Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The role of cyclo-oxygenase (COX) in the regulation of anion secretion (measured as short- circuit current, Isc) in cultured epididymal epithelia from immature rats was investigated. 2. COX inhibitors attenuated the increase of anion secretion caused by bradykinin (LBK) but had no effect on that caused by PGE2, suggesting that prostaglandin synthesis mediates the secretory response of the tissues to LBK. 3. The apparent IC50 values for indomethacin, piroxicam and L-745,337 in inhibiting the LBK-induced Isc were 0.14, 1.34 and 15.7 microM, respectively. This order of potency: indomethacin > piroxicam > L-745,337 >> DFU suggests the involvement of the COX-1 isozyme in the mediation of the secretory response to LBK. 4. Among the COX products (prostaglandins, thromboxane and prostacyclins) tested, only PGE2 and, to a much lesser extent, PGF2alpha stimulated anion secretion by cultured rat epididymal epithelia. 5. The effect of PGE2 was mimicked by 11-deoxyl PGE1, a specific prostaglandin E (EP)2/4 receptor agonist, but not by sulprostone, a specific EP1/3 receptor agonist, indicating that cyclic AMP-coupled EP2/4 receptors are involved in the LBK-stimulated anion secretion. 6. A reverse transcriptase-polymerase chain reaction study detected the expression of COX-1 and COX-2 mRNA in intact rat epididymis and in cultured epididymal epithelia. The expression of COX-1 mRNA was reduced by LBK by 44 %. 7. Immunohistochemical studies demonstrated the presence of COX-1 immunoreactivity in the basal cells of the intact rat epididymis. By comparison, COX-2 immunoreactivity was detected in the apical pole of the principal cells. 8. The role of COX in the formation of the epididymal microenvironment and the implication of long term administration of non-steroidal anti-inflammatory drugs (NSAIDs) on male fertility are discussed.
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PMID:Regulation of anion secretion by cyclo-oxygenase and prostanoids in cultured epididymal epithelia from the rat. 988 52

In vitro, prostaglandins (PG) have strong inhibitory effects on T cell activation and proliferation and inhibitors of PG synthesis (NSAID) increase proliferation and activation of T cells. Although most studies have failed to demonstrate cyclooxygenase (COX) activity in lymphocytes, there is contradictory evidence on the synthesis of different PG. We have studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot the expression of COX-1 and -2 mRNA and protein in resting and activated peripheral blood or Jurkat T cells. Cells were activated by T cell receptor triggering with OKT3 antibodies and activation confirmed by flow cytometric analysis of surface CD69. COX enzymatic activity was measured by determination of arachidonic acid (AA)-induced PG synthesis. Both peripheral blood and Jurkat T cells expressed COX-1 and -2 mRNA and protein. COX-1 was constitutively expressed and did not change after OKT3 stimulation. COX-2 was inducible upon OKT3-induced activation. In spite of the presence of COX mRNA and immunoreactive protein, AA-induced PG synthesis was not detected at the EIA detection (pM) level. The potential role of cyclooxygenases in T cells deserves further study, since no PG of the studied series seem to be synthesized by T cells.
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PMID:Cyclooxygenase-1 and -2 are expressed by human T cells. 993 24

We used the techniques of reverse transcriptase-polymerase chain reaction, Western blotting and immunohistochemistry to evaluate the expression of cyclooxygenase (COX)-1 and -2 in brain and peripheral organs of Alzheimer disease (AD) and control cases. We found both COX-1 and COX-2 to be constitutively expressed in all organs tested, i.e., brain, heart, liver, kidney, spleen and intestine. COX-2 was substantially upregulated in affected areas of AD brain and in infarcted areas of human heart. COX-1 was only mildly upregulated in AD brain. Immunohistochemically, COX-2 was strongly expressed in the perinuclear, dendritic and axonal areas of pyramidal neurons, with enhanced staining in AD. These data suggest a special role for COX-2 in neuronal function.
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PMID:Distribution of cyclooxygenase-1 and cyclooxygenase-2 mRNAs and proteins in human brain and peripheral organs. 1036 79

