHS-1 did not have a significant effect on fibroblast proliferation. Finally, we showed that the antiproliferative effect of dexamethasone and PGHS-2 inhibitors was significantly antagonized when PGE2 was added to the culture medium. Our results suggest that PGHS-2 and prostaglandins such as PGE2 might play an important role in the regulation of 3T6 fibroblast growth stimulated by growth factors of serum.

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29

Richard, Charissa, Ju Gao, Bonnie LaFleur, Brian W. Christman, Judy Anderson, Naoko Brown, and Jeff Reese. "Patency of the preterm fetal ductus arteriosus is regulated by endothelial nitric oxide synthase and is independent of vasa vasorum in the mouse." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 3 (September 2004): R652—R660. http://dx.doi.org/10.1152/ajpregu.00049.2004.

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Patency of the fetal ductus arteriosus (DA) is maintained in an environment of low relative oxygen tension and a preponderance of vasodilating forces. In addition to prostaglandins, nitric oxide (NO), a potent vasodilator in the pulmonary and systemic vasculatures, has been implicated in regulation of the fetal DA. To further define the contribution of NO to DA patency, the expression and function of NO synthase (NOS) isoforms were examined in the mouse DA on days 17–19 of pregnancy and after birth. Our results show that endothelial NOS (eNOS) is the predominant isoform expressed in the mouse DA and is localized in the DA endothelium by in situ hybridization. Despite rapid constriction of the DA after birth, eNOS expression levels were unchanged throughout the fetal and postnatal period. Pharmacological inhibition of prostaglandin vs. NO synthesis in vivo showed that the preterm fetal DA on day 16 is more sensitive to NOS inhibition than the mature fetal DA on day 19, whereas prostaglandin inhibition results in marked DA constriction on day 19 but minimal effects on the day 16 DA. Combined prostaglandin and NO inhibition caused additional DA constriction on day 16. The contribution of vasa vasorum to DA regulation was also examined. Immunoreactive platelet endothelial cell adhesion molecule and lacZ tagged FLK1 localized to DA endothelial cells but revealed the absence of vasa vasorum within the DA wall. Similarly, there was no evidence of vasa vasorum by vascular casting. These studies indicate that eNOS is the primary source of NO in the mouse DA and that vasomotor tone of the preterm fetal mouse DA is regulated by eNOS-derived NO and is potentiated by prostaglandins. In contrast to other species, mechanisms for DA patency and closure appear to be independent of any contribution of the vasa vasorum.

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30

Hörnsten, Lena, Chao Su, Anne E. Osbourn, Paola Garosi, Ulf Hellman, Christer Wernstedt, and Ernst H. Oliw. "Cloning of Linoleate Diol Synthase Reveals Homology with Prostaglandin H Synthases." Journal of Biological Chemistry 274, no. 40 (October 1, 1999): 28219–24. http://dx.doi.org/10.1074/jbc.274.40.28219.

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31

Nakatani, Yoshihito, Makoto Murakami, and Ichiro Kudo. "Prostaglandin E2 synthase." Ensho Saisei 21, no. 5 (2000): 577–82. http://dx.doi.org/10.2492/jsir.21.577.

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32

Garavito, R. Michael, Daniel Picot, and Patrick J. Loll. "Prostaglandin H synthase." Current Opinion in Structural Biology 4, no. 4 (January 1994): 529–35. http://dx.doi.org/10.1016/s0959-440x(94)90215-1.

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33

Murakami, Makoto, Yoshihito Nakatani, Toshihiro Tanioka, and Ichiro Kudo. "Prostaglandin E synthase." Prostaglandins & Other Lipid Mediators 68-69 (August 2002): 383–99. http://dx.doi.org/10.1016/s0090-6980(02)00043-6.

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34

Watanabe, Kikuko. "Prostaglandin F synthase." Prostaglandins & Other Lipid Mediators 68-69 (August 2002): 401–7. http://dx.doi.org/10.1016/s0090-6980(02)00044-8.

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35

Mevkh, Alevtina T., Konstantin A. Miroshnikov, Natalia D. Igumnova, and Sergey D. Varfolomeev. "Prostaglandin H synthase." FEBS Letters 321, no. 2-3 (April 26, 1993): 205–8. http://dx.doi.org/10.1016/0014-5793(93)80109-8.

