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 influence of solar irradiance and seasons on prostaglandin (PG) and arachidonic acid (AA) content in the marine red alga Gracilaria verrucosa (Huds.) Papenf. (unattached form) was investigated. PGA(2), PGE(2), PGF(2), and 15-keto-PGE(2) were isolated from the alga, quantitatively analyzed as 4-methyl-7-methoxycoumarin esters by high-performance liquid chromatography, and their chemical structures were confirmed by 1H NMR. In June-September, the PG content in the alga was relatively stable (420 microg/g of dry wt. of PGE(2)+PGF(2); 40 microg/g of PGA(2)) and it increased 1.5 times in October. The highest level of PGs was detected in November (2500 microg/g of PGE(2)+PGF(2); 74 microg/g of PGA(2)) when water temperature was fairly low (5-10 degrees C). Algae grown for five months at 50% of incident photosynthetic active radiation (PAR(0)) contained two times less PGE(2) and PGF(2) than algae grown under natural conditions, but the amount of these PG in algae grown at 5% of PAR(0) was close to the normal level. On the contrary, when algae were grown at 5% of PAR(0) the content of PGA(2) increased up to 4 times compared to algae cultivated at 100% PAR(0). In June-November, the amount of AA in total algal lipids slightly varied from 48.9 to 56.7% and did not virtually depend on the light intensity. The probable reasons of the PG content variation in response to environmental factors are discussed.
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PMID:Response of prostaglandin content in the red alga Gracilaria verrucosa to season and solar irradiance. 1173 Aug 70

High concentrations of PGE(2) and PGF(2alpha) were identified by radio-immunoassay (RIA) and/or gas chromatography/mass spectrometry (GC/MS) in the hemolymph, salivary glands and saliva of the lone star tick Amblyomma americanum (L.). Binding studies indicated that PGE(2) was free and not bound to any proteins in the hemolymph. A small amount of 6-keto-PGF(1alpha) (breakdown product of PGI(2); prostacyclin) was also found in the salivary glands but not in the hemolymph or saliva. Neither PGD(2) nor PGA(2)/B(2) was detected in any tick material investigated. Although PGE(2) was found in the gut contents, only small amounts of label crossed the gut into the hemolymph during artificial feeding with labeled PGE(2), indicating that the high amounts of PGE(2) in hemolymph and salivary glands are not sequestered from the host blood meal. Isolated salivary glands and salivary gland homogenates demonstrated robust synthesis of PGE(2) at high concentrations of exogenous arachidonic acid. Synthesis by the salivary glands was monitored by measuring increasing PGE(2) with increasing arachidonic acid by RIA, GC/MS and labeled PGE(2) in the presence of labeled arachidonic acid. Synthesis was inhibited in a dose-dependent manner by indomethacin indicating that the cyclooxygenase synthesizing prostaglandins in ticks shares similarities to the enzyme found in mammals.
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PMID:Identity and synthesis of prostaglandins in the lone star tick, Amblyomma americanum (L.), as assessed by radio-immunoassay and gas chromatography/mass spectrometry. 1180 5

We describe prostaglandin (PG) biosynthesis by microsomal-enriched fractions of fat body prepared from larvae of the tenebrionid beetle, Zophobas atratus. PG biosynthesis was sensitive to incubation time, temperature, pH, substrate and protein concentration. Optimal PG biosynthesis conditions of those we examined included 2 mg of microsomal-enriched protein, incubated at 22 degrees C for 2 min at pH 6. These preparations yielded four major PGs: PGA(2), PGE(2), PGD(2) and PGF(2 alpha). PGA(2) and PGF(2 alpha) were the predominant eicosanoids produced under these conditions. Two non-steroidal anti-inflammatory drugs, indomethacin and naproxen, effectively inhibited PG biosynthesis in low concentrations. In vitro PG biosynthetic reaction conditions, using vertebrate or invertebrate enzyme sources, usually include a cocktail of reaction co-factors. The Z. atratus preparation similarly performs better in the presence of co-factors. Arch.
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PMID:Prostaglandin biosynthesis by fat body from larvae of the beetle Zophobas atratus. 1181 23