Resveratrol (3,5,4'-trihydroxy-trans-stilbene) is a naturally occurring compound shown to inhibit carcinogen-induced preneoplastic lesion formation in mouse mammary organ culture and tumorigenesis in the two-stage mouse skin model. Cancer chemopreventive potential was also suggested in various assays reflective of the three major stages of carcinogenesis. Anti-initiation activity was indicated by its antioxidant and antimutagenic effects, inhibition of the hydroperoxidase function of cyclooxygenase (COX), and induction of phase II drug-metabolizing enzymes. Antipromotion activity was indicated by antiinflammatory effects, inhibition of production of arachidonic acid metabolites catalyzed by either COX-1 or COX-2, and chemical carcinogen-induced neoplastic transformation of mouse embryo fibroblasts. Antiprogression activity was demonstrated by its ability to induce human promyelocytic leukemia (HL-60) cell differentiation. Moreover, pretreatment of mouse skin with resveratrol significantly counteracted 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative stress, as evidenced by numerous biochemical responses. Resveratrol reduced the generation of hydrogen peroxide, and normalized levels of myeloperoxidase and oxidized-glutathione reductase activities. It also restored glutathione levels and superoxide dismutase activity. As judged by the reverse transcriptase-polymerase chain reaction, resveratrol selectively inhibited TPA-induced expression of c-fos and transforming growth factor-beta 1 (TGF-beta 1), but did not affect other TPA-induced gene products including COX-1, COX-2, c-myc, c-jun, and tumor necrosis factor-alpha. These data indicate that resveratrol may interfere with reactive oxidant pathways and/or modulate the expression of c-fos and TGF-beta 1 to inhibit tumorigenesis in mouse skin. As reported herein, in addition to the activities described above, resveratrol inhibited the de novo formation of inducible nitric oxide synthase (iNOS) in mouse macrophages stimulated with lipopolysaccharide. This finding suggests an additional mechanism by which resveratrol may function as a cancer chemopreventive agent.
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PMID:Cancer chemopreventive activity of resveratrol. 1037 Aug 67

Nitric oxide (NO) and prostaglandins (PGs) modulate inflammatory and immune responses in the central nervous system (CNS). Both NO and PG synthesis have been described in appropriately stimulated astrocytes. In other systems, both positive and negative modulation of cyclooxygenase (COX) activity, hence PG synthesis, have been described by NO. Since interferon (IFN)-gamma is known to upregulate the production of NO from astrocytes, the present study was designed to investigate the effect of IFNgamma on PG production from activated astrocytes and to determine whether this effect is mediated by NO. Astrocytic PG production was induced by exposure of murine cortical cultures to lipopolysaccharide (LPS). This induction was time- and concentration-dependent, and prevented by inhibitors of transcription and translation, as well as the selective COX-2 inhibitor, NS-398. LPS-induced expression of COX-2 mRNA and protein was confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. Exposure of LPS-treated astrocytes to IFNgamma resulted in a concentration-dependent decrease in PGE2 accumulation which was accompanied by a striking parallel increase in NO formation. However, the NOS inhibitors, N(G)-nitro-L-arginine or N6-(1-iminoethyl)-lysine, failed to reverse the IFNgamma-mediated diminution of LPS-induced PGE2 production, indicating that the IFN-gamma-mediated reduction in COX-2-dependent PGE2 production occurred independent of NO formation. Additional experiments demonstrated that IFN-gamma acted mainly by downregulating the expression of COX-2 protein. Present results indicate that PG and NO synthesis in mouse cortical astrocytes in vitro are under the direct reciprocal control of IFNgamma.
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PMID:Interferon-gamma reduces cyclooxygenase-2-mediated prostaglandin E2 production from primary mouse astrocytes independent of nitric oxide formation. 1037 46