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36

Bambai, Bijan, and Richard J. Kulmacz. "Prostaglandin H Synthase." Journal of Biological Chemistry 275, no. 36 (September 2000): 27608–14. http://dx.doi.org/10.1074/jbc.m003982200.

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37

Herschman, Harvey R. "Prostaglandin synthase 2." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1299, no. 1 (January 1996): 125–40. http://dx.doi.org/10.1016/0005-2760(95)00194-8.

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38

Liu, Shu Fang, Robert Newton, Timothy W. Evans, and Peter J. Barnes. "Differential Regulation of Cyclo-Oxygenase-1 and Cyclo-Oxygenase-2 Gene Expression by Lipopolysaccharide Treatment in vivo in the Rat." Clinical Science 90, no. 4 (April 1, 1996): 301–6. http://dx.doi.org/10.1042/cs0900301.

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1. Prostaglandins are important regulatory mediators of cardiovascular and pulmonary functions which may become disordered in patients with sepsis. The mechanisms controlling their synthesis and release under these circumstances remain unclear. Cyclo-oxygenase (COX, prostaglandin G/H synthase) is a key enzyme in prostaglandin synthesis and has two isoforms (COX-1 and COX-2). COX-1 is constitutively expressed and is probably responsible for prostaglandin release under physiological conditions, whereas COX-2 is expressed at high levels upon induction. 2. We investigated the effect of lipopolysaccharide treatment in vivo on differential COX-1 and COX-2 mRNA expression in the rat. 3. The 2.8 kb COX-1 message was detected in all lungs and seven hearts of eight control rats. In lipopolysaccharide-treated animals, COX-1 expression was reduced by approximately 5-fold in lungs and 2-fold in hearts as quantified by densitometry. In parallel, a marked upregulation of COX-2 mRNA expression was observed. The 4.4 kb COX-2 transcript was absent or expressed at low level in control lungs and hearts, but was increased by approximately 7- and 12-fold in lipopolysaccharide-treated lungs and hearts respectively. Neither the down-regulation of COX-1 nor the upregulation of COX-2 mRNA induced by lipopolysaccharide was significantly affected by pretreatment with dexamethasone in lung and heart, although expression of inducible nitric oxide synthase, induced by lipopolysaccharide, was markedly inhibited in the same tissues. 4. The down-regulation of COX-1 and upregulation of COX-2 may contribute to the multi-organ failure seen in sepsis.

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39

Båge, Tove, Thomas Modéer, Tomomi Kawakami, Hernan Concha Quezada, and Tülay Yucel-Lindberg. "Regulation of prostaglandin E synthases: Effects of siRNA-mediated inhibition of microsomal prostaglandin E synthase-1." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1773, no. 10 (October 2007): 1589–98. http://dx.doi.org/10.1016/j.bbamcr.2007.07.008.

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40

Lugea, A., A. Salas, F. Guarner, and J. R. Malagelada. "Adaptive cytoprotection of the rat duodenum is not dependent on nitric oxide-induced changes in blood flow." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 5 (May 1, 1993): G994—G1000. http://dx.doi.org/10.1152/ajpgi.1993.264.5.g994.

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Mild irritation of the rat duodenum enhances mucosal resistance to acid via a prostaglandin-mediated mechanism. Prostaglandins increase mucosal blood flow, but it is not known whether such changes in blood flow significantly contribute to adaptive cytoprotection. We induced blood flow changes by manipulating the arginine-nitric oxide pathway, which is independent from prostaglandin synthesis, and determined the resulting effects on the cytoprotective response. In anesthetized rats, we tested the effects of intraduodenal infusion of mild acid on duodenal blood flow and on the prevention of mucosal damage by subsequent strong acid in control, indomethacin-pretreated, and NG-nitro-L-arginine-pretreated rats (NG-nitro-L-arginine inhibits the nitric oxide synthase). Additional experiments tested the effects of the prostaglandin analogue 16,16-dimethyl-prostaglandin (PG) E2 or sodium nitroprusside (nitric oxide donor) on duodenal blood flow and on mucosal protection against acid. Exposure of the duodenal mucosa to mild acid increased duodenal blood flow and mucosal resistance to acid. Instillation of 16,16-dimethyl-PGE2 also increased blood flow and mucosal resistance to acid. However, sodium nitroprusside increased blood flow without increasing mucosal resistance to acid, and NG-nitro-L-arginine inhibited the change in blood flow induced by acid while preserving the adaptive cytoprotection phenomenon intact. In conclusion, adaptive cytoprotection of the duodenal mucosa appears to be independent of changes in blood flow.

