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Characterization of a rabbit kidney prostaglandin F(2{alpha}) receptor exhibiting G(i)-restricted signaling that inhibits water absorption in the collecting duct.
H├ębert RL, Carmosino M, Saito O, Yang G, Jackson CA, Qi Z, Breyer RM, Natarajan C, Hata AN, Zhang Y, Guan Y, Breyer MD
(2005) J Biol Chem 280: 35028-37
MeSH Terms: Amino Acid Sequence, Animals, Base Sequence, Calcium, Cell Line, Cloning, Molecular, DNA, Complementary, Dinoprost, Female, GTP-Binding Protein alpha Subunits, Gi-Go, Genetic Vectors, Humans, In Situ Hybridization, Kidney, Kidney Tubules, Collecting, Lac Operon, Latanoprost, Ligands, Molecular Sequence Data, Ovary, Perfusion, Pertussis Toxin, Prostaglandins, Prostaglandins F, Synthetic, Protein Binding, RNA, Messenger, Rabbits, Reverse Transcriptase Polymerase Chain Reaction, Ribonucleases, Sequence Homology, Amino Acid, Signal Transduction, Time Factors, Tissue Distribution, Transfection, Water
Show Abstract · Added December 21, 2013
PGF(2alpha) is the most abundant prostaglandin detected in urine; however, its renal effects are poorly characterized. The present study cloned a PGF-prostanoid receptor (FP) from the rabbit kidney and determined the functional consequences of its activation. Nuclease protection assay showed that FP mRNA expression predominates in rabbit ovary and kidney. In situ hybridization revealed that renal FP expression predominates in the cortical collecting duct (CCD). Although FP receptor activation failed to increase intracellular Ca(2+), it potently inhibited vasopressin-stimulated osmotic water permeability (L(p), 10(-7) cm/(atm.s)) in in vitro microperfused rabbit CCDs. Inhibition of L(p) by the FP selective agonist latanoprost was additive to inhibition of vasopressin action by the EP selective agonist sulprostone. Inhibition of L(p) by latanoprost was completely blocked by pertussis toxin, consistent with a G(i)-coupled mechanism. Heterologous transfection of the rabbit FPr into HEK293 cells also showed that latanoprost inhibited cAMP generation via a pertussis toxin-sensitive mechanism but did not increase cell Ca(2+). These studies demonstrate a functional FP receptor on the basolateral membrane of rabbit CCDs. In contrast to the Ca(2+) signal transduced by other FP receptors, this renal FP receptor signals via a PT-sensitive mechanism that is not coupled to cell Ca(2+).
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35 MeSH Terms
Evidence of free radical-mediated injury (isoprostane overproduction) in scleroderma.
Stein CM, Tanner SB, Awad JA, Roberts LJ, Morrow JD
(1996) Arthritis Rheum 39: 1146-50
MeSH Terms: Adult, Aged, Female, Humans, Male, Middle Aged, Oxidative Stress, Prostaglandins F, Synthetic, Scleroderma, Systemic, Thromboxane B2
Show Abstract · Added December 10, 2013
OBJECTIVE - Free radical-induced oxidative stress with consequent lipid peroxidation and resultant tissue damage has been suggested as a potential mechanism of the pathogenesis of scleroderma. However, because reliable measurement of lipid peroxidation in vivo is difficult, it has not been possible to adequately examine this hypothesis. We have previously described a series of bioactive prostaglandin F2-like compounds, termed F2-isoprostanes, produced in vivo in humans by the non-cyclooxygenase, free radical-catalyzed, peroxidation of arachidonic acid and have shown them to be a reliable measure of lipid peroxidation in vivo. In the present study, we determined whether scleroderma is associated with enhanced oxidative stress.
METHODS - As a measure of oxidative stress, we determined urinary concentrations of a tetranor-dicarboxylic acid metabolite of F2-isoprostanes (F2IP-M) by mass spectrometry in 8 patients with scleroderma (representing a wide spectrum of disease, including limited disease with refractory digital ulceration or pulmonary hypertension, and diffuse disease) and in 10 healthy control subjects.
RESULTS - F2IP-M concentrations were significantly higher in patients with scleroderma (mean +/- SEM 3.41 +/- 0.64 ng/mg of creatinine) than in healthy controls (1.22 +/- 0.14 ng/mg of creatinine) (P = 0.002). These elevations occurred in patients with limited disease and in those with diffuse disease.
