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Journal articles on the topic 'Prostaglandine D₂'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

Laverdière, G., J. J. Dufour, G. L. Roy, D. Lavoie, and J. Proulx. "Comparaison de l'effet de deux analogues de la prostaglandine F2α sur la synchronisation de l'œstrus chez la vache de boucherie." Canadian Journal of Animal Science 74, no. 1 (March 1, 1994): 29–36. http://dx.doi.org/10.4141/cjas94-005.

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The objective of this study was to compare the efficiency of cloprostenol and fenprostalene in synchronizing estrus. Before treatment, estrus was detected during 4.5 d for multiparous cows in exp. 1 (n = 105) and 7.5 d for primiparous and nulliparous females in exp. 2 (n = 86). Females that were not in estrus (exp. 1: n = 74 and exp. 2: n = 58) received at random, either 500 μg of cloprostenol (i.m.) or 1 mg of fenprostalene (s.c). Cattle synchronized with cloprostenol or fenprostalene that presented estrus within 5 d showed similar fertility rates (exp. 1: 86.1% vs. 88.0% and exp. 2: 89.3% vs. 72.2% for cloprostenol and fenprostalene, respectively) and PGF2α-estrus intervals (exp. 1: 68 h vs. 73 h and exp. 2: 57 h vs. 57 h). However, the incidence of synchronization (exp. 1: 97.3% vs. 67.6%, P < 0.001; and exp. 2: 93.3% vs. 64.3%, P < 0.01) and pregnancy rates (exp. 1: 83.8% vs. 59.5%, P < 0.05; and exp. 2: 83.3% vs. 46.4%, P < 0.01) were statistically higher for cloprostenol than for fenprostalene. In exp. 2, primiparous cows and heifers obtained similar reproductive performances. The fertility rate of cattle treated with cloprostenol in exp. 2 was higher than that of untreated cattle (89.3% vs. 50.0%, P < 0.001, n = 56). In exp. 1, the variance of interval to estrus was similar for both analogues, but in exp. 2, it was less variable after the administration of cloprostenol (P < 0.05). Intervals between cloprostenol injection and estrus (0–10 and 0–15 d) were shorter (P < 0.05) and less variable (P < 0.001) than fenprostalene–estrus intervals. These results indicate that cloprostenol has a better potential for estrus synchronization than fenprostalene. Key words: Cloprostenol, fenprostalene, estrus synchronization, prostaglandin F2α, beef cattle
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2

SHIMURA, Takanori, Masaru MIYAZAKI, Masatoshi KURIHARA, Osamu TAKAHASHI, Shigemi KAWATA, Ikuo UDAGAWA, Hisao KOSHIKAWA, et al. "Effects of prostaglandine-E1 and glucagon-insulin on hepatic regeneration following partial hepatectomy in D-galactosamine induced rat liver." Japanese Journal of Gastroenterological Surgery 20, no. 8 (1987): 1877–82. http://dx.doi.org/10.5833/jjgs.20.1877.

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3

Adachi, Hisanobu, Takehiro Suzuki, Michiaki Abe, Naoki Asano, Hiroya Mizutamari, Masayuki Tanemoto, Toshiyuki Nishio, et al. "Molecular characterization of human and rat organic anion transporter OATP-D." American Journal of Physiology-Renal Physiology 285, no. 6 (December 2003): F1188—F1197. http://dx.doi.org/10.1152/ajprenal.00402.2002.

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We have isolated and characterized a novel human and rat organic anion transporter subtype, OATP-D. The isolated cDNA from human brain encodes a polypeptide of 710 amino acids ( Mr 76,534) with 12 predicted transmembrane domains. The rat clone encodes 710 amino acids ( Mr 76,821) with 97.6% amino acid sequence homology with human OATP-D. Human and rat OATP-D have moderate amino acid sequence homology with LST-1/rlst-1, the rat oatp family, the prostaglandin transporter, and moat1/MOAT1/KIAA0880/OATP-B. Phylogenetic tree analysis revealed that OATP-D is branched in a different position from all known organic anion transporters. OATP-D transports prostaglandin E1 ( Km 48.5 nM), prostaglandin E2 ( Km 55.5 nM), and prostaglandin F2α, suggesting that, functionally, OATP-D encodes a protein that has similar characteristics to those of the prostaglandin transporter. Rat OATP-D also transports prostaglandins. The expression pattern of OATP-D mRNA was abundant mainly in the heart, testis, brain, and some cancer cells. Immunohistochemical analysis further revealed that rat OATP-D is widely expressed in the vascular, renal, and reproductive system at the protein level. These results suggest that OATP-D plays an important role in translocating prostaglandins in specialized tissues and cells.
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4

Watzková, Jarmila, Ludmila Křížová, Aleš Pavlík, Věra Schulzová, Jana Hajšlová, and Jaromír Lojza. "The Effect of Soybean-Derived Phytoestrogens on Concentrations of Plasma Isoflavones, 15-keto-13,14-dihydroprostaglandin F2α and Progesterone in Dairy Cows." Acta Veterinaria Brno 79, no. 4 (2010): 525–32. http://dx.doi.org/10.2754/avb201079040525.

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The objective of the study was to determine the effect of soybean-derived phytoestrogens and their metabolites on the activity of sex hormones during the oestrous cycle in multiparous lactating dairy cows. The experiment was carried out on 4 multiparous lactating Holstein cows in the form of replicated Latin square in double reversal design. The experiment in the total length of 168 days was divided into 4 periods of 42 days, each consisting of a 21-day preliminary period and a 21-day collecting period. Cows were divided into 2 groups of 2 cows. The control group (C) was fed a diet based on extruded rapeseed cake while the experimental group (S) was fed a diet containing extruded full-fat soya. The intake of total isoflavones was 3297 mg/d in S and 58.0 mg/d in C (P < 0.001). The concentrations of individual isoflavones, it is daidzein, genistein and equol in plasma were significantly higher in the experimental group S (49.3, 78.7 and 218.8 ng/ml, respectively) than in the control group C (13.5, 42.9 and 18.3 ng/ml, respectively, P < 0.001). Plasma concentration of progesterone throughout the oestrous cycle was not influenced by the diet used (P > 0.05). Plasma concentration of prostaglandine PGFM throughout the oestrous cycle in the experimental group (S) tended to be higher (P = 0.095) than in the control group (C). No differences in the length of the oestrous cycle between the cows fed different diets were observed.
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5

Kutyrev, Olennikov, Kaschenko, and Mazur. "DYNAMICS OF SECRETION OF PROSTAGLANDINS E2 AND D2 WITH DIBOTHRIOCHEPHALLUS DENDRITICUS (CESTODA) PLEROCERCOIDS IN RESPONSE TO EXPOSURE OF BLOOD SERUM OF BAIKAL CISCO, THE HOST." THEORY AND PRACTICE OF PARASITIC DISEASE CONTROL, no. 21 (May 29, 2020): 180–86. http://dx.doi.org/10.31016/978-5-9902341-5-4.2020.21.180-186.

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Parasites regulate host immune response via secretion of soluble mediators which interact in a certain way with cells and molecules of the immune system. The aim of the study was to determine changes of prostaglandins E2 и D2 content in Dibothriochephallus dendriticus plerocercoids and also in the incubation media during incubation of tapeworms with addition of blood serum from the intermediate host – Baikal cisco. D. dendriticus plerocercoids were retrieved from the host body cavity, ashed in the physiological solution and placed in incubation media. Microcolumn high-performance liquid chromatography was used to detect prostaglandins. Concentration of prostaglandins in the plerocercoid organism increased insignificantly after incubation in the Hanks’ solution with addition of blood serum, when compared with incubation in the Hanks’ solution only. Concentration of prostaglandin E2 increased significantly in the incubation media after incubation of plerocercoids in the Hanks’ solution with addition of blood serum. Prostaglandin D2 was also identified in high concentrations after 12 h and 24 h of incubation, whereas prostaglandin D2 was not quite detected during incubation in Hanks’ solution only.
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6

Zehbe, Rolf, Bernhard Watzer, Rainer Grupp, Sven Halstenberg, Heinrich Riesemeier, C. James Kirkpatrick, Helmut Schubert, and Christoph Brochhausen. "Tomographic and Topographic Investigation of Poly-D,L-Lactide-Co-Glycolide Microspheres Loaded with Prostaglandine E2 for Extended Drug Release Applications." Advanced Materials Research 89-91 (January 2010): 687–91. http://dx.doi.org/10.4028/www.scientific.net/amr.89-91.687.