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41

Salamonsen, LA, RA Cherny, and JK Findlay. "Studies in vitro of effects of steroid hormones and the blastocyst on endometrial function in the sheep." Reproduction, Fertility and Development 4, no. 3 (1992): 275. http://dx.doi.org/10.1071/rd9920275.

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Normal endometrial function is a result of regulation by the combination of ovarian steroids and local agents arising from within the embryo-maternal unit. We have used in vitro techniques to examine the role of steroid hormones and ovine trophoblast interferon on endometrial function in the ewe. Immunolocalization of oestrogen receptors in endometrial tissue demonstrated marked changes throughout the cycle and in early pregnancy with maximal concentrations during the follicular and very early luteal phases. Protein secretion from highly purified cultured ovine stromal and epithelial endometrial cells, and the direction of secretion from polarized epithelial cells, has been examined by incorporation of [35S]methionine and by one- and two-dimensional gel electrophoresis. Protein synthesis is greater in stromal than in epithelial cells and more protein is secreted apically than basally from epithelial cells. A number of common and some different proteins are secreted by the two cell types. One secreted protein is matrix metalloproteinase-3 (stromelysin) which degrades components of basement membranes. Ovine trophoblast interferon attenuates the production of prostaglandins from ovine endometrial cells but its action is not by an effect on localization or concentration of the enzyme prostaglandin synthase or on expression of the gene for prostaglandin synthase. Such studies in vitro contribute to our understanding of how the endometrium is prepared for implantation.

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42

Boiti, C., M. Zerani, D. Zampini, and A. Gobbetti. "Nitric oxide synthase activity and progesterone release by isolated corpora lutea of rabbits in the early and mid-luteal phases of pseudopregnancy are modulated differently by prostaglandin E-2 and prostaglandin F-2alpha via adenylate cyclase and phospholipase C." Journal of Endocrinology 164, no. 2 (February 1, 2000): 179–86. http://dx.doi.org/10.1677/joe.0.1640179.

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By examining in vitro the effects of prostaglandin E-2 (PGE-2) and prostaglandin F-2alpha (PGF-2alpha) induced in the corpora lutea (CL) of pseudopregnant rabbits, we have demonstrated that these prostaglandins modulate luteal nitric oxide synthase (NOS) activity and progesterone production differently, depending on the age of the CL. On CL obtained on day 4 of pseudopregnancy (day-4), PGE-2 was found to depress NOS total activity to 13% of control and to significantly increase basal progesterone secretion by 61%, while PGF-2alpha had no effect. On day-9 CL, PGE-2 was ineffective, but PGF-2alpha caused a 2.5-fold increase of NOS activity and a marked decrease in progesterone production. Using specific inhibitors, we found that the regulatory actions of PGE-2 in vitro are mediated via the adenyl cyclase/protein kinase A (PKA) second messenger system, while the PGF-2alpha-induced luteolytic effects on day-9 CL depend upon activation of the phospholipase C/protein kinase C (PKC) system. The different responsiveness of day-4 and day-9 CL to PGE-2 and PGF-2alpha could depend on receptor availability for these two prostaglandins, even if other cellular mechanisms cannot be excluded. The present study supports a functional role for NOS in regulating the steroidogenic capacity of rabbit CL, and reveals a novel interaction between a stimulatory G-protein-coupled receptor and PKC/PKA-mediated signal transduction modulating NOS activity.

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Rossitto, Moïra, Safdar Ujjan, Francis Poulat, and Brigitte Boizet-Bonhoure. "Multiple roles of the prostaglandin D2 signaling pathway in reproduction." REPRODUCTION 149, no. 1 (January 2015): R49—R58. http://dx.doi.org/10.1530/rep-14-0381.