Exogenous prostaglandin E2 (PGE2) given by inhalation almost completely abrogates aspirin-induced asthma and the accompanying increase in cysteinyl-leukotrienes production. Cyclooxygenase (COX) may be present in cells in both constitutive (COX-1) and inducible (COX-2) forms. To increase the production of the potentially protective endogenous PGE2, COX-2 should be upregulated. We hypothesize that an abnormal regulation of COX-2 will predispose patients with asthma to develop aspirin-intolerant asthma/rhinitis (AIAR). We therefore examined the expression of COX-2 messenger RNA (mRNA) in healthy nasal mucosa (n = 11) and in nasal polyps from both patients with AIAR (n = 8) and those with aspirin-tolerant asthma/rhinitis (ATAR) (n = 20). After total mRNA extraction, COX-1 and COX-2 mRNA expression were measured using a reverse transcriptase (RT)-semiquantitative PCR technique. Hybrid primers of COX-1. glyceraldehyde-3-phosphate dehydrogenase (GAPDH) or COX-2. GAPDH were used to create PCR products that were cloned and used as internal standard controls in the competitive PCR reaction. Results are presented as mean +/- standard error of 10(6) molecules of mRNA/micrograms of total RNA. No differences in COX-1 mRNA expression were found between nasal mucosa and nasal polyps from both patients with ATAR and those with AIAR. However, COX-2 mRNA expression in nasal polyps from the AIAR group (0.38 +/- 0.10) was markedly and significantly lower than in polyps from the ATAR group (2.93 +/- 0. 52, sevenfold, p < 0.0001) and nasal mucosa (2.10 +/- 0.54, sixfold, p < 0.01). These findings suggest that an inadequate COX-2 regulation may be involved in AIAR.
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PMID:Cyclooxygenase-2 mRNA is downexpressed in nasal polyps from aspirin-sensitive asthmatics. 1039 Apr 14

Human labour is associated with increased prostaglandin synthesis within the uterus. The aim of this study was to examine the expression of the two isoforms of the central prostaglandin synthetic enzyme, cyclo-oxygenase (COX-1 and COX-2) in human myometrium throughout pregnancy and to test the hypothesis that COX in the myometrium may play a role in labour onset. Expression of COX-1 and COX-2 at the mRNA level was analysed using reverse transcriptase-polymerase chain reaction (RT-PCR) and at the protein level using Western blotting. No significant changes of COX-1 RNA or protein expression were observed either with gestational age or labour. COX-2 mRNA and protein expression increased at term with significant up-regulation occurring prior to the onset of labour (P < 0.005). These data would suggest that up-regulation of COX-2, rather than COX-1, mediates increased prostaglandin synthesis in human myometrium at term. The increased COX-2 expression observed preceded labour onset, suggesting that COX-2 has a role in labour onset, rather than its presence merely a consequence of labour.
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PMID:Expression of cyclo-oxygenase types-1 and -2 in human myometrium throughout pregnancy. 1046 Feb 28

Retinal pigment epithelium (RPE) cells in culture display selective induction of certain early response transcription factors at the onset of photoreceptor rod outer segment (ROS)-specific phagocytosis (Ershov et al., 1996a). Moreover, this response is modulated by prostaglandins. The purpose of this study is to examine the expression of the key enzymes in prostaglandin synthesis: cyclooxygenase-1 (COX-1, constitutive) and cyclooxygenase-2 (COX-2, inducible), during phagocytosis of ROS by RPE cells. Rat RPE cells in primary cell culture were fed with a suspension of freshly isolated rat ROS. COX-1 and COX-2 mRNA expression was studied by quantitative competitive reverse transcriptase-polymerase chain reaction (RT-PCR). During phagocytosis of ROS by RPE cells, RT-PCR revealed an increase in mRNA expression of COX-2, but not of COX-1. COX-2 was also induced by the phospholipid growth factor lyso-phosphatidic acid (LPA) and by the peptide growth factors platelet derived growth factor (PDGF), basic fibroblast growth factor (FGF), and transforming growth factor (TGFbeta), but not nerve growth factor (NGF). Induction of COX-2 by ROS phagocytosis and growth factors through the modulation of prostanoid synthesis may play an important role in the regulation of cell functions associated with photoreceptor cell renewal.
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PMID:Induction of cyclooxygenase-2 gene expression in retinal pigment epithelium cells by photoreceptor rod outer segment phagocytosis and growth factors. 1050 81