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Polymeric, biodegradable microspheres represent a good reliable system to investigate the release of bioactive substances in both in vitro and in vivo applications. Common biomaterials for the synthesis of these microspheres are aliphatic polyesters of the poly(α-hydroxy)acids, especially poly-L-lactides (PLA) and polyglycolides (PGA) or their copolymers poly-D,L-lactide-co-glycolides (PLGA). In our own previous studies we have developed PLGA microspheres with integrated PGE2 as model substance for a wide range of biomedical applications, especially in angiogenesis, fracture healing and cartilage repair. The synthesis is based on a binary solvent in water emulsion approach, where two different solvents are used to dissolve the active agent and the polymer, while being miscible in each other (CHCl3, ethyl acetate). Both, the degradation of the material and the release profiles were investigated using SEM and mass spectrometry coupled with gas- or high performance liquid chromatography. SEM and AFM measurements indicated a porous structure of the microspheres but could not resolve the true three dimensional structure of the microspheres. Therefore, synchrotron radiation-based µCT (SR-µCT) investigations were performed to link the release profile to the structural design of the microspheres. As a result, we were able to cross validate the experimental data from SEM and AFM with SR-µCT, demonstrating both micro-porosity and nano-porosity. The polymer itself appears to consist of 200 nm – 300 nm sized particles.
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7

Chen, Xiaojie, and Jon D. Levine. "NOS Inhibitor Antagonism of PGE2-Induced Mechanical Sensitization of Cutaneous C-Fiber Nociceptors in the Rat." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 963–66. http://dx.doi.org/10.1152/jn.1999.81.3.963.

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NOS inhibitor antagonism of PGE2-induced mechanical sensitization of cutaneous C-fiber nociceptors in the rat. Prostaglandins, metabolites of arachidonic acid, released during tissue injury and inflammation sensitize primary afferent nociceptors. While it has been suggested that this effect on nociceptors is mediated mainly via the cAMP second messenger system, recent evidence suggests that nitric oxide (NO) is also involved in peripheral pain mechanisms. To test the hypothesis that NO contributes to the sensitization of nociceptors to mechanical stimuli induced by hyperalgesic prostaglandins, we compared von Frey hair mechanical threshold as well as the response evoked by 10-s sustained threshold mechanical stimulation before and after injection of prostaglandin E2(PGE2) alone, and NOS inhibitor N G-methyl-l-arginine (l-NMA) or its inactive stereoisomer N G-methyl-d-arginine (d-NMA) plus PGE2, adjacent to the receptive field of C-fiber nociceptors. The reduction of mechanical threshold and increase in number of action potentials to sustained mechanical stimulation induced by intradermal application of PGE2 was blocked by l-NMA, but not d-NMA. It is suggested that NO contributes to nociceptor sensitization induced by hyperalgesic prostaglandins.
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8

Sawyer, Sara J., Suzanne M. Norvell, Suzanne M. Ponik, and Fredrick M. Pavalko. "Regulation of PGE2and PGI2release from human umbilical vein endothelial cells by actin cytoskeleton." American Journal of Physiology-Cell Physiology 281, no. 3 (September 1, 2001): C1038—C1045. http://dx.doi.org/10.1152/ajpcell.2001.281.3.c1038.

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Disruption of microfilaments in human umbilical vein endothelial cells (HUVEC) with cytochalasin D (cytD) or latrunculin A (latA) resulted in a 3.3- to 5.7-fold increase in total synthesis of prostaglandin E2(PGE2) and a 3.4- to 6.5-fold increase in prostacyclin (PGI2) compared with control cells. Disruption of the microtubule network with nocodazole or colchicine increased synthesis of PGE21.7- to 1.9-fold and PGI21.9- to 2.0-fold compared with control cells. Interestingly, however, increased release of PGE2and PGI2from HUVEC into the media occurred only when microfilaments were disrupted. CytD treatment resulted in 6.7-fold more PGE2and 3.8-fold more PGI2released from HUVEC compared with control cells; latA treatment resulted in 17.7-fold more PGE2and 11.2-fold more PGI2released compared with control cells. Both increased synthesis and release of prostaglandins in response to all drug treatments were completely inhibited by NS-398, a specific inhibitor of cyclooxygenase-2 (COX-2). Disruption of either microfilaments using cytD or latA or of microtubules using nocodazole or colchicine resulted in a significant increase in COX-2 protein levels, suggesting that the increased synthesis of prostaglandins in response to drug treatments may result from increased activity of COX-2. These results, together with studies demonstrating a vasoprotective role for prostaglandins, suggest that the cytoskeleton plays an important role in maintenance of endothelial barrier function by regulating prostaglandin synthesis and release from HUVEC.
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9

Nango, Hiroshi, Yasuhiro Kosuge, Nana Yoshimura, Hiroko Miyagishi, Takanori Kanazawa, Kaname Hashizaki, Toyofumi Suzuki, and Kumiko Ishige. "The Molecular Mechanisms Underlying Prostaglandin D2-Induced Neuritogenesis in Motor Neuron-Like NSC-34 Cells." Cells 9, no. 4 (April 10, 2020): 934. http://dx.doi.org/10.3390/cells9040934.

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Prostaglandins are a group of physiologically active lipid compounds derived from arachidonic acid. Our previous study has found that prostaglandin E2 promotes neurite outgrowth in NSC-34 cells, which are a model for motor neuron development. However, the effects of other prostaglandins on neuronal differentiation are poorly understood. The present study investigated the effect of prostaglandin D2 (PGD2) on neuritogenesis in NSC-34 cells. Exposure to PGD2 resulted in increased percentages of neurite-bearing cells and neurite length. Although D-prostanoid receptor (DP) 1 and DP2 were dominantly expressed in the cells, BW245C (a DP1 agonist) and 15(R)-15-methyl PGD2 (a DP2 agonist) had no effect on neurite outgrowth. Enzyme-linked immunosorbent assay demonstrated that PGD2 was converted to 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) under cell-free conditions. Exogenously applied 15d-PGJ2 mimicked the effect of PGD2 on neurite outgrowth. GW9662, a peroxisome proliferator-activated receptor–gamma (PPARγ) antagonist, suppressed PGD2-induced neurite outgrowth. Moreover, PGD2 and 15d-PGJ2 increased the protein expression of Islet-1 (the earliest marker of developing motor neurons), and these increases were suppressed by co-treatment with GW9662. These results suggest that PGD2 induces neuritogenesis in NSC-34 cells and that PGD2-induced neurite outgrowth was mediated by the activation of PPARγ through the metabolite 15d-PGJ2.
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10

BUHR, M. M., R. M. McKAY, and D. L. GRINWICH. "LUTEOLYTIC ACTION OF PROSTAGLANDINS IN SWINE AND THE EFFECTS OF CLOPROSTENOL ON LUTEINIZING HORMONE RECEPTORS AND MEMBRANE STRUCTURE OF PORCINE CORPORA LUTEA." Canadian Journal of Animal Science 66, no. 2 (June 1, 1986): 415–22. http://dx.doi.org/10.4141/cjas86-043.