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Prostaglandins signaling molecules are involved in numerous physiological processes. They are produced by several enzyme-limited reactions upon fatty acids, which are catalyzed by two cyclooxygenases and prostaglandin synthases. In particular, the prostaglandins E2(PGE2), D2(PGD2), and F2(PGF2α) have been shown to be involved in female reproductive mechanisms. Furthermore, widespread expression of lipocalin- and hematopoietic-PGD2synthases in the male reproductive tract supports the purported roles of PGD2in the development of both embryonic and adult testes, sperm maturation, and spermatogenesis. In this review, we summarize the putative roles of PGD2signaling and the roles of both PGD2synthases in testicular formation and function. We review the data reporting the involvement of PGD2signaling in the differentiation of Sertoli and germ cells of the embryonic testis. Furthermore, we discuss the roles of lipocalin-PGD2synthase in steroidogenesis and spermatogenesis, in terms of lipid molecule transport and PGD2production. Finally, we discuss the hypothesis that PGD2signaling may be affected in certain reproductive diseases, such as infertility, cryptorchidism, and testicular cancer.

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44

Dumont, Isabelle, Pierre Hardy, Krishna G. Peri, Xin Hou, Stéphane Molotchnikoff, Daya R. Varma, and Sylvain Chemtob. "Regulation of endothelial nitric oxide synthase by PGD2 in the developing choroid." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 1 (January 1, 2000): H60—H66. http://dx.doi.org/10.1152/ajpheart.2000.278.1.h60.

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We investigated if prostaglandins might regulate the increased choroidal endothelial (e) nitric oxide synthase (NOS) expression in the perinate. Prostaglandins, eNOS mRNA, immunoreactive protein and activity, and nitrite [stable metabolite of nitric oxide (NO)] production were markedly higher in newborn (1 day old) than juvenile (6–8 wk old) pig choroid. Treatment of isolated newborn choroids with the prostaglandin synthase inhibitor ibuprofen for 24 h reduced eNOS mRNA and nitrite production to values in juveniles. This effect was equally observed with the PGD2 receptor (DP) blocker BW A868C and was prevented by cotreatment with PGD2 but not other prostaglandins; similar observations were made on NOS activity in vivo. PGD2 also increased eNOS expression on choroids of juveniles, and this effect was blocked by BW A868C. The manifestation of this upregulation of eNOS by PGD2 on the control of choroidal vasomotor response was tested by using NO-dependent vasorelaxants, ACh, bradykinin (Bk), and substance P (SP). ACh-, Bk-, and SP-elicited choroidal vasorelaxation was greater in saline-treated newborn than juvenile pigs. Ibuprofen (24 h) decreased ACh-, Bk-, and SP-evoked vasorelaxation in newborns, whereas PGD2 increased that in juveniles and prevented the ibuprofen-induced attenuated relaxation in newborns; infusion of N ω-monomethyl-l-arginine in choroids of those animals treated with PGD2 reversed the augmented vasorelaxation to ACh, Bk, and SP. Finally, PGD2-induced upregulation of NOS in the perinate was also reflected by curtailed choroidal blood flow autoregulatory response to increased perfusion pressure. In conclusion, PGD2 exhibits a major role in upregulating eNOS expression and activity in the choroid, which in turn results in greater NO-mediated vasorelaxation; a new mechanism for eNOS regulation via DP is hereby disclosed. The relationship between PGD2 and eNOS in the developing subject provides an explanation for the interactive role of these two factors in the absent choroidal blood flow autoregulation in the perinate.

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45

Zahner, Gunther, Melanie Schaper, Ulf Panzer, Malte Kluger, Rolf A. K. Stahl, Friedrich Thaiss, and André Schneider. "Prostaglandin EP2 and EP4 receptors modulate expression of the chemokine CCL2 (MCP-1) in response to LPS-induced renal glomerular inflammation." Biochemical Journal 422, no. 3 (August 27, 2009): 563–70. http://dx.doi.org/10.1042/bj20090420.