It has been reported that lipopolysaccharide (LPS) from periodontal pathogens can penetrate gingival tissues and stimulate the production of prostaglandin E2 (PGE2), which is known as a potent stimulator of inflammation and bone resorption. Although biostimulatory effects of low-level laser irradiation such as anti-inflammatory results have been reported, the physiological mechanism is not yet clarified. The purpose of the present study was to determine the effect of laser irradiation on PGE2 production and cyclooxygenase (COX)-1 and COX-2 gene expression in LPS-challenged human gingival fibroblast (hGF) cells in vitro. hGF cells were prepared from healthy gingival tissues and challenged with LPS, and Ga-Al-As diode laser was irradiated to the hGF cells. The amount of PGE2 released in the culture medium was measured by radioimmunoassay, and mRNA levels were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). Irradiation with Ga-Al-As diode low-level laser significantly inhibited PGE2 production in a dose-dependent manner, which led to a reduction of COX-2 mRNA levels. In conclusion, low-level laser irradiation inhibited PGE2 by LPS in hGF cells through a reduction of COX-2 mRNA level. The findings suggest that low-level laser irradiation may be of therapeutic benefit against the aggravation of gingivitis and periodontitis by bacterial infection.
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PMID:Inhibitory effect of low-level laser irradiation on LPS-stimulated prostaglandin E2 production and cyclooxygenase-2 in human gingival fibroblasts. 1070 74

We applied high-resolution laser-scanning microscopy, electron microscopy, and non-radioactive in situ hybridization histochemistry to determine the cellular and intracellular localization of lipocalin-type prostaglandin D synthase, the major brain-derived protein component of cerebrospinal fluid, and its mRNA in leptomeninges, choroid plexus, and parenchyma of the adult rat brain. Both immunoreactivity and mRNA for prostaglandin D synthase were located in arachnoid barrier cells, arachnoid trabecular cells, and arachnoid pia mater cells. Furthermore, meningeal macrophages and perivascular microglial cells, identified by use of ED2 antibody, were immunopositive for prostaglandin D synthase. In the arachnoid trabecular cells, the immunoreactivity for prostaglandin D synthase was located in the nuclear envelope, Golgi apparatus, and secretory vesicles, indicating the active production and secretion of prostaglandin D synthase. In the meningeal macrophages, prostaglandin D synthase was not found around the nucleus but in lysosomes in the cytoplasm, pointing to an uptake of the protein from the cerebrospinal fluid. Furthermore, the existence of meningeal cyclooxygenase (COX) -1 and COX-2 was investigated by Western blot, Northern blot, and reverse transcriptase-polymerase chain reaction (RT-PCR), and the colocalization of COX-2 and prostaglandin D synthase was demonstrated in virtually all cells of the leptomeninges, choroid plexus epithelial cells, and perivascular microglial cells, suggesting that these cells synthesize prostaglandin D(2) actively. Alternatively, oligodendrocytes showed prostaglandin D synthase immunoreactivity without detectable COX-2. The localization of lipocalin-type prostaglandin D synthase in meningeal cells and its colocalization with COX-2 provide evidence for its function as a prostaglandin D(2)-producing enzyme.
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PMID:Cellular localization of lipocalin-type prostaglandin D synthase (beta-trace) in the central nervous system of the adult rat. 1105 25


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