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The luteolytic action of prostaglandin F2α (PGF2α), 15-keto-PGF2α, 15-methyl-PGF2α, and cloprostenol was evaluated in cycling gilts and sows after intramuscular injection on day 13 of the estrous cycle. Only cloprostenol significantly shortened the mean cycle length (18.5 vs. 20.3 d, P < 0.05). Cloprostenol also caused a more rapid decline in serum progesterone concentrations than did the other prostaglandins. Serum concentrations of the prostaglandin metabolite 13,14-dihydro-15-keto-PGF2α (PGFM), showed rapid transitory peaks after PGF2α or 15-keto-PGF2α and a lower, later rise after cloprostenol. A second experiment examined luteal luteinizing hormone (LH) receptors and luteal membrane ultrastructure during the estrous cycle and pregnancy and the effect of cloprostenol on these parameters during the estrous cycle. The number of unoccupied luteal LH receptors, as measured by specific 125I-hCG binding, dropped significantly from mid to late pregnancy and from mid to late cycle. Cloprostenol lowered serum progesterone concentrations but did not affect hCG binding. X-ray diffraction showed no correlation of gel or liquid-crystalline phase lipids in luteal microsomes with the stage of the estrous cycle or pregnancy or cloprostenol treatment. Key words: Swine, luteolysis, estrous cycle, prostaglandins, luteal LH receptors
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11

Romanovsky, Andrej A. "Febrile nonresponsiveness of vagotomized animals: is it due to endotoxin translocation from the gut and tolerance?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 3 (September 1, 1998): R933—R935. http://dx.doi.org/10.1152/ajpregu.1998.275.3.r933.

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The following is the abstract of the article discussed in the subsequent letter: Scammell, Thomas E., John D. Griffin, Joel K. Elmquist, and Clifford B. Saper. Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever. Am. J. Physiol.274 ( Regulatory Integrative Comp. Physiol. 43): R933–R935, 1998.—Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA) to determine which preoptic regions produce the prostaglandins required for fever. Initial experiments demonstrated that intravenous ketorolac blocked the fever normally produced by lipopolysaccharide (LPS) 5 μg/kg iv. Microinjection of ketorolac into the POA had no effect on body temperature, and injection of artificial cerebrospinal fluid into the POA did not alter LPS fever. Injection of ketorolac into the anteroventral POA markedly decreased the fever produced by LPS, compared with injections into more rostral, caudal, or dorsal locations. These observations indicate that prostaglandin synthesis in the anteroventral preoptic region is necessary for the production of fever.
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12

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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13

Hossein Mostafa, Delaram, Aniseh Samadi, Somayeh Niknam, Saman Ahmad Nasrollahi, Alexandre Guishard, and Alireza Firooz. "Efficacy of Cetirizine 1% Versus Minoxidil 5% Topical Solution in the Treatment of Male Alopecia: A Randomized, Single-blind Controlled Study." Journal of Pharmacy & Pharmaceutical Sciences 24 (April 24, 2021): 191–99. http://dx.doi.org/10.18433/jpps31456.

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Purpose: Prostaglandins play a pivotal role in modulating hair growth cycle. Prostaglandin F2α and prostaglandin E have stimulating and prostaglandin D has inhibitory effects on hair follicle. Cetirizine inhibits release of prostaglandin D2 and stimulates the release of prostaglandin E2. In the present study, the efficacy and safety of twice daily application of topical cetirizine 1% versus minoxidil 5% solutions for 16 weeks were compared in male androgenetic alopecia (AGA). Methods: Forty men, aged 18 to 49 years, ‎were randomly divided into two equal groups to apply either cetirizine 1% or minoxidil 5% solutions. The study was divided into two phases, a 16-week treatment phase either with cetirizine or minoxidil (anagen phase), followed by an 8-week ‎ drug-free (telogen phase) with a follow-up when patients used placebo. Efficacy outcomes included the change in total hair density, vellus and terminal hair density, hair diameter and the percentage of hair in anagen and telogen phases from baseline in 16 and 24 weeks. Results: After 16 weeks, we observed a significant increase in total and vellus hair density in both minoxidil and cetirizine groups, but the improvement was much higher in the minoxidil group. The percentage of hair in the anagen phase also increased in both groups after 16 weeks of treatment, but then diminished after 8 weeks of placebo consumption. No significant adverse reactions associated with the administration of cetirizine solution were reported. Conclusion: Cetirizine 1% solution was effective in hair growth without any complications for treatment of male AGA.
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14

Hirata, Masakazu, Fumitaka Ushikubi, and Shuh Narumiya. "Prostaglandin I receptor and prostaglandin D receptor." Journal of Lipid Mediators and Cell Signalling 12, no. 2-3 (October 1995): 393–404. http://dx.doi.org/10.1016/0929-7855(95)00025-l.

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15

Dai, Long-Jun, Brian Bapty, Gordon Ritchie, and Gary A. Quamme. "PGE2 stimulates Mg2+ uptake in mouse distal convoluted tubule cells." American Journal of Physiology-Renal Physiology 275, no. 5 (November 1, 1998): F833—F839. http://dx.doi.org/10.1152/ajprenal.1998.275.5.f833.

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Prostaglandins have diverse effects on renal electrolyte reabsorption, inhibiting NaCl absorption in the thick ascending limb and modulating sodium and calcium transport in cortical collecting cells. It is unclear what effect, if any, prostaglandins have on tubular magnesium handling. The effects of prostaglandin E2(PGE2) were studied on immortalized mouse distal convoluted tubule (MDCT) cells by measuring cellular cAMP formation with radioimmunoassays and Mg2+ uptake with fluorescence techniques. Intracellular free Mg2+ concentration ([Mg2+]i) was measured on single MDCT cells using microfluorescence with mag-fura 2. To assess Mg2+ uptake, MDCT cells were first Mg2+ depleted to 0.22 ± 0.01 mM by culturing in Mg2+-free media for 16 h and then placed in 1.5 mM MgCl2, and the changes in [Mg2+]iwere determined. [Mg2+]ireturned to basal levels, 0.53 ± 0.02 mM, with a mean refill rate, d([Mg2+]i)/d t, of 173 ± 8 nM/s. Indomethacin, 5 μM, diminished basal Mg2+ uptake, suggesting that endogenous prostaglandins may stimulate Mg2+ entry in control cells. PGE2 stimulated Mg2+ entry in a concentration-dependent manner with maximal response of 311 ± 12 nM/s, at a concentration of 10−7 M, which represented an 80 ± 3% increase in uptake rate above control values. This was associated with a sixfold increase in intracellular cAMP generation. PGE2-stimulated Mg2+ uptake was completely inhibited with the Rp diastereoisomer of adenosine 3′,5′-cyclic monophosphothionate (Rp-cAMPS), a protein kinase A inhibitor, and U-73122, a phospholipase C inhibitor, and partially by chelerythrine, a protein kinase C inhibitor. Accordingly, PGE2-mediated Mg2+ entry rates involve multiple intracellular signaling pathways. These studies demonstrate that PGE2 stimulates Mg2+ uptake in a cell line of MDCT.
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Kanaoka, Yoshihide, and Yoshihiro Urade. "Hematopoietic prostaglandin D synthase." Prostaglandins, Leukotrienes and Essential Fatty Acids 69, no. 2-3 (August 2003): 163–67. http://dx.doi.org/10.1016/s0952-3278(03)00077-2.

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17

Martinez, Dominique, Gilles Aumont, M. Moutoussamy, D. Gabriel, A. H. Tatareau, Nicolas Barré, F. Vallée, and Bernard Mari. "Études épidémiologiques sur la dermatophilose dans les Antilles." Revue d’élevage et de médecine vétérinaire des pays tropicaux 46, no. 1-2 (January 1, 1993): 323–27. http://dx.doi.org/10.19182/remvt.9387.