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The pro-inflammatory chemokine CCL2 [chemokine (Cys-Cys motif) ligand 2; also known as MCP-1 (monocyte chemotactic protein-1)] is up-regulated in the glomerular compartment during the early phase of LPS (lipopolysaccharide)-induced nephritis. This up-regulation also occurs in cultured MCs (mesangial cells) and is more pronounced in MCs lacking the PGE2 (prostaglandin E2) receptor EP2 or in MCs treated with a prostaglandin EP4 receptor antagonist. To examine a possible feedback mechanism of EP receptor stimulation on CCL2 expression, we used an in vitro model of MCs with down-regulated EP receptor expression. Selectively overexpressing the various EP receptors in these cells then allows the effects on the LPS-induced CCL2 expression to be examined. Cells were stimulated with LPS and CCL2 gene expression was examined and compared with LPS-stimulated, mock-transfected PTGS2 [prostaglandin-endoperoxide synthase 2, also known as COX-2 (cyclo-oxygenase-2)]-positive cells. Overexpression of EP1, as well as EP3, had no effect on LPS-induced Ccl2 mRNA expression. In contrast, overexpression of EP2, as well as EP4, significantly decreased LPS-induced CCL2 expression. These results support the hypothesis that PTGS2-derived prostaglandins, when strongly induced, counter-balance inflammatory processes through the EP2 and EP4 receptors in MCs.

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Peri, Krishna G., Pierre Hardy, Ding You Li, Daya R. Varma, and Sylvain Chemtob. "Prostaglandin G/H Synthase-2 Is a Major Contributor of Brain Prostaglandins in the Newborn." Journal of Biological Chemistry 270, no. 41 (October 13, 1995): 24615–20. http://dx.doi.org/10.1074/jbc.270.41.24615.

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47

Razandi, M., A. Pedram, T. Rubin, and E. R. Levin. "PGE2 and PGI2 inhibit ET-1 secretion from endothelial cells by stimulating particulate guanylate cyclase." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 4 (April 1, 1996): H1342—H1349. http://dx.doi.org/10.1152/ajpheart.1996.270.4.h1342.

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Prostaglandins (PG)E2 and prostacyclin (PGI2) can cause vasodilation in selective vascular beds and could act in part by inhibiting the production of the vasoconstrictor endothelin-1 (ET-1). We recently reported that these prostanoids inhibit ET-1 production/secretion from cultured endothelial cells via the generation of guanosine 3'-5'-cyclic monophosphate (cGMP). It is unclear whether this results from the stimulation of the particulate (membrane) of soluble (cytosolic) form of guanylate cyclase, and whether these effects are through an intermediate, such as nitric oxide. PGE2 and PGI2 each caused a three- to fourfold increase in both membrane and whole bovine aortic endothelial cell guanylate cyclase activity. The stimulations were significantly reversed (80-90%) by the compound LY-83583, an antagonist to cGMP generation, but were unaffected by methylene blue (MB), an inhibitor of nitric oxide-induced soluble guanylate cyclase. In contrast, the prostaglandins did not generate cGMP in cytosolic fractions. The prostaglandins inhibited ET-1 secretion from the intact cells, which was significantly prevented by LY-83583, but not by MB. Neither prostaglandin stimulated NO synthase activity, an indicator of nitric oxide generation. We conclude that PGE2 and PGI2 are likely to inhibit ET-1 secretion through the activation of the particulate guanylate cyclase, identifying a novel mechanism by which the prostanoids signal in the endothelial cell.

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48

Frasor, Jonna, Aisha E. Weaver, Madhumita Pradhan, and Kinnari Mehta. "Synergistic Up-Regulation of Prostaglandin E Synthase Expression in Breast Cancer Cells by 17β-Estradiol and Proinflammatory Cytokines." Endocrinology 149, no. 12 (August 14, 2008): 6272–79. http://dx.doi.org/10.1210/en.2008-0352.

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Inflammatory mediators, such as cytokines and prostaglandins, play a fundamental role in estrogen-dependent breast cancer through their ability to up-regulate aromatase expression and subsequent local production of estrogens in the breast. To study the link between estrogens and inflammation further, we examined the regulation of prostaglandin E synthase (PTGES), a key enzyme in the production of prostaglandin E2. We found that 17β-estradiol (E2) rapidly and robustly up-regulates PTGES mRNA and protein levels in estrogen receptor (ER)-positive breast cancer cells through ER recruitment to an essential estrogen response element located in the 5′ flanking region of the PTGES gene. PTGES is also up-regulated by the proinflammatory cytokines TNFα or IL-1β. Surprisingly, the combination of E2 and cytokines leads to a synergistic up-regulation of PTGES in an ER and nuclear factor-κB (NFκB)-dependent manner. This is in contrast to the mutual transrepression between ER and NFκB that has been well characterized in other cell types. Furthermore, we found enhanced recruitment of ERα as well as the NFκB family member, p65, to the PTGES estrogen response element by the combination of E2 and TNFα compared with either E2 or TNFα alone. The synergistic up-regulation of PTGES may result in enhanced prostaglandin E2 production, which in turn may further enhance aromatase expression and production of local estrogens. Our findings suggest that a finely tuned positive feedback mechanism between estrogens and inflammatory factors may exist in the breast and contribute to hormone-dependent breast cancer growth and progression.