CONCLUSION - The increased level of urinary F2IP-M supports the hypothesis that free radical-induced oxidative injury occurs in scleroderma and provides a biologic marker whose relationship to disease activity and disease therapy may be important. These findings may also provide a rationale for exploring whether antioxidant therapy may influence the natural course of the disease.
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10 MeSH Terms
Formation of F2-isoprostanes during oxidation of human low-density lipoprotein and plasma by peroxynitrite.
Moore KP, Darley-Usmar V, Morrow J, Roberts LJ
(1995) Circ Res 77: 335-41
MeSH Terms: Antihypertensive Agents, Arachidonic Acid, Arteriosclerosis, Catalysis, Humans, In Vitro Techniques, Lipid Peroxidation, Lipoproteins, LDL, Molsidomine, Nitrates, Nitric Oxide, Oxidation-Reduction, Platelet Aggregation Inhibitors, Prostaglandins F, Synthetic, Superoxide Dismutase, Superoxides, Vasodilator Agents
Show Abstract · Added December 10, 2013
F2-Isoprostanes are novel bioactive prostaglandin F2-like compounds produced by nonenzymatic free radical-catalyzed peroxidation of arachidonic acid. F2-Isoprostanes are initially formed in situ on phospholipids and subsequently released. Quantification of the F2-isoprostanes has been found to represent a valuable and reliable marker of lipid peroxidation. Oxidative modification of low-density lipoprotein (LDL) is a key process for the recognition of LDL by the scavenger receptors on macrophages. The oxidative mechanism responsible for the modification of LDL in vivo remains unclear, but an attractive candidate is the powerful oxidant peroxynitrite, which can be formed by reaction of nitric oxide and superoxide in the vessel wall. To further explore the potential role of peroxynitrite in the oxidative modification of plasma lipids, we investigated whether incubation of LDL and plasma with peroxynitrite or SIN-1, which decomposes to form nitric oxide and superoxide, catalyzes the formation of F2-isoprostanes. Incubation of LDL with peroxynitrite (0.125 to 1 mmol/L) or SIN-1 (0.5 and 1 mmol/L) induced a concentration-dependent increase in the formation of F2-isoprostanes, reaching a maximum of 5.5 +/- 2.05-fold (SEM) and 18.2 +/- 4.0-fold above control values, respectively. The increase of F2-isoprostanes induced by SIN-1 was essentially completely inhibited by superoxide dismutase. Incubation of plasma with peroxynitrite or SIN-1 yielded similar results. These results indicate that peroxynitrite can induce the formation of F2-isoprostanes in lipoproteins. Since F2-isoprostanes can exert potent biological activity such as vasoconstriction, they may contribute to the vascular pathobiology associated with atherosclerosis.
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17 MeSH Terms
Quantitative analysis of two dinor urinary metabolites of prostaglandin I2.
Falardeau P, Oates JA, Brash AR
(1981) Anal Biochem 115: 359-67
MeSH Terms: 6-Ketoprostaglandin F1 alpha, Deuterium, Epoprostenol, Gas Chromatography-Mass Spectrometry, Humans, Prostaglandins, Prostaglandins F, Synthetic, Radioisotope Dilution Technique, Tritium
Added December 10, 2013
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9 MeSH Terms
Quantitation of two dinor metabolites of prostacyclin by GC-MS.
Falardeau P, Brash AR
(1982) Methods Enzymol 86: 585-92
MeSH Terms: 6-Ketoprostaglandin F1 alpha, Adult, Biotransformation, Epoprostenol, Gas Chromatography-Mass Spectrometry, Humans, Prostaglandins, Prostaglandins F, Synthetic
Added December 10, 2013
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8 MeSH Terms
Endogenous prostacyclin biosynthesis and platelet function during selective inhibition of thromboxane synthase in man.