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La dermatophilose est une des maladies les plus importantes des ruminants domestiques des îles caraïbes, où la maladie clinique est associée à la présence de la tique Amblyomma variegatum. Des études séroépidémiologiques ont été effectuées afin d’éclaircir l’épidémiologie de la maladie dans la région, en faisant particulièrement attention au rôle d’A. variegatum. Une banque de 1300 sérums de bovins des Petites Antilles a été examinée par ELISA pour la présence d’anticorps contre Dermatophilus congolensis. Il s’est avéré que des animaux séropositifs existent dans des îles non infestées par A. variegatum, et où la dermatophilose n’est jamais ou rarement observée. De plus, il n’y avait pas de différence significative entre la prévalence d’animaux séropositifs des zones infestées par la tique et des zones non infestées de la Martinique et de Sainte-Lucie, deux îles partiellement infestées et où la dermatophilose n’est observée que dans les parties infestées par la tique. La prévalence était basse dans les petites îles ayant un climat sec. Ceci confirme les résultats expérimentaux indiquant qu’A. variegatum n’est pas indispensable pour la transmission de D. congolensis, qui est très répandu dans la plupart des îles. Les concentrations élevées de prostaglandine E2 (entre 151 et 377 ng/ml) et de prostacycline (entre 124 et 134 ng/ml) trouvées dans la salive des femelles d’A. variegatum, suggèrent fortement que la tique pourrait favoriser le développement des lésions par une activité immunomodulatrice de sa salive. Néanmoins, malgré un certain succès dans la reproduction de la dermatophilose chez des chèvres simultanément infestées avec des adultes d’A. variegatum et scarifiées avec Dermatophilus, on n’a pas observé de différence entre des bovins Créole naturellement résistants et des Brahman hautement sensibles, utilisant le même modèle. Les lésions de la dermatophilose sont restées très bénignes sur les animaux des deux races. Après cette expérience, les Brahman ont développé une dermatophilose généralisée après avoir été mis au pâturage, ce qui indique que le rôle respectif des facteurs de risque identifiés comme étant d’importance majeure pour l’expression de la dermatophilose clinique, n’est pas complètement clarifié et demande d’être étudié davantage.
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18

Caló, Lorenzo, Salvatore Cantaro, Francesco Marchini, Sandro Giannini, Rocco Castrignano, Giovanni Gambaro, Augusto Antonello, et al. "Is hydrochlorothiazide-induced hypocalciuria due to inhibition of prostaglandin E2 synthesis?" Clinical Science 78, no. 3 (March 1, 1990): 321–25. http://dx.doi.org/10.1042/cs0780321.

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1. Since prostaglandin E2 could play a role in idiopathic hypercalciuria, and considering the well-established hypocalciuric action of hydrochlorothiazide, we have evaluated the effect of 15 days' treatment with hydrochlorothiazide in 10 hypercalciuric male stone-formers on urinary Ca2+ and prostaglandin E2, as well as on plasma bicyclo-prostaglandin E2, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and parathyroid hormone. 2. In addition to lowering urinary Ca2+ (P <0.001), hydrochlorothiazide also promoted a significant fall in urinary prostaglandin E2 (P <0.001), plasma bicyclo-prostaglandin E2 (P <0.001) and 1,25-dihydroxyvitamin D (P <0.01), and an increase in plasma parathyroid hormone (P <0.025), whereas plasma 25-hydroxyvitamin D was unchanged. 3. A positive correlation between urinary Ca2+ and prostaglandin E2 was present before (P <0.00005), but not after, hydrochlorothiazide. Plasma bicyclo-prostaglandin E2 and plasma 1,25-dihydroxyvitamin D were positively correlated both before (P <0.005) and after (P <0.005) hydrochlorothiazide, as was also the percentage change in each induced by the drug (P <0.05). Furthermore, the changes in plasma 25-hydroxyvitamin D and plasma 1,25-dihydroxyvitamin D after hydrochlorothiazide were negatively correlated (P <0.05). 4. It is suggested that a block of prostaglandin E2 synthesis plays a role in the effect of hydrochlorothiazide on Ca2+ metabolism, most probably through an inhibition of 1α-hydroxylase activity.
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Nicol, G. D., M. R. Vasko, and A. R. Evans. "Prostaglandins Suppress an Outward Potassium Current in Embryonic Rat Sensory Neurons." Journal of Neurophysiology 77, no. 1 (January 1, 1997): 167–76. http://dx.doi.org/10.1152/jn.1997.77.1.167.

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Nicol, G. D., M. R. Vasko, and A. R. Evans. Prostaglandins suppress an outward potassium current in embryonic rat sensory neurons. J. Neurophysiol. 77: 167–176, 1997. The cellular mechanisms giving rise to the enhanced excitability induced by prostaglandin E2 (PGE2) and carba prostacyclin (CPGI2) in embryonic rat sensory neurons were investigated using the whole cell patch-clamp recording technique. Exposing sensory neurons to 1 μM PGE2 produced a twofold increase in the number of action potentials elicited by a ramp of depolarizing current, but this eicosanoid had no effect on the resting membrane potential or the amplitude of the slow afterhyperpolarization. Characterization of the outward potassium currents in the embryonic sensory neurons indicated that the composition of the total current was variable among these neurons. A steady-state inactivation protocol was used to determine the extent of residual noninactivating current. A conditioning prepulse to +20 mV demonstrated that some of these neurons exhibited only a sustained potassium current with little steady-state inactivation whereas others exhibited some combination of a sustained as well as a rapidly inactivating I A-type current. Treatment with 1 μM PGE2 or 1 μM CPGI2, but not 1 μM prostaglandin F2α (PGF2α) produced a time-dependent suppression of the total potassium current. After a 20-min exposure, PGE2 and CPGI2 inhibited the maximal current obtained at +60 mV by 48 and 40%, respectively. The prostaglandin-induced suppression of the potassium current was not associated with a shift in the voltage dependence for activation. Subtraction of the currents remaining after PGE2 or CPGI2 treatment from their respective control recordings revealed that the prostaglandin-sensitive current had characteristics that were consistent with a sustained-type of potassium current. This idea is supported by the following observation. The steady-state inactivation protocol revealed that for prepulse voltages activating both rapidly inactivating and sustained currents, the relaxation of the current was accelerated after treatment with PGE2 or CPGI2 suggesting the removal of a slower component. This effect was not observed in neurons exhibiting only the sustained type current. These results suggest that pro-inflammatory prostaglandins enhance the excitability of rat sensory neurons, in part, through the suppression of an outward potassium current that may modulate the firing threshold for generation of the action potential.
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20

Kompanowska-Jezierska, Elzbieta, Claus Emmeluth, Lisbeth Grove, Poul Christensen, Janusz Sadowski, and Peter Bie. "Mechanism of vasopressin natriuresis in the dog: role of vasopressin receptors and prostaglandins." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 6 (June 1, 1998): R1619—R1625. http://dx.doi.org/10.1152/ajpregu.1998.274.6.r1619.

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Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg ⋅ min−1 ⋅ kg body wt−1), plasma vasopressin concentration increased to 2.30 ± 0.20 pg/ml compared with 0.12 ± 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 ± 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 ± 15.8 μmol/min) than without vasopressin (4.6 ± 0.4 ml/min and 14.4 ± 4.1 μmol/min, respectively). Deamino-[Cys1,d-Arg8]vasopressin, a V2 receptor agonist (4 pg ⋅ min−1 ⋅ kg−1), mimicked the antidiuretic response (0.20 ± 0.03 ml/min) without changing UNaV (9.7 ± 4.4 μmol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 ± 0.02 ml/min), and abolished the natriuresis (13.4 ± 3.7 μmol/min). During AVP infusion, UNaV was highly correlated ( r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.
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21

Hapangama, Dharani K., Hilary O. D. Critchley, Teresa A. Henderson, and David T. Baird. "Mifepristone-Induced Vaginal Bleeding Is Associated with Increased Immunostaining for Cyclooxygenase-2 and Decrease in Prostaglandin Dehydrogenase in Luteal Phase Endometrium." Journal of Clinical Endocrinology & Metabolism 87, no. 11 (November 1, 2002): 5229–34. http://dx.doi.org/10.1210/jc.2002-020429.

