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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacological differences between muscarinic cholinergic receptors coupled to phosphoinositide turnover and those coupled to adenylate cyclase were studied. Stimulation of muscarinic receptors from SK-N-SH human neuroblastoma cells resulted in phosphoinositide hydrolysis, but not in inhibition of cAMP formation. As has been shown previously, stimulation of muscarinic receptors from NG108-15 neuroblastoma x glioma cells, on the other hand, resulted in inhibition of cAMP formation without any observable phosphoinositide hydrolysis. These two cell lines provide a useful model system in which to study differential coupling of muscarinic cholinergic receptors. Inhibition of [3H]N-methyl scopolamine [( 3H]NMS) binding and inhibition of carbachol-stimulated function by the antagonists pirenzepine, AF-DX 116, and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) were studied in this system. Pirenzepine inhibited [3H]NMS binding in both cell lines with low affinity (Ki of 130 and 160 nM in NG108-15 and SK-N-SH cells respectively), indicating that both cell lines express M2 receptors. None of the three antagonists studied exhibited any clear selectivity for the receptors in one cell line over those of the other. In contrast, several agonists including acetylcholine, bethanechol and carbachol exhibited pronounced selectivity. These agonists inhibited [3H]NMS binding to membranes from SK-N-SH cells with IC50 values that were 17-, 3- and 38-fold higher, respectively, than those of NG108-15 cells. This selectivity was still observed when whole cells rather than membranes were studied. These findings indicate that pharmacological differences between receptors coupled to phosphoinositide turnover and those coupled to cAMP inhibition can be detected with certain agonists, but not with the antagonists pirenzepine, AF-DX 116 or 4-DAMP.
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PMID:Pharmacological differences between muscarinic receptors coupled to phosphoinositide turnover and those coupled to adenylate cyclase inhibition. 247 34

Nerve growth factor (NGF) and glia maturation factor (GMF) reverse some of the transformed characteristics of T9 glioma cells (Marushige et al., Cancer Res 47: 4109-4115, 1987). As an attempt to define the mechanisms of such actions, various chemical agents which modulate second messenger systems were examined for their effects on growth and morphological characteristics of these cells. Administration of bromo-cAMP, forskolin and methylisobutylxanthine retarded cell growth and induced formation of long, branching processes which were similar to those induced by GMF. Perturbation of Ca2(+)-mediated processes by a Ca2+ ionophore, ionomycin, and by calmodulin antagonists, chlorpromazine and W-7, on the other hand, arrested cell growth, and caused clustering of cells, spreading of the cytoplasm and development of lamellipodium-like protrusions which were reminiscent of the effects of NGF. Administration of bromo-cAMP in combination with chlorpromazine, W-7 or ionomycin prevented spreading of the cytoplasm and produced compact cell bodies with well-developed processes. The results of this study demonstrate that modulation of specific second messenger systems by chemical agents are capable of simulating selective morphological changes inducible by NGF and GMF.
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PMID:Chemical control of growth and morphological characteristics of anaplastic glioma cells. 248 3

Comparisons of glycolytic enzymes between rapidly proliferating and Bt2 cAMP-induced differentiated C6 glioma cells have been made. Rapidly proliferating cells had higher concentrations of glucose-6-phosphate, fructose-6-phosphate and fructose-1,6-bisphosphate compared to morphologically differentiated cells. Under maximally activating conditions, the specific activity and Vmax of hexokinase and phosphofructokinase enzymes were reduced by approximately 3- and 28-fold, respectively, in differentiated cells, without any change in Km values. These results suggest that hexokinase and phosphofructokinase occupy special control positions and the rate of glycolysis is correlated with cellular proliferation of C6 glioma cells.
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PMID:Activities of glycolytic enzymes in rapidly proliferating and differentiated C6 glioma cells. 252 90

