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

A novel clonal cell line derived from a human glioma (HOG) was found to express some oligodendrocyte-specific proteins including a 15-kDa form of myelin basic protein (MBP) and high 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) activity. Expression of the myelin lipids galactosylceramide and sulfogalactosylceramide (sulfatide) was low. HOG cells did not express the characteristic astrocyte markers glial fibrillary acidic protein (GFAP) or significant glutamine synthetase (GS) activity. After initial plating, HOG cells were flat and epitheloid and thus showed a limited oligodendrocyte-like morphology. However, after cells became more confluent, some cells were phase-bright and elaborated short processes. Receptor types expressed by HOG cells included A2-adenosine, prostaglandin E1 (PGE1), and beta 2-adrenergic receptors (beta-ARs) linked to stimulation of adenylate cyclase, and muscarinic cholinergic and H1-histamine coupled to phosphatidyinositol turnover (Post and Dawson, 1991). HOG cells should therefore provide a useful model for studying the extracellular regulation and phosphorylation of oligodendrocyte-specific proteins.
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PMID:Characterization of a cell line derived from a human oligodendroglioma. 132 95

Previous studies from this laboratory have shown that C-6 rat glioma cells (2B clone) exhibit specific phenotypic characteristics depending on passage in culture and that these populations respond differentially to addition of various exogenous compounds to the medium. Early passage (less than 25) C-6 glial cells express low glutamine synthetase activity (a marker for astrocytes) and with increasing cell passage (greater than 70) C-6 glial cells express more astrocytic properties with respect to both glutamine synthetase (GS) and morphology. In this study, cells from both early (glioblastic) and late (astrocytic) passage were examined for their response to the phospholipid, platelet-activating factor (PAF). We found that PAF increased GS activity in early passage (glioblastic) cells and more importantly it increased GS activity in late passage cells, already committed to the astrocytic phenotype. Furthermore, cells from both passages failed to respond to addition of lyso-PAF, the non-biologically active analog of PAF, to the medium. By following the uptake of 3H-PAF into cells, we observed that greater than 90% of the phospholipid was taken into the cells within the first hour of incubation. We compared the PAF effects with that of dibutyryl cyclic AMP (dBcAMP) and RO20-1724, a phosphodiesterase inhibitor. Cells from the early passage responded to both dBcAMP and RO20-1724 treatments with a significant increase in GS activity whereas cells from the late passage showed no significant change, confirming earlier reports from this laboratory. These findings indicate that the response of C-6 glioma cells to PAF (at least in the late passage) is not mediated via cyclic AMP. We suggest that in early passage cells PAF promotes expression of the astrocytic phenotype and in late passage cells PAF mediates a gliosis-type response.
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PMID:Platelet-activating factor increases glutamine synthetase activity in early and late passage C-6 glioma cells. 167 34

Flat, amorphous astroblasts in culture differentiate into rounded process-bearing cells after removal of serum from the media or following addition of dibutyryl cyclic-AMP (dbcAMP). We report here that addition of thrombin (10 nM) to rat primary astroglial cultures reversed both the spontaneous morphological differentiation of astroblasts caused by serum removal, and the more extensive morphological differentiation caused by pre-treatment with dbcAMP. The astroblasts retained the ability to differentiate upon removal of thrombin from the medium. Proteolytic activity of thrombin was required for the reversal of differentiation. Moreover, addition of serine protease inhibitors active against thrombin elicited a prolonged morphological differentiation rivaling that induced by dbcAMP, suggesting that inactivation of cell-associated thrombin might be sufficient for morphological differentiation to occur. Two other serine proteases with a cleavage specificity similar to thrombin were ineffective in reversing differentiation. Both the induction of morphological differentiation by dbcAMP and its reversal by thrombin were rapid, being essentially complete by 1 h. With more prolonged treatments, thrombin also reduced the dbcAMP-mediated increase in glutamine synthetase, a biochemical marker for astroglial differentiation. Thrombin also inhibited morphological differentiation in C6 glioma and altered the morphology of microglial cells; however, thrombin did not prevent neurite outgrowth in primary central neuronal cultures in contrast to its previously reported effects on the neuroblastoma 2a cell line. These findings indicate that a proteolytic mechanism mediated by thrombin and its inhibitors may underlie the regulation of astroglial differentiation.
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PMID:Thrombin and its inhibitors regulate morphological and biochemical differentiation of astrocytes in vitro. 197 84

A human glioma-derived cell line which expresses both the astrocytic markers, glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) and cell surface gangliosides recognised by the A2B5 monoclonal antibody has been cloned. Two clones are described, which are A2B5-positive and A2B5-negative, respectively. These neoplastic clones may provide a suitable in vitro model with which to assess the significance of surface ganglioside expression in relation to function and lineage of mammalian glia.
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PMID:A2B5 surface ganglioside binding distinguishes between two GFAP-positive clones from a human glioma-derived cell line. 197 73

The tricyclic antidepressant desipramine, when added to culture medium, gave rise in C6 rat glioma cells to a decrease of the activity of the enzyme asialofetuin sialyltransferase. The inhibition was dose and time dependent and was observed in both multiplying cells and cells blocked with 2 mM thymidine or depletion of amino acids. This inhibition was rather specific to the sialyltransferase, as under the conditions where this enzyme was inhibited up to 70%, other enzymes such as dolichol phosphate mannose synthetase, glutamine synthetase, and glycerol phosphate dehydrogenase remained unaffected. This inhibition was not reversed after removal of desipramine from the medium and was not observed by direct addition of desipramine to the sialyltransferase incubation assay. Under the same conditions, W-7 [N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide], which is known to be a potent calmodulin antagonist and an inhibitor of calmodulin-dependent kinases, gave the same concentration-dependent inhibition profile of sialyltransferase as desipramine, whereas H-7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine], which is an inhibitor of protein kinase C and cyclic nucleotide-dependent kinases, had no effect. So, it is suggested that desipramine inhibits the sialyltransferase activity in C6 glioma cells through a calmodulin-dependent system.
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PMID:Effect of desipramine on a glycoprotein sialyltransferase activity in C6 cultured glioma cells. 229 42

