Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cannabimimetic drugs have been shown to inhibit adenylate cyclase activity in N18TG2 neuroblastoma cells. This investigation examines the possible role of opioid receptors in the cannabimimetic response. Opioid receptors of the delta subtype were found on N18TG2 membranes using [3H]D-Ala2-D-Leu5-enkephalin. No mu or kappa receptors were detected using selective ligands for these sites. The delta binding affinity and capacity were unaltered by cannabimimetic drugs. To test if cannabimimetic drugs may modulate opioid effector mechanisms, cyclic AMP metabolism was determined in intact cells and in membranes. N18TG2 adenylate cyclase was inhibited by the cannabimimetic drugs delta 9-tetrahydrocannabinol and desacetyllevonantradol, and by the opioid agents morphine, etorphine, and D-Ala2-Met5-enkephalinamide. The opioid inhibition was reversed by naloxone and naltrexone; however, the cannabimimetic response was unaffected. Both cannabimimetic and opioid drugs decreased cyclic AMP accumulation in intact cells, but opioid antagonists blocked the response only to the latter. Thus, cannabimimetic effects are observed even though opioid receptors are blocked by antagonist drugs. The interaction between desacetyllevonantradol and etorphine was neither synergistic nor additive at maximal concentrations, suggesting that these two drugs operate via the same effector mechanism. Other neuronal cell lines having an opioid response were also examined. The cannabimimetic inhibition of cyclic AMP accumulation in NG108-15 neuroblastoma X glioma cells was not as great as the response in N18TG2. N4TG1 neuroblastoma cells did not respond to cannabimimetic drugs under any conditions tested. Thus, the cannabimimetic inhibition of adenylate cyclase is not universally observed, and the efficacy of the cannabimimetic response does not correlate with the efficacy of the opioid response.
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PMID:An assessment of the role of opioid receptors in the response to cannabimimetic drugs. 300 17

When membranes from neuroblastoma X glioma NG108-15 hybrid cells were incubated in a cell-free system with opioid agonists, a time-, temperature-, and dose-dependent desensitization to opioid inhibition of adenylate cyclase activity was observed. The composition of the system during the incubation was manipulated to elucidate the biochemical mechanisms of desensitization. Receptor coupling appeared to be a prerequisite for desensitization, because both magnesium and sodium, which are necessary for coupling, were required for desensitization. Removal of ATP and addition of cyclic AMP or cyclic GMP had no effect on desensitization.
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PMID:Cell-free desensitization of opioid inhibition of adenylate cyclase in neuroblastoma X glioma NG108-15 hybrid cell membranes. 301 85

We have compared the effects of norepinephrine, forskolin, and dibutyryl cyclic AMP (Bt2cAMP) on the regulation of the cytosolic enzyme glycerol phosphate dehydrogenase (GPDH) in the C6 rat glioma cell line. Forskolin and Bt2cAMP elicit a dose-dependent increase in the levels of the enzyme that was, however, unaffected by norepinephrine. The half-maximal effect of forskolin was obtained at 7-8 microM, and the effect was maximal at 30 microM. Dexamethasone at a 50 nM concentration produced a two- to sixfold induction of GPDH after 48 h. The combination of dexamethasone with forskolin or Bt2cAMP leads to an elevation in GPDH levels that is higher than that produced by one of the compounds alone. This potentiation is found when both agents are added together with or after the glucocorticoid. The increase in uninduced and dexamethasone-induced GPDH activity was blocked by cycloheximide and actinomycin D, indicating that de novo protein and RNA synthesis are required. The activity of cytosolic lactate dehydrogenase activity did not change after incubation with dexamethasone, but increased with forskolin or Bt2cAMP.
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PMID:Regulation of glycerol phosphate dehydrogenase and lactate dehydrogenase activity by forskolin and dibutyryl cyclic AMP in the C6 glial cells. 302 Jan 71

Regulation of preproenkephalin gene expression was studied in NG108-15 neuroblastoma-glioma hybrid cells. Untreated cells contain 20-120 fg preproenkephalin mRNA per microgram cellular RNA. Treatment of cells with a glucocorticoid (e.g. dexamethasone) for 24 hr or 8 days elevated the abundance of this mRNA to 3 or 9 times the control, respectively. Treatment with 8-bromo-cyclic AMP or an adenylate cyclase activator such as prostaglandin E1 or forskolin elevated preproenkephalin mRNA to twice the control or less. Treatment with both glucocorticoid and forskolin for 24 hr or 8 days markedly increased preproenkephalin mRNA to 5-8 and 30 times the control, respectively. Intracellular Met-enkephalin immunoreactivity was increased in parallel with the mRNA abundance. The results demonstrate that preproenkephalin gene expression is synergistically regulated by glucocorticoids and cAMP.
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PMID:Glucocorticoids and cyclic AMP synergistically regulate the abundance of preproenkephalin messenger RNA in neuroblastoma-glioma hybrid cells. 302 Nov 19

