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)

The relationship between prostaglandins (PG) and interferon (IFN) was investigated. IFN induced the synthesis of immunoreactive PGE and PGA at early and late stages, respectively, of vaccinia virus infection in mouse L fibroblasts. Only species-specific IFN possessed this activity and PG synthesis was stimulated in virus-infected cells, while normal L cells were not affected. The vaccinia virus infection did not significantly alter PG synthesis in the absence of IFN. Indomethacin increased the rate of vaccinia virus replication and partially inhibited the IFN-induced protection of L cells. The addition of exogenous PGA1 only partially reversed this effect. Finally, short-term PGA treatment induced the synthesis of two enzymes (protein kinase and 2,5A synthetase) thought to be partially responsible for the antiviral action of interferon. These findings suggest that a prostaglandin or PG-related compound seems to mediate at least one aspect of IFN action.
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PMID:The relationship between the antiviral action of interferon and prostaglandins in virus-infected murine cells. 619 67

The inhibitory effect of various prostaglandin analogues on the anchorage independent growth of murine and human melanoma cells was measured. PGA analogues (which were modified at C-16 and C-18) did not demonstrate any major improvement in activity over PGA alone. These included 16,16-dimethyl PGA1, 16,16-dimethyl-PGA2, 16,16-dimethyl-18-oxa-PGA2 and trans-delta-2-15-alpha acetoxy-16,16-dimethyl-18-oxa-11-deoxy-PGE1-methylester. The thromboxane synthetase inhibitor, U51605, demonstrated weak anti-proliferative activity. PGD2 (with a ketone at C-11 versus C-9 for PGA and PGE) was the most potent prostaglandin tested. Cells from melanoma lines displayed species differences in their sensitivities. PGA1 and PGE1 were the most potent inhibitors of the anchorage independent growth of murine melanoma cells. On human melanoma cells PGD2 was the most active prostaglandin, 2-3 times more potent than PGA1; PGE1 was a very weak inhibitor.
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PMID:In vitro modulation of human and murine melanoma growth by prostanoid analogues. 658 9

Following close intra-arterial administration to the carotid and femoral arterial beds of the anaesthetised dog the rank order of potency for producing vasodilation was PGE greater than 11-deoxy PGE0 greater than PGA greater than PGI2 greater than PGB with the 1- and 2-series prostaglandins equipotent. PGI2 was about 60 times weaker than PGE1. In the mesenteric arterial bed the rank order of potency for producing vasodilation was the same except PGI2 was about equipotent with PGE1. The absolute potency of the prostaglandins, with the exception of PGI, was similar on all three vascular beds. A similar differential action of PGI2 relative to PGE1 was also observed following both left intraventricular and intravenous administration. We suggest that all three arterial beds contain PGE-receptors mediating vasodilatation at which the E-series prostaglandins are potent and PGI2 is weak. In addition the mesenteric bed contains PGI2-receptors which are absent or sparse in the carotid and femoral beds.
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PMID:Comparison of the potencies of some prostaglandins as vasodilators in three vascular beds of the anaesthetised dog. 674 31

Human lung explants maintained in culture for 7 d incorporate [(3)H]glucosamine into mucous glycoproteins. Ethanol-precipitable, glucosamine-labeled mucous secretion was measured, and the effects of different pharmacologic agents upon this secretion were investigated. Anaphylaxed human lung generates prostaglandin (PG) synthesis and increased mucous release. Arachidonic acid (AA), PGA(2), PGD(2), and PGF(2alpha) significantly increased mucous glycoprotein release, whereas PGE(2) significantly reduced release. Evidence which suggests that lipoxygenase products of AA augment mucous release includes the following: (a) Nonsteroidal anti-inflammatory drugs (NSAID: acetylsalicylic acid and indomethacin) increase mucous release while preventing prostaglandin formation. (b) The increase in mucous release induced by AA or NSAID is additive once the agents are combined. (c) Several nonspecific lipoxygenase inhibitors (eicosa-5,8,11,14-tetraynoic acid; vitamin E; nordihydroguaiaretic acid; and alpha-naphthol) inhibit mucous release. Three additional lines of evidence directly indicate that monohydroxyeicosatetraenoic acid (HETE) causes increased mucous release: (a) the addition of a mixture of synthetic HETE (24-600 nM) increases mucous release; (b) pure 12-HETE (1-100 nM) also increases mucous release; (c) mucous release is increased synergistically by the combination of HETE and NSIAD. These data taken together demonstrate that HETE are capable of increasing mucous release and that conditions which may influence HETE production alter mucous release. Thus, although not directly demonstrating HETE production by human airways, the data strongly suggest that lipoxygenase products of AA in airways may profoundly influence mucous release; and it seems possible that lipoxygenase inhibitors may have a role in treating bronchorrhea.
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PMID:Effects of arachidonic acid, monohydroxyeicosatetraenoic acid and prostaglandins on the release of mucous glycoproteins from human airways in vitro. 678 82