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Yang, C. Y., and C. L. Meng. "Regulation of PG Synthase by EGF and PDGF in Human Oral, Breast, Stomach, and Fibrosarcoma Cancer Cell Lines." Journal of Dental Research 73, no. 8 (August 1994): 1407–15. http://dx.doi.org/10.1177/00220345940730080301.

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Prostaglandins may inhibit or promote tumor cell replication, depending on the cell system that is investigated. In our laboratory, we have established and characterized four different specific human cancer cell lines. The objectives of this study were to examine and compare the prostaglandin endoperoxide synthase (PG synthase, EC 1.14.99.1) activity of these cell lines by measuring the conversion of arachidonate to 3H-PGE2 and 3H-PGF2α. We found that the oral epidermal carcinoma cell line (OEC-M1) had a moderate degree of PG synthase activity. Enzyme activity could be partially blocked (statistically significant) by the addition of epidermal growth factor (EGF) at 20 ng/mL and almost completely inhibited by platelet-derived growth factor at (PDGF) 20 mU/mL. By contrast, we discovered that the human breast adenocarcinama cell line (BC-M1) did not contain significant PG synthase, and enzyme activity could be significantly activated by the addition of epidermal growth factor at 20 ng/mL and platelet-derived growth factor at 20 mU/mL. We also found that the human stomach adenocarcinoma cell line (SCM-1) had a significant amount of PG synthase activity, and these PG synthase activities were not activated or inhibited by EGF at 20 ng/mL or PDGF at 20 mU/mL. Furthermore, the human fibrosarcoma (FS-Ml) cell line also contained a moderate degree of PG synthase activity, which could be significantly inhibited by PDGF at 20 mU/mL but was not inhibited by EGF at 20 ng/mL. The results suggest that EGF and PDGF may be involved in the regulation of the PG synthase activities of human oral, breast, stomach, and fibrosarcoma cancer cells.

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Gookin, Jody L., Laurel L. Duckett, Martha U. Armstrong, Stephen H. Stauffer, Colleen P. Finnegan, Michael P. Murtaugh, and Robert A. Argenzio. "Nitric oxide synthase stimulates prostaglandin synthesis and barrier function inC. parvum-infected porcine ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 3 (September 2004): G571—G581. http://dx.doi.org/10.1152/ajpgi.00413.2003.

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Cell culture models implicate increased nitric oxide (NO) synthesis as a cause of mucosal hyperpermeability in intestinal epithelial infection. NO may also mediate a multitude of subepithelial events, including activation of cyclooxygenases. We examined whether NO promotes barrier function via prostaglandin synthesis using Cryptosporidium parvum-infected ileal epithelium in residence with an intact submucosa. Expression of NO synthase (NOS) isoforms was examined by real-time RT-PCR of ileal mucosa from control and C. parvum-infected piglets. The isoforms mediating and mechanism of NO action on barrier function were assessed by measuring transepithelial resistance (TER) and eicosanoid synthesis by ileal mucosa mounted in Ussing chambers in the presence of selective and nonselective NOS inhibitors and after rescue with exogenous prostaglandins. C. parvum infection results in induction of mucosal inducible NOS (iNOS), increased synthesis of NO and PGE2, and increased mucosal permeability. Nonselective inhibition of NOS ( NG-nitro-l-arginine methyl ester) inhibited prostaglandin synthesis, resulting in further increases in paracellular permeability. Baseline permeability was restored in the absence of NO by exogenous PGE2. Selective inhibition of iNOS [l- N6-(1-iminoethyl)-l-lysine] accounted for ∼50% of NOS-dependent PGE2synthesis and TER. Using an entire intestinal mucosa, we have demonstrated for the first time that NO serves as a proximal mediator of PGE2synthesis and barrier function in C. parvum infection. Expression of iNOS by infected mucosa was without detriment to overall barrier function and may serve to promote clearance of infected enterocytes.

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Journal articles on the topic 'Prostaglandines – Synthèse'

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