Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of inhibitors of prostaglandin synthetase to chicken embryos produced myopathies in their skeletal muscles which were characterized by ringbinden, loss of Z-discs, M-bands, and thick and thin filaments and decreased myoblast proliferation and type 2 myotube formation. The effect of administration of prostaglandins on myoblast proliferation was also examined and PGE was found to suppress proliferation. There was also a tendency for PGF2 alpha to suppress and PGI2 to stimulate proliferation, although neither of these effects were statistically significant. PGA, PGB and PGD did not affect myoblast proliferation.
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PMID:Characterization of a myopathy caused by prostaglandin dysfunction. 297 78

The profile of urinary metabolites of 3H-arbaprostil was characterized in the male dog after intravenous administration. The major metabolites were purified and their structures deduced by gas chromatography/mass spectrometry (GC/MS) studies after conversion to the methyl ester-methoxime-trimethylsilyl ether derivatives, aided by GC with simultaneous radioactivity monitoring. The identified metabolites accounted for 96% of the urinary excretion products. beta-Oxidation of the carboxy side-chain of arbaprostil to 15-methyl-2,3,4,5-tetranor PGE1, via the 15-methyl-2,3-dinor PGE2 intermediate, appeared to be the most significant metabolic pathway. In contrast to the rat, the following were observed in the dog: glucuronic acid conjugation of the 15-methyl-2,3,4,5-tetranor PGE, and PGA metabolites; detection of the 15-methyl-2,3-dinor PGE2 intermediate; absence of 19-hydroxyl-15-methyl-2,3,4,5-tetranor PGA, and PGB metabolites; oxidation at C-20; and excretion of some parent drug.
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PMID:Isolation and characterization of the urinary metabolites of arbaprostil in the male dog after intravenous administration. 320 90

Effects of prostaglandins on the incorporation of [4,5-(3)H]leucine into growth hormone and its subsequent release into the incubation medium were studied. Incubation of rat anterior pituitary glands with 10(-6) M prostaglandin PGE(1) in tissue culture medium 199 for 7 hr caused a 40-300% increase in the release of labeled growth hormone into the incubation medium. PGE(1) at 10(-8) M increased growth hormone synthesis but not release. At 10(-6) M, PGE(2) had effects similar to PGE(1); PGA(1) increased growth hormone synthesis but not release. PGF(2alpha) was without effect on either synthesis or release of growth hormone.Prolactin synthesis and release were not affected by prostaglandins. All of the prostaglandins, at 10(-4) M, increased adenyl cyclase activity in the pituitary gland but phosphodiesterase activity was unaltered. Dibutyryl cyclic AMP, with or without caffeine, caused an up to 300% increase in labeled growth hormone release. No consistent effect of prolactin was observed. If potassium concentration was increased 10-fold, a 215% increase in growth hormone release was observed. A combination of hypertonic potassium and 10(-6) M PGE(1) increased growth hormone release 325%, suggesting that potassium and prostaglandins act by independent mechanisms. Addition of theophylline to pituitary gland, incubated in vitro, increased both the synthesis and release of growth hormone. Although fluoride greatly stimulated growth hormone release, it completely inhibited the incorporation of leucine into the hormone. Similarly, puromycin inhibited synthesis of growth hormone but did not block release induced by prostaglandin, dibutyryl cyclic AMP, theophylline, or fluoride. Prostaglandins increase pituitary adenyl cyclase activity and, presumably via cyclic AMP, increase growth hormone release, independently of protein synthesis.
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PMID:Release of pituitary growth hormone by prostaglandins and dibutyryl adenosine cyclic 3':5'-monophosphate in the absence of protein synthesis. 432 Sep 73

1. Prostaglandins were injected into the third ventricle of unanaesthetized cats and rabbits whilst rectal temperature was recorded.2. In cats prostaglandin E(1) and E(2) (PGE(1) and PGE(2)) produced hyperthermia which mostly began within a minute of injection and lasted 1 or more hours. With PGE(1) the hyperthermia was shown to be dose dependent between 10 ng and 10 mug (2.8 x 10(-11) and 2.8 x 10(-8)M). The hyperthermia was associated with vigorous shivering, skin vasoconstriction and piloerection. In several experiments a secondary rise in temperature occurred a few hours after the injection but such an effect was sometimes observed with control injections of 0.9% NaCl solution as well.3. None of the other prostaglandins (A(1), F(1alpha), F(2alpha)) examined in cats had an immediate or strong effect on temperature comparable to the hyperthermia produced by PGE(1) and PGE(2).4. In rabbits PGE(1) (2 mug) also caused hyperthermia which began shortly after the injection and lasted for hours. PGF(2alpha) and PGA(1), did not affect temperature.5. In cats it was seen that an intraperitoneal injection of 4-acetamidophenol (paracetamol 50 mg/kg) did not affect the initial strong hyperthermia produced by PGE(1) and PGE(2) but abolished the secondary rise.6. The possibility is discussed that PGE(1) plays a role as a central transmitter or modulator in temperature regulation.
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PMID:Effects on body temperature of prostaglandins of the A, E and F series on injection into the third ventricle of unanaesthetized cats and rabbits. 433 Sep 29