Effects of the administration of PGs A-1, E-2 and F-2 alpha (150 micrograms/rat b.i.d. for 10 days) were studied. Significant increase in testicular weight was observed only in PGE-2 treated group. Testicular ascorbic acid content reduced significantly by treatment with all the PGs. PGE-2 treatment caused a significant decrease in the content of testicular cholesterol, while no change was observed in the same and prostatic acid phosphatase activity in any of the PG treated groups. Blood plasma levels of testosterone drastically reduced by both PGE-2 and PGF-2 alpha, while there was no change in the levels of plasma LH in any of the groups. Plasma FSH levels increased significantly in PGA-1 treated rats only. The results suggest that 1) There is a direct action of PG particularly PGE-2 on testicular weight. PGE-2 increases testicular weight possibly by preventing degeneration of spermatids, 2) PGE-2 acting directly on the testis, reduces testicular ascorbic acid content, stimulates the conversion of cholesterol to pregnenolone but depresses the conversion of the latter to testosterone.
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PMID:Effect of prostaglandins A-1, E-2 and F-2 alpha on blood plasma levels of testosterone, LH and FSH in male rats. 678 15

1. The effect of i.v. administration of prostaglandin (PG) E(2) (10-40 mug kg(-1) h(-1)), 16,16-dimethyl PGE(2) (0.1-0.5 mug kg(-1) h(-1)), PGE(1) (16-20 mug kg(-1) h(-1)), PGA(1) (5-11 mug kg(-1) h(-1)) and PGF(2alpha) (40 mug kg(-1) h(-1)) on the relationship between [H(+)] and flow of gastric juice during stimulation of gastric secretion by pentagastrin was investigated in conscious cats prepared with cannulated gastric fistulae.2. A- and E-type prostaglandins significantly reduced pentagastrin-stimulated acid output. This inhibition was associated with a reduction of the [H(+)] of the gastric juice such that the [H(+)] observed at any flow rate tended to be lower than the normal range observed with pentagastrin alone. With the highest doses of these prostaglandins the mean [H(+)] values were well below the normal range with pentagastrin alone.3. At the dose tested, PGF(2alpha) had little effect on acid output, and did not alter the relationship between [H(+)] and gastric flow.4. There is a linear relationship between acid output and gastric flow and this relationship is similar during stimulation of gastric secretion by pentagastrin, histamine or insulin. Gastric acid inhibitory doses of cimetidine, atropine and somatostatin did not alter this relationship. In contrast the A- and E-type prostaglandins displaced this relationship to the right of the normal line observed with the acid stimulants alone. A- and E-type prostaglandins reduced the slope of the line relating acid output and gastric flow from approximately 150-170 muequiv/ml(-1) to approximately 100-120 muequiv ml(-1), this being taken as evidence of dilution of the parietal H(+) secretion with a non-parietal secretion.5. The volume of non-parietal gastric secretion was calculated as the gastric flow at zero acid output by extrapolation of linear plots of acid output versus gastric flow. Unstimulated gastric flow measured directly was 0.75 ml 15 min(-1). The calculated non-parietal flow was in the range 0.52-0.90 ml 15 min(-1) during stimulation of gastric secretion with pentagastrin, histamine and insulin, and inhibition of pentagastrin-stimulated acid secretion with cimetidine, atropine and somatostatin. PGE(2) (1.51 ml 15 min(-1)) and 16,16-dimethyl PGE(2) (1.20 ml 15 min(-1)) nearly doubled the calculated non-parietal flow.6. These data demonstrate that gastric acid inhibitory doses of A- and E-type prostaglandins can reduce the [H(+)] in the bulk fluid of the gastric lumen during stimulation of acid secretion. The data provide evidence that these prostaglandins stimulate a non-parietal component of gastric secretion. This might be gastric bicarbonate and mucus secretion.
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PMID:Prostaglandins alter the relationship between gastric hydrogen ion concentration and flow: evidence for stimulation of non-parietal secretion in the cat. 694 8

Urinary immunoreactive PGA and PGE, plasma and urinary aldosterone, and plasma renin activity (PRA) were determined in eleven control subjects and four patients with diabetic hyporeninaemic hypoaldosteronism (HH) before and during 4 days of sodium chloride restriction and frusemide administration. Aldosterone and PRA increased steadily in control subjects, but not in patients with HH. Increases in urinary PGA and PGE were observed during volume depletion. The basal levels and increases observed were comparable in both groups. The apparently normal stimulation of PGA and PGE in subjects with diabetic HH suggests that this syndrome is not associated with abnormal prostaglandin metabolism, despite the fact that drug-induced abnormalities of the latter may precipitate or aggravate the clinical syndrome in susceptible individuals. The increase in PGA and PGE following frusemide treatment and salt depletion supports the possibility of a relationship between renal prostaglandin metabolism, frusemide-induced natriuresis and/or renin secretion. While the nature of this relationship remains obscure, the increases in PGA and PGE in the absence of increases in renin-angiotensin levels in subjects with HH suggests that these changes are not due to activation of the renin-angiotensin system.
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PMID:Urinary prostaglandins following frusemide treatment and salt depletion in normal subjects and subjects with diabetic hyporeninaemic hypoaldosteronism. 701 40

