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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.
Hébert 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
Allergen-induced synthesis of F(2)-isoprostanes in atopic asthmatics. Evidence for oxidant stress.
Dworski R, Murray JJ, Roberts LJ, Oates JA, Morrow JD, Fisher L, Sheller JR
(1999) Am J Respir Crit Care Med 160: 1947-51
MeSH Terms: Administration, Inhalation, Adult, Allergens, Asthma, Beclomethasone, Bronchial Provocation Tests, Bronchoalveolar Lavage Fluid, Cross-Over Studies, Cyclooxygenase Inhibitors, Double-Blind Method, Forced Expiratory Volume, Glucocorticoids, Humans, Hypersensitivity, Immediate, Mass Spectrometry, Methacholine Chloride, Middle Aged, Oxidative Stress, Prostaglandins F, Reactive Oxygen Species, Skin Tests
Show Abstract · Added December 10, 2013
It is thought that reactive oxygen species (ROS) participate in the inflammation which characterizes asthma, but the evidence supporting this contention is incomplete. F(2)-isoprostanes (F(2)-IsoPs) are arachidonate products formed on membrane phospholipids by the action of ROS and thereby represent a quantitative measure of oxidant stress in vivo. Using a mass spectrometric assay we measured urinary release of F(2)-IsoPs in 11 patients with mild atopic asthma after inhaled allergen challenge. The excretion of F(2)-IsoPs increased at 2 h after allergen (1.5 +/- 0.2 versus 2.6 +/- 0.3 ng/mg creatinine) and remained significantly elevated in all urine collections for the 8-h period of the study (analysis of variance [ANOVA]). The measured compounds were of noncyclooxygenase origin because neither aspirin nor indomethacin given before challenge suppressed them. Urinary F(2)-IsoPs remained unchanged after inhaled methacholine challenge. In nine atopic asthmatics, F(2)-IsoPs were quantified in bronchoalveolar lavage fluid (BALF) at baseline values and in a separate segment 24 h after allergen instillation. F(2)-IsoPs were elevated late in the BALF (0.9 +/- 0.2 versus 11.4 +/- 3.0 pg /ml, baseline versus allergen, respectively, p = 0.007). The increase was inhibited by pretreatment of the subjects with inhaled corticosteroids. These findings provide a new evidence for a role for ROS and lipid peroxidation in allergen-induced airway inflammation.
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21 MeSH Terms
Evidence against an increase in capillary permeability in subjects exposed to high altitude.
Kleger GR, Bärtsch P, Vock P, Heilig B, Roberts LJ, Ballmer PE
(1996) J Appl Physiol (1985) 81: 1917-23
MeSH Terms: Acclimatization, Acute-Phase Proteins, Altitude, Capillary Permeability, Cytokines, Free Radicals, Humans, Prostaglandins F, Pulmonary Edema
Show Abstract · Added December 10, 2013
A potential pathogenetic cofactor for the development of acute mountain sickness and high-altitude pulmonary edema is an increase in capillary permeability, which could occur as a result of an inflammatory reaction and/or free radical-mediated injury to the lung. We measured the systemic albumin escape by intravenously injecting 5 muCi of 125I-labeled albumin and the plasma concentrations of cytokines, F2-isoprostanes (products of lipid peroxidation), and acute-phase proteins in 24 subjects exposed to 4,559 m. Ten subjects developed acute mountain sickness, and four subjects developed high-altitude pulmonary edema. The transcapillary escape rate of albumin was 6.9 +/- 2.0%/h (SD) at low (550 m) and 6.3 +/- 1.9%/h at high (4,559 m) altitude (P = 0.23; n = 24). The subjects with high-altitude pulmonary edema had a modest but insignificant increase in the transcapillary escape rate of albumin (4.6 +/- 1.9%/h at low vs. 5.7 +/- 1.9%/h at high altitude; P = 0.42; n = 4). Plasma concentrations of fibrinogen, alpha 1-acid glycoprotein, C-reactive protein, and interleukin-6 were unchanged in the early phases and significantly increased by the end of the observation period in the subjects with high-altitude pulmonary edema, whereas tumor necrosis factor-alpha and F2-isoprostanes did not change at all. This suggests that the inflammatory reaction was rather a consequence than a causative factor of high-altitude pulmonary edema. In summary, these data argue against a dominant role for increased systemic capillary permeability in the development of acute mountain sickness and high-altitude pulmonary edema.
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9 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
Metabolism of the prostaglandins and thromboxanes.
Oates JA, Roberts LJ, Sweetman BJ, Maas RL, Gerkens JF, Taber DF
(1980) Adv Prostaglandin Thromboxane Res 6: 35-41
MeSH Terms: Animals, Epoprostenol, Half-Life, Humans, Hypercalcemia, Kinetics, Prostaglandins, Prostaglandins D, Prostaglandins E, Prostaglandins F, Thromboxanes
Added December 10, 2013
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11 MeSH Terms
Quantitation of the major urinary metabolite of PGF2 alpha in the human by GC-MS.
Brash AR
(1982) Methods Enzymol 86: 579-85
MeSH Terms: Biotransformation, Dinoprost, Gas Chromatography-Mass Spectrometry, Humans, Male, Prostaglandins F
Added December 10, 2013
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6 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
Endometrial prostaglandins and phospholipase activity related to implantation in rabbits: effects of dexamethasone.
Hoffman LH, Davenport GR, Brash AR
(1984) Biol Reprod 30: 544-55
MeSH Terms: 6-Ketoprostaglandin F1 alpha, Animals, Dexamethasone, Dinoprost, Dinoprostone, Embryo Implantation, Endometrium, Female, Indomethacin, Phospholipases, Pregnancy, Prostaglandins, Prostaglandins E, Prostaglandins F, Rabbits
Show Abstract · Added December 10, 2013
The anti-inflammatory steroid, dexamethasone, was demonstrated to have an antifertility effect in rabbits when administered systemically on Days 5-7 of pregnancy. The effects of this agent on prostaglandin (PG) concentrations and phospholipase activity in endometrium were determined. Using a highly specific and sensitive gas chromatography-mass spectometry (GC-MS) method, it was established that PGF2 alpha, PGE2 and 6-keto-PGF1 alpha concentrations are all significantly elevated in implant site endometrium relative to nonimplant regions on Day 7 postcoitus (p.c.). Although these levels were strikingly lowered in indomethacin-treated females, the administration of dexamethasone altered the balance between the various PGs but did not reduce tissue levels greatly. Determinations of PG levels in uterine venous plasma likewise demonstrated that neither synthesis nor release of PGs had been drastically curtailed by dexamethasone treatment. Endometrial phospholipase activity was determined on Days 6, 7 and 8 of pregnancy. Enzyme activity was elevated on Day 7 relative to the other days and implant site activity was significantly greater than nonimplant region activity on both Days 6 and 7. Treatment with either dexamethasone or indomethacin reduced the Day 7 activity to baseline levels and obliterated the differential between implant and nonimplant regions. The dexamethasone effect appears to be mediated by induction of a transferable inhibitory factor. Thus, while indomethacin and dexamethasone have similar effects on pregnancy when present during the implantation period, their respective mechanisms of action may be different. Even though dexamethasone inhibits endometrial phospholipase activity, this is not attended by inhibition of PG generation.
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15 MeSH Terms