Incubation of L-929 and L-2071 fibroblasts with prostaglandin E(1) (PGE(1)) caused a rapid increase in the cyclic AMP content of these cells. A maximal effect was produced with 0.2 mug PGE(1) per ml. At a concentration of 4 mug/ml, PGE(2) was almost equally effective, but PGF(2alpha) and PGA(2) were much less so. 2.6 muM epinephrine, 0.4 mM serotonin, and 0.2% ethanol were without effect. In L-929 cells, cyclic AMP concentrations remained elevated for 2-5 hr, and then declined, although even after a 24-hr incubation the medium contained PGE(1) in a concentration sufficient to increase maximally the cyclic AMP content of cells not previously exposed to this compound. A second addition of PGE(1) after 5 or 24 hr did not produce another increase in the concentration of cyclic AMP. After incubation with PGE(1) for 24 hr, cyclic AMP phosphodiesterase activity, assayed with 0.56 muM substrate, was increased 30-100%; the activity rose further between 24 and 48 hr. It is suggested that the increase in phosphodiesterase activity that appears to be a consequence of prolonged elevation of cyclic AMP concentration may account at least in part for the apparent "refractoriness" to PGE(1) that develops after incubation for several hours with this compound.
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PMID:Prostaglandin E 1 effects on adenosine 3':5'-cyclic monophosphate concentration and phosphodiesterase activity in fibroblasts (mouse L cells-tissue culture-enzyme kinetics-prostaglandin homologues). 433 44

Prostaglandins E(1) and E(2) significantly stimulated the synthesis of aldosterone, corticosterone, and to a lesser degree, cortisol in the outer slices of beef adrenal tissue. PGA, PGF(1a), and PGF(2a) were ineffective.PGE(1) was found to stimulate steroidogenesis in a manner similar to that of adrenocorticotropin (ACTH) in (a) needing calcium, (b) being inhibited by puromycin but not actinomycin D, (c) increasing the levels of cyclic AMP, and (d) not having an additive effect to exogenous cyclic AMP. PGE(1) did not produce an additive effect with either submaximal or maximal amounts of ACTH but did have an additive effect with angiotensin. These results are in keeping with the hypothesis that PGE(1) shares a receptor site on the plasma membrane with ACTH.
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PMID:Adrenocortical steroidogenesis: the effects of prostaglandins. 434 27

1. The relationship between the vasodilator and inhibitory effects of prostaglandin E(1) (PGE(1)), E(2) and A(2) on responses to nerve stimulation, noradrenaline and angiotensin was evaluated in the dog hindlimb preparation.2. PGE(1) and PGE(2) were equipotent as vasodilators in the hindlimb; however, PGE(1) was much more potent as an inhibitor of vasoconstrictor responses to nerve stimulation, noradrenaline and angiotensin.3. PGA(2) and PGE(2) were approximately equal as inhibitors of vasoconstrictor responses to noradrenaline, nerve stimulation and angiotensin; however, PGE(2) was far more potent as a vasodilator.4. Since there is no relationship between the vasodilator and inhibitory effects of PGE(1), E(2) and A(2), and since the inhibitory effect of PGA(2) was present at a time when hindlimb perfusion pressure had returned to control value, it is concluded that the inhibitory action is probably not the result of a physiological antagonism.5. Since each prostaglandin inhibited responses to nerve stimulation and noradrenaline to approximately the same extent and responses to angiotensin were also inhibited, it is suggested that these agents antagonize vasoconstrictor responses by a nonspecific depressant effect on smooth muscle cells.
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PMID:Effect of prostaglandins E 1 , E 2 and A 2 on vascular resistance and responses to noradrenaline, nerve stimulation and angiotensin in the dog hindlimb. 434 79