We describe prostaglandin (PG) biosynthesis by isolated midgut preparations from tobacco hornworms, Manduca sexta. Microsomal-enriched midgut preparations yielded four PGs, PGA/B(2), PGD(2), PGE(2) and PGF(2alpha), all of which were confirmed by analysis on gas chromatography--mass spectrometry (GC--MS). PGA and PGB are double bond isomers which do not resolve on TLC but do resolve by GC; for convenience, we use the single term PGA(2) for this product. PGA(2) was the major product under most conditions. The midgut preparations were sensitive to reaction conditions, including radioactive substrate, protein concentration (optimal at 1mg/reaction), reaction time (optimal at 0.5 min), temperature (optimal at 22 degrees C), buffer pH (highest at pH 6), and the presence of a co-factor cocktail composed of reduced glutathione, hydroquinine and hemoglobin. In vitro PG biosynthesis was inhibited by two cyclooxygenase inhibitors, indomethacin and naproxen. Subcellular localization of PG biosynthetic activity in midgut preparations, determined by ultracentrifugation, revealed the presence of PG biosynthetic activity in the cytosolic and microsomal fractions, although most activity was found in the cytosolic fractions. This is similar to other invertebrates, and different from mammalian preparations, in which the activity is exclusively associated with the microsomal fractions. Midgut preparations from M. sexta pupae, adult cockroach, Periplaneta americana, and corn ear worms, Helicoverpa zea, also produced the same four major PG products. We infer that insect midguts are competent to biosynthesize PGs, and speculate they exert important, albeit unrevealed, actions in midgut physiology.
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PMID:Prostaglandin biosynthesis by midgut tissue isolated from the tobacco hornworm, Manduca sexta. 1188 78

Many inflammatory mediators retard granulocyte apoptosis. Most natural PGs studied herein (e.g., PGE(2), PGA(2), PGA(1), PGF(2 alpha)) either delayed apoptosis or had no effect, whereas PGD(2) and its metabolite PGJ(2) selectively induced eosinophil, but not neutrophil apoptosis. This novel proapoptotic effect does not appear to be mediated via classical PG receptor ligation or by elevation of intracellular cAMP or Ca(2+). Intriguingly, the sequential metabolites Delta(12)PGJ(2) and 15-deoxy-Delta(12,) Delta(14)-PGJ(2) (15dPGJ(2)) induced caspase-dependent apoptosis in both granulocytes, an effect that did not involve de novo protein synthesis. Despite the fact that Delta(12)PGJ(2) and 15dPGJ(2) are peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activators, apoptosis was not mimicked by synthetic PPAR-gamma and PPAR-alpha ligands or blocked by an irreversible PPAR-gamma antagonist. Furthermore, Delta(12)PGJ(2) and 15dPGJ(2) inhibited LPS-induced I kappa B alpha degradation and subsequent inhibition of neutrophil apoptosis, suggesting that apoptosis is mediated via PPAR-gamma-independent inhibition of NF-kappa B activation. In addition, we show that TNF-alpha-mediated loss of cytoplasmic I kappa B alpha in eosinophils is inhibited by 15dPGJ(2) in a concentration-dependent manner. The selective induction of eosinophil apoptosis by PGD(2) and PGJ(2) may help define novel therapeutic pathways in diseases in which it would be desirable to specifically remove eosinophils but retain neutrophils for antibacterial host defense. The powerful proapoptotic effects of Delta(12)PGJ(2) and 15dPGJ(2) in both granulocyte types suggest that these natural products control the longevity of key inflammatory cells and may be relevant to understanding the control and resolution of inflammation.
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PMID:Prostaglandin D2 and its metabolites induce caspase-dependent granulocyte apoptosis that is mediated via inhibition of I kappa B alpha degradation using a peroxisome proliferator-activated receptor-gamma-independent mechanism. 1205 37