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Abstract The mechanism of mifepristone-induced vaginal bleeding and endometrial shedding was investigated in 13 women who took 200 mg mifepristone in the midluteal phase on d 8 after the onset of the urinary LH surge (LH+8). Endometrial biopsies were collected, 6–24 h after mifepristone (group 1, n = 7) or 36–48 h after mifepristone (group 2, n = 6), and compared with those from a control group in the midluteal phase (n = 7). All women reported vaginal bleeding commencing 36–48 h after taking mifepristone. Treatment with mifepristone significantly reduced serum progesterone levels in all women, when compared with the controls (13.2 nmvs. 34.8 nm, P = 0.001). After mifepristone, a significant increase in cyclooxygenase-2 immunoreactivity was apparent at 36–48 h (P = 0.0018), whereas prostaglandin 15 dehydrogenase enzyme-positive immunostaining declined, to be virtually absent by 36–48 h in both glands and in stroma (P &lt; 0.05). There was no change in intensity or distribution of staining for steroid receptors after mifepristone. The changes in immunostaining for cyclooxygenase-2 and prostaglandin 15 dehydrogenase strongly support the hypothesis that an increase in the local concentration of prostaglandins in the endometrium is involved in the mechanism of bleeding induced by mifepristone in the luteal phase.
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22

Schwertschlag, U., J. G. Gerber, J. S. Barnes, and A. S. Nies. "Increased PGE2 excretion by dDAVP in humans depends on state of hydration." American Journal of Physiology-Renal Physiology 250, no. 6 (June 1, 1986): F1008—F1012. http://dx.doi.org/10.1152/ajprenal.1986.250.6.f1008.

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The relationship of renal prostaglandin E2 (PGE2) excretion (UPGEV) to water deprivation, water diuresis, and subsequent antidiuresis by 1-desamino-8-D-arginine vasopressin (dDAVP) was studied in female volunteers. After 16 h of water deprivation, the subjects began a sustained water diuresis for 8 h. This diuresis caused a transient twofold rise in UPGEV at 2 h (P less than 0.05), which then fell back to or below baseline levels. dDAVP given during the water diuresis caused a transient rise of UPGEV as urine volume decreased and plasma osmolality fell from 277 +/- 1.5 to 271 +/- 2 mosmol/kg (P less than 0.01). Another group of subjects had the water diuresis discontinued after 4 h with dDAVP given at the 5th h when urine volume was decreasing and urine osmolality was increasing. In this setting dDAVP did not produce as great a fall in plasma osmolality nor did it increase UPGEV. These data indicate that renal prostaglandin synthesis (as determined by UPGEV) is increased transiently by an acute water load; dDAVP given during continued water ingestion results in a fall in plasma osmolality and increased PGE excretion; however, dDAVP does not increase UPGEV during normal hydration; and UPGEV is independent of changes in urine flow. These findings imply that renal prostaglandins may have a functional role in humans to inhibit the hydroosmotic actions of antidiuretic hormone, and thus hasten the excretion of a water load, and to prevent overhydration when inappropriate antidiuresis occurs. However, there is no evidence that the stimulus for prostaglandin production is dDAVP per se.
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23

Lieberthal, W., M. L. Vasilevsky, C. R. Valeri, and N. G. Levinsky. "Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney." American Journal of Physiology-Renal Physiology 252, no. 2 (February 1, 1987): F331—F337. http://dx.doi.org/10.1152/ajprenal.1987.252.2.f331.

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Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.
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24

Tsubosaka, Yoshiki, Toko Maehara, Daiki Imai, Tatsuro Nakamura, Koji Kobayashi, Nanae Nagata, Wataru Fujii, and Takahisa Murata. "Hematopoietic prostaglandin D synthase–derived prostaglandin D 2 ameliorates adjuvant‐induced joint inflammation in mice." FASEB Journal 33, no. 6 (February 27, 2019): 6829–37. http://dx.doi.org/10.1096/fj.201802153r.

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25

Urade, Yoshihiro. "New Aspects on Prostaglandin D Synthases." Folia Pharmacologica Japonica 110, supplement (1997): 56–58. http://dx.doi.org/10.1254/fpj.110.supplement_56.

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26

Urade, Yoshihiro, Kikuko Watanabe, and Osamu Hayaishi. "Prostaglandin D, E, and F synthases." Journal of Lipid Mediators and Cell Signalling 12, no. 2-3 (October 1995): 257–73. http://dx.doi.org/10.1016/0929-7855(95)00032-l.

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27

Santos, R. M., and J. L. M. Vasconcelos. "Eficácia da dose reduzida de gonadorelina e diferentes prostaglandinas no protocolo ovsynch em vacas holandesas." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 60, no. 6 (December 2008): 1323–28. http://dx.doi.org/10.1590/s0102-09352008000600005.

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Avaliou-se a eficácia da dose de 0,10 ou de 0,25mg de gonadorelina nas taxas de ovulação e de sincronização no protocolo Ovsynch e de 150mcg de D-cloprostenol ou 0,530mg de cloprostenol sódico na regressão do corpo lúteo (CL) de sete dias e de todos os CL. Foram utilizadas 136 vacas lactantes da raça Holandesa, com média de produção de leite de 23,75,8kg/dia, com 138,4±72,0 dias em lactação. As vacas foram distribuídas aleatoriamente em quatro grupos, de acordo com a dose de gonadorelina e o tipo da prostaglandina. As taxas de ovulação e de sincronização foram de 52,9% e 80,9% para 0,10mg de gonadorelina e de 57,4% e 80,9% para 0,25mg de gonadorelina, respectivamente. A taxa de regressão do CL de sete dias foi de 97,1% para o D-cloprostenol e de 97,5% para o cloprostenol sódico. A taxa de prenhez não foi influenciada pelos tratamentos, mas foi influenciada pela taxa de ovulação à primeira aplicação de gonadorelina, 16,0% vs. 6,6% para as vacas que ovularam e não ovularam, respectivamente. Conclui-se que 0,10mg de gonadorelina foi eficiente e ambas prostaglandinas podem ser usadas em protocolos de sincronização da ovulação.
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28

Mizushima, Y. "Lipo-prostaglandin preparations." Prostaglandins, Leukotrienes and Essential Fatty Acids 42, no. 1 (January 1991): 1–6. http://dx.doi.org/10.1016/0952-3278(91)90058-d.

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29

YAMADA, Kenji. "The Effect of Prostaglandin D2 on Rat Testicular Testosterone Levels." Folia Endocrinologica Japonica 65, no. 10 (1989): 1180–85. http://dx.doi.org/10.1507/endocrine1927.65.10_1180.

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30

Hammad, Hamida, Mirjam Kool, Thomas Soullié, Shuh Narumiya, François Trottein, Henk C. Hoogsteden, and Bart N. Lambrecht. "Activation of the D prostanoid 1 receptor suppresses asthma by modulation of lung dendritic cell function and induction of regulatory T cells." Journal of Experimental Medicine 204, no. 2 (February 5, 2007): 357–67. http://dx.doi.org/10.1084/jem.20061196.

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Prostaglandins (PGs) can enhance or suppress inflammation by acting on different receptors expressed by hematopoietic and nonhematopoietic cells. Prostaglandin D2 binds to the D prostanoid (DP)1 and DP2 receptor and is seen as a critical mediator of asthma causing vasodilation, bronchoconstriction, and inflammatory cell influx. Here we show that inhalation of a selective DP1 agonist suppresses the cardinal features of asthma by targeting the function of lung dendritic cells (DCs). In mice treated with DP1 agonist or receiving DP1 agonist-treated DCs, there was an increase in Foxp3+ CD4+ regulatory T cells that suppressed inflammation in an interleukin 10–dependent way. These effects of DP1 agonist on DCs were mediated by cyclic AMP–dependent protein kinase A. We furthermore show that activation of DP1 by an endogenous ligand inhibits airway inflammation as chimeric mice with selective hematopoietic loss of DP1 had strongly enhanced airway inflammation and antigen-pulsed DCs lacking DP1 were better at inducing airway T helper 2 responses in the lung. Triggering DP1 on DCs is an important mechanism to induce regulatory T cells and to control the extent of airway inflammation. This pathway could be exploited to design novel treatments for asthma.
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31

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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32

Helliwell, Rachel J. A., Jeffrey A. Keelan, Keith W. Marvin, Linda Adams, Maxwell C. Chang, Ashmit Anand, Timothy A. Sato, et al. "Gestational Age-Dependent Up-Regulation of Prostaglandin D Synthase (PGDS) and Production of PGDS-Derived Antiinflammatory Prostaglandins in Human Placenta." Journal of Clinical Endocrinology & Metabolism 91, no. 2 (February 2006): 597–606. http://dx.doi.org/10.1210/jc.2005-1982.