Each of a range of pharmacological agents which function to increase intracellular levels of cAMP caused a morphological 'differentiation' of neuroblastoma x glioma hybrid, NG108-15, cells grown in tissue culture. Associated with this differentiation, increased incorporation of [32P]ADP-ribose catalysed by pertussis toxin was noted into a band of some 39-40 kDa in membranes derived from these cells. Immunoblotting using two antipeptide antisera which identify different regions of Go alpha demonstrated marked increases in the levels of this polypeptide in membranes of the differentiated cells. However, levels of the beta-subunit did not increase appreciably with differentiation.
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PMID:Elevated levels of the guanine nucleotide binding protein, Go, are associated with differentiation of neuroblastoma x glioma hybrid cells. 253 44

The effects of morphine on the basal cAMP level in the neuroblastoma X glioma NG108-15 hybrid cell line have been studied. Morphine (10 microM) added to the incubation media at hr 0 caused a rapid and significant decrease in the cAMP level up to hr 1; the level then slowly returned to the control at hr 6, and gradually increased to its peak at hr 36, returning to the control at hr 60. These results provide the first evidence for a delayed rebound increase of cAMP during morphine treatment. Naloxone (10 microM) added at hr 0 concomitantly with morphine blocked the morphine-induced decrease in cAMP level at hr 1 and attenuated its increase at hr 36. However, when naloxone was added at hr 5.5, the cAMP level significantly increased at hr 6, and at hr 36 the cAMP level increase was the same as in the case of morphine alone. Furthermore when naloxone was added 0.5 hr prior to harvesting the cells at hr 6, 12, 24 and 36, the cAMP level showed an immediate increase at each time point up to about the same level as observed with morphine alone at hr 36. Chloramphenicol, a protein synthesis inhibitor (100 microM) itself caused little or no change in the cAMP level. Added 30 min before morphine, chloramphenicol decreased the morphine-induced rebound increase at hr 36 in a concentration-dependent manner without any significant effect on cAMP decrease at hr 1. However when chloramphenicol was added at hr 5.5, the morphine-induced rebound increase at hr 36 was also attenuated, thereby suggesting an involvement of macromolecular synthesis in the rebound increase of cAMP which may be used as a model for the development of morphine dependence.
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PMID:Rebound increase of basal cAMP level in NG108-15 cells during chronic morphine treatment: effects of naloxone and chloramphenicol. 253 45

When added to intact C6 glioma cells in the micromolar range of concentrations, ADP and ATP induce an inhibition of the isoproterenol-elicited cAMP responses. ATP is rapidly hydrolyzed by the ectonucleotidases present on these cells, with an apparent Km of 50 microM and a Vmax of 1.1 nmol/min/10(6) cells. cAMP responses are also inhibited by millimolar concentrations of either ATP in the presence of an ATP-regenerating system to prevent ADP accumulation or AMP-PCP. These observations show that, in C6 glioma cells, ADP is a more potent inhibitor of cAMP production than ATP, the latter acting indirectly, via its rapid hydrolysis to ADP. The additive inhibition of isoproterenol-elicited cAMP responses induced, on one hand, by the treatment of the cells with a phorbol ester and by addition of ADP to the cells, and, on the other hand, by the progressive disappearance of the effects of ADP and ATP when cells are treated with increasing concentrations of Pertussis toxin, demonstrate that ADP and ATP exert their action in C6 glioma cells via a P2 purinoceptor probably negatively coupled to adenylate cyclase and a G regulatory protein.
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PMID:ADP and, indirectly, ATP are potent inhibitors of cAMP production in intact isoproterenol-stimulated C6 glioma cells. 255 Dec 69