Heme oxygenase-1 (HO-1) is induced as a beneficial and adaptive response in cells and tissues exposed to oxidative stress. Herein we examined how various eicosanoids affect the induction of HO-1, and the possible mechanism underlying 15-deoxy-Delta(12,14)- prostaglandin J(2) (15d-PGJ(2))-induced HO-1 expression. PGH(2), PGD(2) and its metabolites of the PGJ(2) series, and PGA(1) markedly induced the protein expression of HO-1. Arachidonic acid (AA), docosahexaenoic acid (DHA), PGE(2), PGF(2 alpha), and thromboxane B(2) (TXB(2)) were shown to have no effect on the induction of HO-1. 15d-PGJ(2) was the most potent activator achieving significance at 5 microM. Although 15d-PGJ(2) significantly activated the MAPKs of JNK and ERK, the activation of JNK and ERK did not contribute to the induction of HO-1 as determined using transfection of dominant-negative plasmids and MAPKs inhibitors. Additional experiment indicated that 15d-PGJ(2) induced HO-1 expression through peroxisome proliferator-activated receptor (PPAR)-independent pathway. 15d-PGJ(2) significantly decreased the intracellular level of reduced glutathione; and the thiol antioxidant, N-acetyl-L-cysteine (NAC), and the thiol-reducing agent, dithiothreitol (DTT), inhibited the induction of HO-1 by 15d-PGJ(2). Finally, NAC and DTT exhibited significant inhibition of HO-1 mRNA and HO-1 promoter reporter activity induced by 15d-PGJ(2). These results suggest that thiol antioxidant and reducing agents attenuate the expression of HO-1 induced by 15d-PGJ(2), and that the cellular thiol-disulfide redox status may be linked to HO-1 activation.
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PMID:Thiol antioxidant and thiol-reducing agents attenuate 15-deoxy-delta 12,14-prostaglandin J2-induced heme oxygenase-1 expression. 1499 22

Efficient RIA procedures are required for determination of prostaglandins (PGF(2alpha), PGE(2), PGI(2) and their metabolites) in bovine blood plasma to elucidate their significance in reproductive endocrinology. A new rapid efficient prepurification was developed using commercial octadecyl silicagel cartridges. Prepurification is especially necessary for the determination of 13,14-dihydro-15-keto-PGE(2) (PGEM). After prepurification, PGEM was first converted into the more stable 13,14-dihydro-15-keto-PGA(2) (PGAM) and measured in a RIA-system for PGAM. For PGF(2alpha), 13,14-dihydro-15-keto-PGF(2alpha) (PGFM), PGE(2) and 6-keto-PGF(1alpha) direct tests using 50 mul plasma per tube were elaborated. The validity of the tests was monitored by high performance liquid chromatography radioimmunoassay (HPLC RIA ). Infusion studies using PGF(2alpha) and PGE(2) showed that about 10% of these hormones remained unmetabolized after the first passage through the lungs. The biological half life of the metabolites PGFM and PGEM in bovines was estimated to be 4 min. Thus, PGFM and PGEM measurements in the peripheral circulation reflect even short-term secretory changes of PGF(2alpha) and PGE(2). During the infusion of PGF(2alpha) the levels of progesterone decreased but were not affected by PGE(2). Both prostaglandins caused increased oxytocin secretion. In the cow peripartum first PGEM elevations were measured 5 to 8 d ante partum, whereas PGFM increased 1 to 2 d ante partum. Then both prostaglandins increased simultaneously until parturition. In the postpartal phase PGFM was higher than PGEM, and both prostaglandins remained elevated for several days. Prostacyclin levels remained unchanged during the peripartal period.
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PMID:Improvement of radioimmunoassays for prostaglandins in bovine blood plasma and their application to monitor reproductive functions. 1672 87

Mass spectral measurements by electrospray ionization mass spectrometry (ESI-MS) detected the ions of beta-cyclodextrin (betaCD) or branched betaCDs (glucosyl-, galactosyl-, mannosyl- and maltosyl-betaCD)-prostaglandins (PGs: PGA(2), PGD(2), PGE(1), PGE(2), PGF(2alpha) and PGJ(2)) complexes, i.e., betaCD-PG complexes, with a host:guest ratio of 1:1 in the negative ion mode. This is the first study to report the ions of branched betaCD-PG complexes using ESI-MS. The inclusion complexes were determined by a flow injection analysis using acetonitrile/water. We could confirm by this method the presence of a betaCD-PGE(2) complex with a host:guest ratio of 1:1 in a solution-dissolved pharmaceutical formulation consisting of betaCD-PGE(2) (Prostarmon E tablet).
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PMID:Determination of branched beta-cyclodextrin-prostaglandin complexes using electrospray ionization mass spectrometry. 1868 84