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33

Umeda, Fumio, Tatsuya Kuroki, and Hajime Nawata. "Prostaglandins and diabetic nephropathy." Journal of Diabetes and its Complications 9, no. 4 (October 1995): 334–36. http://dx.doi.org/10.1016/1056-8727(95)80035-d.

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34

Nakahata, Yuta, Shigeru Shimamoto, Tadayasu Ohkubo, Kosuke Aritake, Yoshihiro Urade, and Yuji Hidaka. "Structural Analysis of Lipocalin-Type Prostaglandin D Synthase Complexed with Prostaglandin J2." Biophysical Journal 108, no. 2 (January 2015): 510a. http://dx.doi.org/10.1016/j.bpj.2014.11.2792.

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35

Shimamoto, Shigeru, Yuta Nakahata, Yusuke Nakagawa, Yutaro Fukuda, Kosuke Aritake, Yoshihiro Urade, and Yuji Hidaka. "Structural Analysis of Lipocalin-Type Prostaglandin D Synthase Complexed with Prostaglandin J2." Biophysical Journal 110, no. 3 (February 2016): 379a. http://dx.doi.org/10.1016/j.bpj.2015.11.2048.

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36

Garrelds, Ingrid M., Graham R. Elliott, Freek J. Zijlstra, and Iván L. Bonta. "Effects of short- and long-term feeding of L-carnitine and congeners on the production of eicosanoids from rat peritoneal leucocytes." British Journal of Nutrition 72, no. 5 (November 1994): 785–93. http://dx.doi.org/10.1079/bjn19940080.

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The effect of short- and long-term feeding with L-carnitine, L-acetyl carnitine and L-propionyl carnitine on the production of eicosanoids front in vitro stimulated carrageenan-induced rat peritoneal macrophages was investigated. Both young (4 weeks) and old (18 months) rats were used. A lower number of cells was isolated from the peritonea of treated than control young rats after 4 d feeding, but after 60 d no differences were observed. A similar reduction in cell number was found when old animals were given L-acetyl carnitine or L-propionyl carnitine (acutely) or L-acetyl carnitine or L-carnitine (chronically). Plasma carnitine levels were higher in young rats given carnitine both chronically and acutely. Carnitine derivatives were without effect. In contrast, levels of total carnitine in the plasma of old rats given L-carnitine and L-acetyl carnitine for 4 d and 60 d were higher than in controls. There was no correlation between total plasma carnitine level and effects on prostaglandin, thromboxane and leukotriene B4 (LTB4) production. In young rats the most important changes were observed in relation to the production of prostacyclin (PGI2), measured as 6 keto-prostaglandin Flα. Prostacyclin production was higher in the groups given carnitine or its derivatives. The net result of the changes in PGI2 was that the 6 keto-prostaglandin F1α: thromboxane B2 and the 6 keto-prostaglandin Flα:LTB4 ratios tended to be higher in cells from young animals following short-term feeding with L-carnitine. When young rats were given carnitine compounds for 60 d PGI2 production was lower in cells from L-acetyl carnitine- and L-propionyl carnitine-fed animals. The net result of the changes in PGI2 was that the 6 keto-prostaglandin F1α: thromboxane B2 and the 6 keto-prostaglandin F1α:LTB4 ratios were lower in cells from animals fed with carnitine compounds. In old rats the PGI2 production was lower after short-term feeding with carnitine compounds and was higher after long-term feeding. LTB4 production was lower after L-carnitine and L-acetyl carnitine treatment for 4 d and also lower after 60 d treatment with L-acetyl carnitine. The net results of the changes in PGI2 were that the 6 keto-prostaglandin F1α: thromboxane B2 and the 6 keto-prostaglandin F1α:LTB4 ratios were lower after short-term feeding of all three compounds and higher after the long-term treatment with L-acetyl carnitine and L-propionyl carnitine in old rats. By long-term treatment with low-dose aspirin of patients with heart failure and claudication, the 6 keto-prostaglandin F1α: thromboxane B2 ratio is positively increased, which is a beneficial cardioprotective effect. The mechanism of action of carnitine in heart failure and claudication could also be achieved by an increase of this ratio. Our results suggest that elderly patients could be treated chronically by carnitine to obtain this beneficial effect.
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37

Daniel, Larry W., Vicki A. Sciorra, and Sujoy Ghosh. "Phospholipase D, tumor promoters, proliferation and prostaglandins." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1439, no. 2 (July 1999): 265–76. http://dx.doi.org/10.1016/s1388-1981(99)00099-2.

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38

Mahmud, Ishtiaq, Natsuo Ueda, Hiroko Yamaguchi, Rieko Yamashita, Shozo Yamamoto, Yoshihide Kanaoka, Yoshihiro Urade, and Osamu Hayaishi. "Prostaglandin D Synthase in Human Megakaryoblastic Cells." Journal of Biological Chemistry 272, no. 45 (November 7, 1997): 28263–66. http://dx.doi.org/10.1074/jbc.272.45.28263.

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39

Toh, Hiroyuki. "Molecular evolutionary studies on prostaglandin D synthase." Prostaglandins 51, no. 4 (April 1996): 299. http://dx.doi.org/10.1016/0090-6980(96)86804-3.

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40

Liszewska, Ewa, Pierrette Reinaud, Emmanuelle Billon-Denis, Olivier Dubois, Philippe Robin, and Gilles Charpigny. "Lysophosphatidic Acid Signaling during Embryo Development in Sheep: Involvement in Prostaglandin Synthesis." Endocrinology 150, no. 1 (September 4, 2008): 422–34. http://dx.doi.org/10.1210/en.2008-0749.

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We investigated the lysophosphatidic acid (LPA) pathway during early pregnancy in sheep. LPA was detected in the uteri of early-stage pregnant ewes. Using quantitative RT-PCR, the expression of autotaxin, the LPA-generating enzyme, was found in the endometrium and conceptus. In the latter autotaxin, transcript levels were low on d 12–14 and increased on d 15–16, in parallel with the level of LPA. Autotaxin was localized in the luminal epithelium and superficial glands of the endometrium and in trophectoderm cells of the conceptus. The expression of G protein-coupled receptors for LPA was also examined in the ovine conceptus. LPA receptor LPAR1 and LPAR3 transcripts were expressed during early pregnancy and displayed a peak on d 14, whereas the highest level of protein for both receptors was observed at d 17. LPAR1 was localized in cellular membranes and nuclear compartments of the trophectoderm cells, whereas LPAR3 was revealed only in membranes. LPA activated phosphorylation of the MAPK ERK1/2 in ovine trophectoderm-derived cells. Moreover, the bioactive lipid increased the proliferation of trophectoderm cells in culture, as shown by thymidine and bromodeoxyuridine incorporation. Furthermore, LPA induced changes to the organization of β-actin and α-tubulin, suggesting a role for it in rearrangement of trophectoderm cells cytoskeleton. Because a link had previously been established between prostaglandin and LPA pathways, we analyzed the effect of LPA on prostaglandin synthesis. LPA induced an increase in the release of prostaglandin F2α and prostaglandin E2, with no significant modifications to cytosolic phospholipase A2α and prostaglandin synthase-2 expression. Taken together, our results suggest a new role for LPA-mediated signaling in the ovine conceptus at the time of implantation. Lysophosphatidic acid (LPA) receptor 1 (R1) and LPAR3 mediate signaling of lysophosphatidic acid produced by autotaxin and induce prostaglandin biosynthesis and cytoskeleton changes in ovine trophectoderm cells at implantation time.
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41

Stephens, L. A., and R. Rajamahendran. "A comparison of two estrus synchronization methods in beef heifers." Canadian Journal of Animal Science 78, no. 3 (September 1, 1998): 437–39. http://dx.doi.org/10.4141/a98-043.