Three cows and 2 sheep were passively immunized against prostaglandin (PG) F on Day 16 and Days 13-15 of the oestrous cycle respectively. The PGF antiplasma was raised in ovariectomized ewes against a PGF-2 alpha-bovine serum albumin complex and showed 100%, 12.5%, 0.3%, less than 0.05% and less than 0.01% cross-reactivity with PGF-2 alpha, PGE-2, PGA-2, PGB-2 and arachidonic acid, respectively. Control animals were given an equivalent amount of ovariectomized ewe plasma. In all passively immunized animals there was evidence of a persistent corpus luteum as indicated by plasma progesterone concentration and the failure of the animals to return to oestrus until at least 29 days after treatment. These data are consistent with previous proposals that PGF-2 alpha is the uterine luteolytic factor in sheep and cattle.
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PMID:Prolongation of the oestrous cycle in cows and ewes after passive immunization with PGF antibodies. 719 12

Suspensions of aggregated chondrocytes display active prostaglandin (PG) production. Radioimmunoassay of culture media and thin layer chromatographic analysis suggests that PGE2 is the primary PG synthesized. In order of decreasing concentration, the following PG were tentatively identified; PGE greater than PGI greater than PGA + PGB greater than or equal to PGF1+2 greater than TxB. An inverse logarithmic relationship was identified between PG synthesis and cells cultured at densities of 1.5 to 7.5 x 10(6) cells/ml. Little or no change in the PG distribution profile was seen at these high cell densities. Maximum PG synthesis was attained after 36 hours of incubation with persistence of high synthetic levels up to 48 hours. PGE2 production measured at various post-isolation intervals indicated an initial high rate of synthesis during the first 4 hours which decreased with time up to 24 hours. Cartilage explant organ cultures demonstrated a similar level of PG synthesis suggesting minimal effect of matrix on cellular PG production. Indomethacin (5 microgram/ml) inhibited PG synthesis by 70% within 4 hours and 85% after 24 hours of exposure. Arachidonic acid supplementation (10 microM) stimulated PG synthesis by 300%.
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PMID:The prostaglandins of articular cartilage. I. Correlates of prostaglandin activity in a chondrocyte culture system. 720 51

1 The sensitivity and contractility of isolated canine intrapulmonary arteries and veins to a variety of primary prostaglandin compounds was studied.2 Intrapulmonary arteries produced no measurable contractile responses to prostaglandin A(1) (PGA(1)), PGA(2), PGB(1), PGD(2), PGE(1), PGE(2) or to PGF(1alpha). However, high concentrations of both PGB(2) (> 10(-7) M) and PGF(2alpha) (> 10(-6) M) elicited concentrated-related, but weak, contractile responses, measuring only 5-25% of KCl-induced maximum contractions.3 Intrapulmonary arteries, partially contracted by 5-hydroxytryptamine (5-HT), exhibited concentration-related relaxations in response to PGE(1); PGE(2), PGA(1) or PGA(2) produced only weak superimposed contractions.4 In contrast to intrapulmonary arteries, intrapulmonary veins contracted in a concentration-related fashion to all prostaglandins tested, where the contractile sensitivity was (based on EC(50) s and threshold concentrations): PGB(2) > PGB(1) > PGD(2) > PGF(2alpha) > PGA(2) >> PGA(1) > PGF(1alpha) > PGE(2) > PGE(1).5 In terms of the ability to generate maximum contractile responses on intrapulmonary veins, the prostaglandins were also variable, with PGA(2) and PGB(2) being the most potent and PGD(2) the least potent.6 Intrapulmonary veins, partially contracted by 5-HT, exhibited concentration-related relaxations to PGE(1) at low concentrations, followed by secondary contractile responses at higher concentrations.7 Neither PGA(1) nor PGA(2) (3.4 x 10(-8) to 3.4 x 10(-5) M) inhibited or potentiated 5-HT responses of intrapulmonary arteries.8 These data suggest that there are species, regional and major qualitative and quantitative, differences in the responsiveness of intrapulmonary arteries and veins to prostaglandin.
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PMID:Differential effects of prostaglandins on canine intrapulmonary arteries and veins. 727 85


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