The prostaglandin (PG) content of mitogen- and antigen-stimulated leukocyte cultures was examined by a radioimmunoassay procedure empolying an antiserum reactive with PGB(1) and PGB(2), the alkaline dehydration products of PGE and PGA. At 48 h, mitogen-activated mouse spleen cell cultures showed 2-10-fold increases in the PGE, but not in the PGA, component of immunoreactive PG (iPG) fractionated by silicic acid column chromatography. Increases in iPG were detectable by h 16 in spleen cell cultures incubated with staphylococcal enterotoxin B. Since iPG levels rose only in the culture supernates and not in cells exposed to mitogens for 48 h, increases reflected extracellular release of PG. The validity of the radioimmunoassay determinations of PGE in spleen cell cultures was supported by the results of concomitant assessment of the PGE(2) content of basal and enterotoxin-stimulated cultures by gas chromatography/mass spectrometry. By the latter method, the PGE(2) content was three-fold higher in enterotoxin-activated, compared to basal, cultures at 48 h. Aspirin effectively suppressed increases in both iPG and PGE(2). In spleen cell cultures prepared from mice previously inoculated with an attenuated strain of yellow fever virus in vivo and then incubated with this virus in vitro, iPG levels increased twofold over basal at 48 h. By contrast, iPG content of spleen cell cultures prepared from saline-inoculated mice was not appreciably altered by exposure to the virus in vitro. The enhancement of iPG release from cultured spleen cells by mitogens did not correlate with an ability of these agents to increase cellular cyclic AMP (cAMP) levels. Moreover, epinephrine and cholera toxin markedly increased spleen cell cAMP content but had no demonstrable effect on basal iPG levels, suggesting iPG release from these cells was not mediated by cAMP. Incubation with mitogens also enhanced the iPG content of 72-cultures of human peripheral leukocytes and of human lymphocytes isolated by nylon chromatography. However, the iPG of cultures of human lymphocytes purified by glass bead chromatography and of mouse thymocytes was not appreciably altered when these cells were cultured with mitogens, even though DNA synthesis in both instances was markedly increased. Accordingly, iPG release was not an invariable concomitant of increased DNA synthesis in lymphoid cell cultures. In summary, the results demonstrate that mitogen and antigen stimulation of leukocytes in culture may be accompanied by enhanced release of PGE. The mechanisms mediating this phenomenon and its biologic significance remain to be delineated, but participation of PGE in immunologically induced inflammatory responses seems possible.
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PMID:Release of prostaglandin by mitogen- and antigen-stimulated leukocytes in culture. 436 90

The effects of agents that elevate intracellular cyclic adenosine 3',5'-monophosphate (cAMP) have been studied with respect to phagocytosis by guinea pig polymorphonuclear leukocytes. The investigation depends upon the use of a precise method for following ingestion. Theophylline, dibutyryl cAMP, and prostaglandins inhibited the phagocytosis of starch particles. The inhibitions caused by prostaglandins E(1), E(2), and F(2alpha) (PGE(1), PGE(2), and PGF(2alpha)) were synergistic with that due to theophylline. Inhibition by PGA(1) and PGA(2) was not. At equal concentrations the order of increasing inhibition of phagocytosis (assayed at 10 min) by the prostaglandins was PGE(1) < PGF(2alpha) < PGE(2) < PGA(1) = PGA(2). Our results are consistent with the hypothesis that increased intracellular levels of cAMP impair the phagocyte's ability to ingest particles. The mechanism of the inhibition has not been defined. The increment in oxidation of [1-(14)C]glucose to (14)CO(2) that normally accompanies phagocytosis was found to be depressed in the presence of PGE(1) or theophylline, together or individually as expected from the inhibition of phagocytosis. Paradoxically, oxygen consumption although depressed by theophylline or PGE(1) plus theophylline, was stimulated by PGE(1) alone.
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PMID:The depression of phagocytosis by exogenous cyclic nucleotides, prostaglandins, and theophylline. 437 83

By use of two novel techniques for detecting extremely small amounts of PGs, studies were conducted elucidating the mechanism of urate crystal-induced inflammation. Rats deficient in EFA and thus deficient in PGs received injections of monosodium urate crystals into the footpad. The EFA-deficient animals developed less swelling than did normal animals. However, when a 1-ng dose of PGE-1, PGE-2, PGA-2, or PGF-2-alpha was added along with the urate injection the swelling was enhanced to approximately normal levels. In the second technique the swelling induced by injection of two different urate crystals was compared. Urate crystals heated to 200 degrees C produced less swelling in normal rats than did similar urate crystals heated only to 50 degrees C. However when a 1-ng dose of PGE-1, PGE-2 or PGF-2-alpha was added to the heated urate crystals injection the swelling increased to approximately the swelling in normal controls receiving urate heated to 50 degrees C. Comments are presented suggesting that urate crystal inflammation may be a membrane disease.
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PMID:Effect of prostaglandins in urate crystal inflammation. 445 26


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