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This study compared the use of two injections of prostaglandin F2α(PGF2α) given 11 d apart with the use of gonadotropin releasing hormone (GnRH) followed by PGF2α after 7 d for synchronizing estrus in beef heifers. Heifers synchronized with GnRH and PGF2α showed weak signs of estrus and were more difficult to inseminate. There were no significant differences in synchronization rate and pregnancy rate. Key words: Estrus synchronization, beef heifers, gonadotropin releasing hormone, prostaglandin F2α
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42

Sitter, T., B. Haslinger, S. Mandl, H. Fricke, E. Held, and A. Sellmayer. "High glucose increases prostaglandin E2 synthesis in human peritoneal mesothelial cells: role of hyperosmolarity." Journal of the American Society of Nephrology 9, no. 11 (November 1998): 2005–12. http://dx.doi.org/10.1681/asn.v9112005.

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Peritoneal mesothelial cells are considered the predominant source of peritoneal prostanoid formation because they represent the largest resident cell population in the peritoneal cavity. The present study was designed to evaluate the effect of D-glucose, which is widely used in commercially available peritoneal dialysis fluids as an osmotic compound, on the synthesis of prostaglandins in cultured human mesothelial cells (HMC). Analysis of eicosanoid synthesis in HMC by reversed-phase HPLC revealed that 6-keto-PGF1alpha, the spontaneous hydrolysis product of prostacyclin (PGI2), and prostaglandin E2 (PGE2) were the main eicosanoids produced. Addition of D-glucose resulted in a time- and concentration-dependent (30 to 120 mM) increase in PGE2 production in HMC (24 h, 90 mM: 3.9+/-0.5 ng/10(5) cells versus 2.3+/-0.3 in untreated cells; P < 0.05). Mannitol (90 mM) or L-glucose (90 mM). nonmetabolizable osmotic compounds, also led to a significant (P < 0.05) but less intense increase in PGE2 synthesis (3.3+/-0.4 and 3.2+/-0.5 ng/10(5) cells, respectively). Increased PGE2 synthesis was completely blunted by coincubation with the specific protein kinase C (PKC) inhibitor Ro 31-8220 or downregulation of PKC activity by preincubation with phorbol myristate acetate for 16 h. Furthermore, coincubation with PD 98059, an inhibitor of the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway, also inhibited increased PGE2 synthesis by D-glucose or mannitol. In contrast, the iso-osmolar glucose polymer icodextrin, which is used as an alternative to D-glucose in peritoneal dialysis solutions, had no effect on PGE2 synthesis. These data indicate that D-glucose and metabolically inert sugars increase PGE2 synthesis in HMC at least in part by hyperosmolarity and that this effect requires activation of PKC and the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway of intracellular signaling.
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43

Elliott, G. R., A. P. M. Lauwen, and I. L. Bonta. "The effect of acute feeding of carnitine, acetyl carnitine and propionyl carnitine on basal and A23187-stimulated eicosanoid release from rat carrageenan-elicited peritoneal macrophages." British Journal of Nutrition 64, no. 2 (September 1990): 497–503. http://dx.doi.org/10.1079/bjn19900049.

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Little is known about the ability of carnitine to modulate cell functions. As carnitine plays an important role in lipid metabolism we investigated the acute effect of L-carnitine, L-acetyl carnitine and L-propionyl carnitine (300 mg/kg per d; 4 d) on the basal and calcium-ionophore (A23187)-stimulated release of arachidonic acid metabolites from rat carrageenan-elicited peritoneal macrophages. A decrease in the number of peritoneal carrageenan-elicited macrophages was observed after feeding all three compounds. The basal release of prostaglandin E2, 6 keto-prostaglandin F1α and leukotriene B4 was stimulated by all treatments. In contrast, thromboxane B2 production was diminished by feeding carnitine and acetyl carnitine. A23187-stimulated synthesis of 6 keto-prostaglandin F1α and leukotriene B4 was further enhanced by all three compounds. Acetyl carnitine and propionyl carnitine also enhanced thromboxane B2 synthesis. However, no effects on prostaglandin E2 formation were detected. The 6 keto-prostaglandin F1α: thromboxane B2 ratio, calculated from the basal and A23187-stimulated values, was increased by carnitine treatment. In the presence of A23187 there was also an increase in the 6 keto-prostaglandin F1α: leukotriene B4 ratio. We conclude that carnitine, and possibly some of its derivatives, could modify the macrophage component of an inflammation in vivo.
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44

Westover, Alana J., Stuart B. Hooper, Megan J. Wallace, and Timothy J. M. Moss. "Prostaglandins mediate the fetal pulmonary response to intrauterine inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 7 (April 1, 2012): L664—L678. http://dx.doi.org/10.1152/ajplung.00297.2011.

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Intra-amniotic (IA) lipopolysaccharide (LPS) induces intrauterine and fetal lung inflammation and increases lung surfactant and compliance in preterm sheep; however, the mechanisms are unknown. Prostaglandins (PGs) are inflammatory mediators, and PGE2 has established roles in fetal lung surfactant production. The aim of our first study was to determine PGE2 concentrations in response to IA LPS and pulmonary gene expression for PG synthetic [prostaglandin H synthase-2 (PGHS-2) and PGE synthase (PGES)] and PG-metabolizing [prostaglandin dehydrogenase (PGDH)] enzymes and PGE2 receptors. Our second study aimed to block LPS-induced increases in PGE2 with a PGHS-2 inhibitor (nimesulide) and determine lung inflammation and surfactant protein mRNA expression. Pregnant ewes received an IA saline or LPS injection at 118 days of gestation. In study 1, fetal plasma and amniotic fluid were sampled before and at 2, 4, 6, 12, and 24 h after injection and then daily, and fetuses were delivered 2 or 7 days later. Amniotic fluid PGE2 concentrations increased ( P < 0.05) 12 h and 3–6 days after LPS. Fetal lung PGHS-2 mRNA and PGES mRNA increased 2 ( P = 0.0084) and 7 ( P = 0.014) days after LPS, respectively. In study 2, maternal intravenous nimesulide or vehicle infusion began immediately before LPS or saline injection and continued until delivery 2 days later. Nimesulide inhibited LPS-induced increases in PGE2 and decreased fetal lung IL-1β and IL-8 mRNA ( P ≤ 0.002) without altering lung inflammatory cell infiltration. Nimesulide decreased surfactant protein (SP)-A ( P = 0.05), -B ( P = 0.05), and -D ( P = 0.0015) but increased SP-C mRNA ( P = 0.023). Thus PGHS-2 mediates, at least in part, fetal pulmonary responses to inflammation.
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45

Hoff, K. K., E. T. Zawada, F. K. Alavi, J. W. Leyse, and R. N. Santella. "Effects of ketorolac tromethamine on erythropoietin levels in Sprague Dawley rats." International Journal of Artificial Organs 17, no. 12 (December 1994): 629–34. http://dx.doi.org/10.1177/039139889401701203.

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Ketorolac tromethamine (KT) is a potent analgesic, most often used in its injectable form postoperatively. Similar to other nonsteroidal antiinflammatory drugs (NSAIDs), it inhibits prostaglandin (PG) synthesis. Prostaglandins have been shown to be involved in the regulation of renal function as well as erythropoietin (Ep) production. The intent of this study was to determine the effect of KT on plasma Ep levels in Sprague Dawley (SD) rats. Twenty rats received either 15 mg/kg/d or the KT vehicle IM for 5d. Blood samples (1 ml) were collected via tail vein each day of treatment. Plasma Ep levels were significantly higher in the KT rats than normal controls with the greatest difference occurring on d4 of treatment (70.1 ± 10.8 vs 30.9 ± 10.84 mU/ml, p < 0.01). This change in Ep corresponded with a significant reduction in hematocrit (KT, 29.5 ± 2.2 vs C, 40.8 ± 2.2%, p< 0.01). Presence of fecal blood was noted in the KT treated rats. A similar second experiment was designed to determine if blood loss was the cause of altered Ep production. In this experiment controls (HC) were bled via tail vein, to match the hematocrits of KT treated animals. Repeated administration of KT led to a steady reduction in hematocrit. When compared, hematocrit matched animals showed no difference in plasma Ep levels on all days of treatment (KT, 48.0 ± 4.9 vs HC, 44.6 ± 3.1 mU/ml, N.S.). In conclusion, repeated administration of KT showed no impairment of Ep production and release in response to reduced hematocrit, suggesting that in this instance, prostaglandin inhibition plays a minimal role in Ep production or release.
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46

Meyer, D. J., and M. Thomas. "Characterization of rat spleen prostaglandin H d-isomerase as a sigma-class GSH transferase." Biochemical Journal 311, no. 3 (November 1, 1995): 739–42. http://dx.doi.org/10.1042/bj3110739.