FitzGerald GA, Brash AR, Oates JA, Pedersen AK
(1983) J Clin Invest 72: 1336-43
MeSH Terms: Adult, Bleeding Time, Depression, Chemical, Dose-Response Relationship, Drug, Epoprostenol, Humans, Imidazoles, Male, Oxidoreductases, Platelet Aggregation, Prostaglandins F, Synthetic, Thromboxane B2, Thromboxane-A Synthase
Show Abstract · Added December 10, 2013
The consequences of inhibiting the metabolism of prostaglandin G2 to thromboxane A2 in man were studied by using an inhibitor of thromboxane synthase, 4-[2-(IH-imidazol-1-yl)ethoxy] benzoic acid hydrochloride (dazoxiben). Single doses of 25, 50, 100, and 200 mg of dazoxiben were administered to healthy volunteers at 2-wk intervals in a randomized, placebo-controlled, double-blind manner. Serum thromboxane B2 and aggregation studies in whole blood and platelet-rich plasma were measured before dosing and at 1, 4, 6, 8, and 24 h after dosing. Both serum thromboxane B2 and the platelet aggregation response to arachidonic acid (1.33 mM) were reversibly inhibited in a dose-dependent manner. Aggregation induced by 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (0.4 and 4.0 microM) in platelet-rich plasma as well as both aggregation and nucleotide release induced by collagen (95 micrograms/ml) in platelet-rich plasma and whole blood were unaltered by dazoxiben. Additional evidence for a platelet-inhibitory effect of the compound was a significant prolongation of the bleeding time at 1 h after administration of the highest dose (200 mg) of dazoxiben. Endogenous prostacyclin biosynthesis was assessed by measurement of the major urinary metabolite of prostacyclin, 2,3-dinor-6-keto-PGF1 alpha (PGI-M). PGI-M excretion was increased by dazoxiben; it rose a mean 2.4-fold from predosing control values at 0-6 h after administration of the highest dose studied (200 mg).
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13 MeSH Terms
Aspirin inhibits endogenous prostacyclin and thromboxane biosynthesis in man.
FitzGerald GA, Maas RL, Lawson JA, Oates JA, Roberts LJ, Brash AR
(1983) Adv Prostaglandin Thromboxane Leukot Res 11: 265-6
MeSH Terms: Aspirin, Humans, Kinetics, Prostaglandins F, Synthetic, Thromboxane B2, Thromboxanes
Added December 10, 2013
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6 MeSH Terms
Formation of unique biologically active prostaglandins in vivo by a non-cyclooxygenase free radical catalyzed mechanism.
Morrow JD, Hill KE, Burk RF, Nammour TM, Badr KF, Roberts LJ
(1991) Adv Prostaglandin Thromboxane Leukot Res 21A: 125-8
MeSH Terms: Animals, Carbon Tetrachloride, Dinoprost, Diquat, Free Radicals, Isomerism, Kidney, Oxidation-Reduction, Oxygen, Prostaglandins F, Synthetic, Rats, Superoxides
Added December 10, 2013
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2 Members
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12 MeSH Terms
Prostaglandin thromboxane, and 12-hydroxy-5,8,10,14-eicosatetraenoic acid production by ionophore-stimulated rat serosal mast cells.
Roberts LJ, Lewis RA, Oates JA, Austen KF
(1979) Biochim Biophys Acta 575: 185-92
MeSH Terms: Animals, Anti-Bacterial Agents, Arachidonic Acids, Calcimycin, Epoprostenol, Female, Gas Chromatography-Mass Spectrometry, Hydroxy Acids, Mast Cells, Peritoneum, Pleura, Prostaglandins, Prostaglandins D, Prostaglandins E, Prostaglandins F, Prostaglandins F, Synthetic, Rats, Thromboxane B2
Show Abstract · Added December 10, 2013
Production of several metabolites of arachidonic acid by purified rat serosal mast cells in response to stimulation with the ionophore A23187 was assessed by stable isotope dilution assay using gas chromatography-mass spectrometry. Compounds quantified were prostaglandins D2, E2, F2 alpha, 6-keto-F1 alpha, thromboxane B2, and 12-hydroxy-5,8,10,14-eicosatetraenoic acid. Mast cells incubated at 37 degrees C for 30 min without ionophore produced measurable quantities of all metabolites assayed. 4 microM A23187 resulted in substantial increased synthesis of all metabolites compared to control cells. Of the metabolites quantified, prostaglandin D2 and prostacyclin were the major products derived from arachidonic acid in ionophore-stimulated rat mast cells.
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18 MeSH Terms