Rat glioma C6 cells, cultured in the presence of the tricyclic antidepressant desipramine, lost a significant number of beta-adrenergic receptors in a time- and dose-dependent manner. A similar loss was observed whether binding was determined on intact cells with the hydrophilic beta-adrenergic antagonist (+/-)-[3H]4-(3-tert-butylamino-2-hydroxypropoxyl)benzimidazole-2-o n HCl ([3H]CGP-12177) or on cell lysates with the more hydrophobic antagonists [125I]iodocyanopindolol or [3H]dihydroalprenolol. When stimulated with the agonist isoproterenol, desipramine-treated cells accumulated less cyclic AMP than control cells. The affinity of the beta-adrenergic receptors for either antagonist or agonist was unchanged after desipramine treatment. Desipramine interacted only weakly with the receptors and competed for [125I]iodocyanopindolol binding with a Ki of 30 microM. The presence in the culture medium of alprenolol or propranolol, potent beta-adrenergic antagonists, however, did not prevent the reduction in receptors by desipramine. Desipramine also caused a loss of beta-adrenergic receptors from cells maintained in serum-free medium and the cells themselves did not contain or secrete endogenous catecholamines. Although desipramine is a potent inhibitor of catecholamine uptake, it appears unlikely that the observed loss of beta-adrenergic receptors in rat glioma C6 cells exposed to the drug is due to an increase in extracellular catecholamine levels or to a direct interaction with the receptors.
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PMID:Effect of the tricyclic antidepressant desipramine on beta-adrenergic receptors in cultured rat glioma C6 cells. 303 98

Incubation of C6-BU1 glioma cells in the presence of isoproterenol and Ro20-1724--a potent cAMP phosphodiesterase inhibitor--results in a transient increase in intracellular cAMP levels, followed by a rapid efflux of cyclic AMP from the cells into the media. Two distinct types of morphological changes could be seen: rounded cell bodies with multipolar processes and beadings after 30 minutes of incubation--this period coincides with a 70-80-fold increase in intracellular cAMP levels, and elongated cell bodies with extended bipolar processes after 24-48 hours. By this time the intracellular cAMP concentration dropped to a low level, which was only three- to four fold higher than that in control. The transient increase in intracellular cAMP concentration results in retardation of cell growth, diminished uptake of 3H-2-deoxyglucose, and abolition of enhanced synthesis of cyclic AMP by concanavalin A.
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PMID:Transient increase in intracellular concentration of adenosine 3':5'-cyclic monophosphate results in morphological and biochemical differentiation of C6 glioma cells in culture. 303 2

Glial fibrillary acidic protein (GFAP) was induced in rat C6 glioma cells grown in M199 and HAM F10 media by addition of 1 mM dibutyryl cyclic AMP. The amount of GFAP per cell increased 7- and 33-fold in M199 and HAM F10 media, respectively. GFAP could be induced in each phase of the cell culture except for the lag phase, where GFAP synthesis was delayed until the onset of the logarithmic growth. The induction took place under conditions where the total protein content of the cell decreased. Measurement of the amount of vimentin indicated that GFAP was induced under conditions of low vimentin concentration. Our results do not support the hypothesis that GFAP induction depends on cell-cell contact or cell proliferation. They indicate a shift from vimentin to GFAP synthesis by an as yet unknown mechanism.
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PMID:Expression of glial fibrillary acidic protein in rat C6 glioma relates to vimentin and is independent of cell-cell contact. 303 25

The neuroblastoma-glioma NG108 cell line has been shown to contain both a delta-opiate receptor and enkephalin peptides. In this paper, the presence of authentic proenkephalin mRNA and proenkephalin-derived peptides are demonstrated. Growth of the cells in the presence of etorphine for 5-7 days resulted in a 3-fold increase of proenkephalin mRNA, which was accompanied by comparable increases in proenkephalin peptides and free enkephalin. The effect was mimicked by either morphine or [D-Ala2,D-Met5]enkephalinamide, and was blocked by naloxone. The EC50 for the effect of etorphine was 10(-9) M. The cyclic AMP content of cells grown for 5 days in the presence of etorphine was the same as that of control cells. Forskolin treatment also increased the proenkephalin mRNA content of the cells: the effect was not additive with that of etorphine, suggesting that the effect of opiate agonists was not occurring through their inhibition of adenylate cyclase. The results suggest that proenkephalin synthesis in NG108 cells can be regulated by two different mechanisms, one involving cyclic AMP while the other, regulated by the opiate receptor, is yet to be determined.
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PMID:Chronic exposure to opiate agonists increases proenkephalin biosynthesis in NG108 cells. 338 39

A method for measuring respiratory activity in anchorage-dependent cultured cells has been developed. This method is based on a technique that permits the perfusion of standard plastic culture dishes with attached cells. Basal respiratory activities were studied in two continuous cell lines of neural origin, neuroblastoma C1300 clone 41A3 and glioma 138MG. As compared to traditional measurements on detached cells, a fourfold increase in value was obtained. Investigations on membrane permeability suggested that the observed difference could be attributed to alterations in cell membrane integrity. Pretreatment with dibutyryl cyclic AMP, known to induce a morphological and biochemical differentiation in C1300 and 138MG cells, caused in both cell lines an enhanced respiration.
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PMID:Use of a perfusion technique for measurements of respiratory activity in cultured cells. 406 1

Long-term regulation of the cyclic nucleotide phosphodiesterase of the C-6 rat glioma cell line has been studied. Both the low K(m) and high K(m) activities can be induced by elevation of intracellular cyclic AMP levels following either dibutyryl cyclic AMP or norepinephrine treatment of the cells. The enzymes are maximally induced by 3-4 hr. The presence of either cycloheximide or actinomycin D prevents induction by either dibutyryl cyclic AMP or norepinephrine. Evidence is presented that the norepinephrine effect is mediated by the beta-catecholamine receptor. The increased phosphodiesterase activity causes a partial refractoriness to a second challenge with norepinephrine, which can be overcome by blockade of the induction with cycloheximide. The results suggest that just as short-term regulation of cyclic AMP levels occurs via changes in the rates of synthesis or degradation, long-term alterations of the system may also involve either the adenylate cyclase or the phosphodiesterase.
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PMID:Cyclic AMP-mediated induction of the cyclic AMP phosphodiesterase of C-6 glioma cells. 415 39


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