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The prostaglandin H D-isomerase of rat immune accessory cells has been purified from spleen by a simple procedure, and its high specificity and activity [Urade, Fujimoto, Ujihara and Hayaishi (1987) J. Biol. Chem. 262, 3820-3825] have been confirmed in an assay coupled to prostaglandin H synthase. The enzyme also decreases the formation of 12[S]-hydroxy-5,8,10-heptadecatrienoic acid formed by the synthase in the presence of GSH and increases the overall rate of arachidonate oxidation. A partial amino acid sequence shows a strong relationship to GSH transferases of parasitic helminths and molluscs, indicating that it is the first example of a vertebrate sigma-class GSH transferase, and suggesting that certain helminth GSH transferases may be involved in prostaglandin synthesis.
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47

Song, Wen-Liang, Emanuela Ricciotti, Xue Liang, Tilo Grosser, Gregory R. Grant, and Garret A. FitzGerald. "Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice." Journal of Pharmacology and Experimental Therapeutics 367, no. 3 (October 10, 2018): 425–32. http://dx.doi.org/10.1124/jpet.118.250936.

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48

Dixon, B. S., R. Breckon, J. Fortune, R. J. Vavrek, J. M. Stewart, R. Marzec-Calvert, and S. L. Linas. "Effects of kinins on cultured arterial smooth muscle." American Journal of Physiology-Cell Physiology 258, no. 2 (February 1, 1990): C299—C308. http://dx.doi.org/10.1152/ajpcell.1990.258.2.c299.

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The present study uses various kinin agonists and antagonists to examine the cellular mechanisms of bradykinin's actions on intracellular calcium, prostaglandins, and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cultured arterial smooth muscle cells (casmc) obtained from rat mesenteric arteries. Exposure to bradykinin produced a rapid release of calcium (peak less than or equal to 20 s) from intracellular stores and an increase in prostaglandin (PG) E2 and cAMP production in casmc. Compared with bradykinin, the bradykinin B1-agonist [des-Arg9]BK produced only a small increase in intracellular calcium. The bradykinin-mediated increase in intracellular calcium was competitively blocked by the B2 receptor antagonist [D-Arg-O-Hyp3-Thi5,8-D-Phe7]BK (B4307) but not the B1-antagonist ([des-Arg9-Leu8]BK). In addition, the similarity of the dose-response curves for the bradykinin-mediated increase in Ca2+, PGE2, and cAMP (half-maximal stimulation of 12, 11, and 13 nM, respectively) and the ability of the B2-antagonist (B4307) to block each of these effects of bradykinin suggest that all three effects are mediated by the same bradykinin (B2) receptor. Further studies revealed that increases in intracellular calcium are necessary for the bradykinin-mediated increase in PGE2 formation and the subsequent PGE2-dependent formation of cAMP. Taken together, these results suggest that bradykinin acts via a B2-receptor on arterial smooth muscle cells to release calcium from intracellular stores, leading to increases in PGE2 production and the PGE2-dependent activation of adenylate cyclase.
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49

Waclawik, Agnieszka, Adolfo Rivero-Muller, Agnieszka Blitek, Monika M. Kaczmarek, Leon J. S. Brokken, Kikuko Watanabe, Nafis A. Rahman, and Adam J. Ziecik. "Molecular Cloning and Spatiotemporal Expression of Prostaglandin F Synthase and Microsomal Prostaglandin E Synthase-1 in Porcine Endometrium." Endocrinology 147, no. 1 (January 1, 2006): 210–21. http://dx.doi.org/10.1210/en.2005-0880.

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Endometrial prostaglandins (PGs) and the PGE2/PGF2α ratio play an important role in regulating the estrous cycle and establishment of pregnancy. The enzymes downstream of cyclooxygenase-2 may determine the PGE2/PGF2α ratio in the porcine uterus. Thus, we have cloned porcine PGF synthase (PGFS) and microsomal PGE synthase-1 (mPGES-1) and characterized their expression in porcine endometrium during the estrous cycle and early pregnancy. PGFS and mPGES-1 amino acid sequences possessed a high degree (&gt;67% and &gt;77%, respectively) of identity with the other mammalian homologs. There was little modulation of mPGES-1 throughout the estrous cycle; however, PGFS expression was highly up-regulated in endometrium around the time of luteolysis. During early pregnancy, PGFS at the protein level showed a time-dependent increase (low on d 10–13, intermediate on d 14–23, and high on d 24–25). In pregnancy, expression of mPGES-1 was intermediate on d 10–11 and low on d 14–17 and then increased after d 22, reaching the maximum on d 24–25. Immunohistochemistry showed localization of PGFS and mPGES-1 proteins mainly in luminal and glandular epithelium. Concluding, the spatiotemporal expression of PGFS throughout the estrous cycle indicates an involvement of PGFS in regulating luteolysis in the pig. The comparison of endometrial PGFS and mPGES-1 expression on d 10–13 of the estrous cycle and pregnancy suggest a supportive role of these enzymes in determining the increase of uterine PGE2/PGF2α ratio during maternal recognition of pregnancy. Moreover, high expression of both PG synthases after initiation of implantation may indicate their significant role in placentation.
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50

Kong, Deping, Qiangyou Wan, Juanjuan Li, Shengkai Zuo, Guizhu Liu, Qian Liu, Chenchen Wang, et al. "DP1 Activation Reverses Age-Related Hypertension Via NEDD4L-Mediated T-Bet Degradation in T Cells." Circulation 141, no. 8 (February 25, 2020): 655–66. http://dx.doi.org/10.1161/circulationaha.119.042532.

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Background: Blood pressure often rises with aging, but exact mechanisms are still not completely understood. With aging, the level of proinflammatory cytokines increases in T lymphocytes. Prostaglandin D 2 , a proresolution mediator, suppresses Type 1 T helper (Th1) cytokines through D-prostanoid receptor 1 (DP1). In this study, we aimed to investigate the role of the prostaglandin D 2 /DP1 axis in T cells on age-related hypertension. Methods: To clarify the physiological and pathophysiological roles of DP1 in T cells with aging, peripheral blood samples were collected from young and older male participants, and CD4 + T cells were sorted for gene expression, prostaglandin production, and Western blot assays. Mice blood pressure was quantified by invasive telemetric monitor. Results: The prostaglandin D 2 /DP1 axis was downregulated in CD4 + T cells from older humans and aged mice. DP1 deletion in CD4 + T cells augmented age-related hypertension in aged male mice by enhancing Th1 cytokine secretion, vascular remodeling, CD4 + T cells infiltration, and superoxide production in vasculature and kidneys. Conversely, forced expression of exogenous DP1 in T cells retarded age-associated hypertension in mice by reducing Th1 cytokine secretion. Tumor necrosis factor α neutralization or interferon γ deletion ameliorated the age-related hypertension in DP1 deletion in CD4 + T cells mice. Mechanistically, DP1 inhibited Th1 activity via the PKA (protein kinase A)/p-Sp1 (phosphorylated specificity protein 1)/neural precursor cell expressed developmentally downregulated 4-like (NEDD4L) pathway–mediated T-box-expressed-in-T-cells (T-bet) ubiquitination. T-bet deletion or forced NEDD4L expression in CD4 + T cells attenuated age-related hypertension in CD4 + T cell–specific DP1-deficient mice. DP1 receptor activation by BW245C prevented age-associated blood pressure elevation and reduced vascular/renal superoxide production in male mice. Conclusions: The prostaglandin D 2 /DP1 axis suppresses age-related Th1 activation and subsequent hypertensive response in male mice through increase of NEDD4L–mediated T-bet degradation by ubiquitination. Therefore, the T cell DP1 receptor may be an attractive therapeutic target for age-related hypertension.
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