To elucidate the mechanisms by which hormones regulate cAMP phosphodiesterases (PDEs), a group of cDNA clones that had been isolated from a rat Sertoli cell library were characterized. These cDNAs are derived from a single gene (ratPDE3). The deduced amino acid sequence of the ratPDE3 cDNA corresponds to a 66,200-Da protein homologous to other testicular PDEs, to the Drosophila melanogaster dunce-encoded cAMP PDE, and to bovine and yeast PDEs. Expression of ratPDE3 in eukaryotic and prokaryotic cells leads to the appearance of a cAMP PDE with properties identical to the cAMP PDE purified from Sertoli cells. Although of different size, transcripts corresponding to ratPDE3 were present in all organs studied. In the immature Sertoli cell in culture, the level of mRNA transcripts of ratPDE3 was increased more than 100-fold by follicle-stimulating hormone or N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate treatment. Stimulation of ratPDE3 mRNA by N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate was also observed in a C6 glioma cell line. These data demonstrate that cAMP regulates the expression of one of its own degrading enzymes by an intracellular feedback mechanism that involves changes in mRNA levels.
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PMID:The mRNA encoding a high-affinity cAMP phosphodiesterase is regulated by hormones and cAMP. 255 3

The effect of dibutyryladenosine 3',5'-cyclic monophosphate (dibutyryl cAMP) on the expression of glutathione S-transferase placental type (GST-P) was examined in rat glioma cell line using an immunohistochemical technique. Cultured T9 glioma cells were negative for GST-P activity under normal conditions. However, treatment with 1 mM dibutyryl cAMP produced GST-P expression in about 50% of the cells, as well as some morphological changes. The expression of GST-P was increased with addition of dibutyryl cAMP together with 1 microgram/ml allyl isothiocyanate (AITC) or 0.1 microgram/ml benzyl isothiocyanate (BITC). With these combinated treatments, almost all cultured cells showed a strong positive reaction for GST-P, although AITC or BITC alone elicited GST-P in only 5% of the cultured cells. The results of the present study indicate that dibutyryl cAMP causes functional as well as morphological differentiation of T9 glioma cells.
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PMID:Induction of glutathione S-transferase, placental type in T9 glioma cells by dibutyryladenosine 3',5'-cyclic monophosphate and modification of its expression by naturally occurring isothiocyanates. 255 81

The activity of beta-adrenergic receptors at the plasma membrane level was investigated in viable, electropermeabilized C6 glioma cells. Electric field pulses were applied directly to the plated cells without any previous proteinase treatment. The affinity for isoproterenol and the density of the beta-adrenergic receptors, as judged from the number of [3H]CGP-12177 binding sites, were not affected by the electropermeabilization whereas the isoproterenol-stimulated cAMP accumulation was transiently impaired. This decrease in activity is due to an electropermeabilization-induced GTP leak. Normal activity could be obtained either by treating the cells by the electric field in a GTP-containing buffer, or by spontaneous recovery of the cells after the resealing of the plasma membrane, with a delay depending on the temperature. The activity of the receptors was not affected by the structural organization of the membrane associated to its electropermeabilization.
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PMID:Signal transduction by membrane receptors in viable electropermeabilized cells: isoproterenol-stimulated cyclic AMP synthesis in C6 glioma cells. 256 94

Cells from gliomas induced by N-ethyl-N-nitrosourea have a high basal level of plasminogen activator activity compared with cells from normal tissue. Plasminogen activator activity is known to be affected by many substances but whether inhibition or stimulation occurs depends on the cell and agent involved. It is not clear whether tumour and control cells from the same type of tissue respond similarly. A comparison has been made of the effect of several factors on both cell associated and secreted enzyme activity of cloned lines from a glioma and normal tissue. The effect of two cAMP elevating compounds was stimulatory while that of the steroid, dexamethasone, was generally inhibitory for both cells. However, the polypeptide hormone, epidermal growth factor, had a differential effect. It caused an increase in secreted enzyme activity in the tumour line but had no such effect on the control clone. The precise mechanism by which this occurs is unknown. Co-operative effects of the enzyme and growth hormone could result in more aggressive behaviour of the tumour cells.
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PMID:A comparison of the effect of several factors on the plasminogen activator activity of cloned lines from an ethylnitrosourea-induced glioma and from normal tissue. 262 4


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