Isoprostanes are endogenously formed end products of lipid peroxidation. Furthermore, they are markers of oxidative stress and independent risk markers of coronary heart disease. In patients experiencing coronary heart disease, impaired angiogenesis may exacerbate insufficient blood supply of ischemic myocardium. We therefore hypothesized that isoprostanes may exert detrimental cardiovascular effects by inhibiting angiogenesis. We studied the effect of isoprostanes on vascular endothelial growth factor (VEGF)-induced migration and tube formation of human endothelial cells (ECs), and cardiac angiogenesis in vitro as well as on VEGF-induced angiogenesis in the chorioallantoic membrane assay in vivo. The isoprostanes 8-iso-PGF(2alpha), 8-iso-PGE(2), and 8-iso-PGA(2) inhibited VEGF-induced migration, tube formation of ECs, and cardiac angiogenesis in vitro, as well as VEGF-induced angiogenesis in vivo via activation of the thromboxane A(2) receptor (TBXA2R): the specific TBXA2R antagonists SQ-29548, BM 567, and ICI 192,605 but not the thromboxane A(2) synthase inhibitor ozagrel blocked the effect of isoprostanes. The isoprostane 8-iso-PGA(2) degraded into 2 biologically active derivatives in vitro, which also inhibited EC tube formation via the TBXA2R. Moreover, short hairpin RNA-mediated knockdown of the TBXA2R antagonized isoprostane-induced effects. In addition, Rho kinase inhibitor Y-27632 reversed the inhibitory effect of isoprostanes and the thromboxane A(2) mimetic U-46619 on EC migration and tube formation. Finally, the various isoprostanes exerted a synergistic inhibitory effect on EC tube formation. We demonstrate for the first time that isoprostanes inhibit angiogenesis via activation of the TBXA2R. By this mechanism, isoprostanes may contribute directly to exacerbation of coronary heart disease and to capillary rarefaction in disease states of increased oxidative stress.
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PMID:Isoprostanes inhibit vascular endothelial growth factor-induced endothelial cell migration, tube formation, and cardiac vessel sprouting in vitro, as well as angiogenesis in vivo via activation of the thromboxane A(2) receptor: a potential link between oxidative stress and impaired angiogenesis. 1894 27

Cyclooxygenase (COX) and lipoxygenase (LOX) can catalyze the oxidation of C20 fatty acids to produce certain eicosanoids, which play roles in mediating immune responses in insects. Despite their critical role in insect immunity, there have been few studies of the unique effects of different eicosanoids on immune responses. This study analyzed cellular and humoral immune responses of the beet armyworm, Spodoptera exigua, using seven eicosanoids selected from two major eicosanoid subgroups: prostaglandin (PG) and leukotriene (LT), derived from catalytic activities of COX and LOX respectively. Upon bacterial challenge, all seven eicosanoids (PGA(1), PGB(2), PGD(2), PGE(1), PGE(2), PGF(1alpha), and LTB(4)) significantly induced hemocyte nodulation and phagocytosis in the presence of dexamethasone, an eicosanoid biosynthesis inhibitor. However, only PGs induced cell lysis of oenocytoids to release prophenoloxidase, which resulted in an increase in phenoloxidase activity. These seven eicosanoids also induced expression of humoral immune-associated genes, including prophenoloxidase, serpin, dopa decarboxylase, cecropin, and lysozyme, in which PGB(2) and PGE(1) did not induce gene expression of prophenoloxidase. To understand the interactions between different eicosanoids, mixture effects of these eicosanoids were compared with their individual eicosanoid effects on mediating nodule formation in response to bacterial challenge. All six single PGs showed increases in nodule formation in a dose-dependent manner without significant difference among the different types. LTB(4) was more potent than the tested PGs in mediating the cellular immune response. At low doses, all combinations of two eicosanoids showed significant additive effects on nodule formation. These results indicate that immune target cells, such as hemocyte and fat body, of S. exigua can respond to different COX and LOX products to express cellular and humoral immune responses, and their overlapping, additive effects on nodulation suggest that in target cells, these eicosanoids share a hypothetical common eicosanoid signal pathway.
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PMID:Various eicosanoids modulate the cellular and humoral immune responses of the beet armyworm, Spodoptera exigua. 1973 70


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