C6 glioma cells contain two types of receptors for adrenocorticoids. Glucocorticoid (Type II) receptors are present at higher density and mediate increases in glycerol phosphate dehydrogenase and glutamine synthetase activity. The function of mineralocorticoid (Type I) receptors present at low density in C6 cells is unknown. Since mineralocorticoid (Type I) receptors in renal epithelial cells regulate cation transport, we sought to determine whether adrenocorticoid receptors located in glioma cells are similarly linked to electrolyte transporting activity. Occupation of mineralocorticoid receptors in C6 glioma by adrenocorticoids did not alter Na+ or K+ transport, in contrast to their effects on renal epithelial and vascular smooth muscle cells. Occupation of glucocorticoid receptors produced a 20-25% decrease in K+ uptake into C6 cells, but did not alter Na+ influx. Stimulation of Na+ influx with the ionophore monensin produced a large ouabain-sensitive increase in glucose utilization, as measured by 2-deoxyglucose uptake. However, mineralocorticoid receptor occupation did not alter glucose utilization, providing further evidence that these receptors do not influence Na+ transport in C6 cells. These studies provide evidence that mineralocorticoid receptors in glioma cells do not regulate Na+ or K+ transport. Glial glucocorticoid receptors have an inhibitory effect on glial K+ influx, which may contribute to glucocorticoid hormone effects on brain excitability.
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PMID:Effect of adrenocorticoid receptors on potassium and sodium flux in rat C6 glioma cells. 282 17

We established and characterized five cell lines derived from human malignant gliomas (four glioblastomas multiforme and one highly anaplastic astrocytoma). All cell lines exhibited tumor cell morphology and growth kinetics, and anchorage-independent growth in soft agar. Cytogenetic analysis revealed significant aneuploidy in all five cases as well as clonal chromosomal alterations unique to each cell line. No cell line was tumorigenic in athymic mice. Two of the cell lines were sensitive to carmustine (BCNU) in monolayer and soft-agar cultures. Electron microscopy showed marked variability between cell lines in the number and structure of intracytoplasmic organelles; SF-126 formed collagen fibers in vitro. Immunohistochemical analysis of the surgical specimens showed variable expression of glial fibrillary acidic protein (GFAP) in malignant astrocytes; positive immunostaining for glycoproteins of the extracellular matrix was found predominantly in perivascular regions. In early-passage cultures, only cell line SF-295 expressed GFAP; at establishment, none of the cell lines expressed GFAF or glutamine synthetase. Fibronectin and laminin were expressed by all cell lines in early-passage culture, but expression of these glycoproteins at establishment was variable. Only SF-126 was positively identified by immunostains for procollagen III; this was also the only cell line in which DEAE-cellulose chromatography and SDS-PAGE demonstrated interstitial collagen synthesis. These well-characterized glioma-derived cell lines may now serve as useful tools with which to study the cell biology of gliomas. The synthesis of interstitial collagen by a glioma-derived cell line may suggest a derivation from vascular mesenchymal elements, either reactive or transformed, in the original heterogeneous malignant glioma, rather than from a glial precursor cell.
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PMID:Establishment and characterization of five cell lines derived from human malignant gliomas. 282 96

Cellular supply of glutamine, an essential substrate for growth, is derived from extracellular fluid and de novo synthesis. We investigated the relative importance of these sources to the growth of six human anaplastic glioma- and one human medulloblastoma-derived permanent cell lines. Exogenous glutamine was limiting for the proliferation of glioma-derived lines D-54 MG, U-118 MG, and U-251 MG. In contrast, medulloblastoma-derived line TE-671 and glioma-derived lines U-373 MG, D-245 MG, and D-259 MG grew in the absence of supplemental glutamine. Two cell lines with contrasting glutamine requirements, D-54 MG and TE-671, were used to explore the pharmacological interference with glutamine metabolism. DL-alpha-Aminoadipic acid, a reported glutamic acid analogue with gliotoxic properties, significantly inhibited the growth of both lines. These effects were reversed by increasing glutamine, suggesting that the major action of DL-alpha-aminoadipic acid is as a glutamine antagonist. In contrast, the glutamine synthetase inhibitor delta-hydroxylysine demonstrated activity only against TE-671. Acivicin and 6-diazo-5-oxo-L-norleucine, glutamine analogues available for clinical use, reduced the proliferation of both cell lines at pharmacological concentrations. Methionine sulfoximine, a glutamine synthetase inhibitor previously used clinically, produced marked growth inhibition only against TE-671. These findings indicate that the synthesis and utilization of glutamine are potentially exploitable targets for the chemotherapy of some human gliomas and medulloblastomas.
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PMID:Influence of glutamine on the growth of human glioma and medulloblastoma in culture. 286 94

Incubation of L929 cells with three different glucocorticoids, hydrocortisone, dexamethasone and triamcinolone acetonide, rendered the cells unable to support plaque formation by several unrelated DNA and RNA viruses. The establishment of this antiviral state by dexamethasone coincided with an inhibition of cell growth and induction of glutamine synthetase activity. These steroid-mediated activities occurred only in cultures of L929 cells and not in cultures of rabbit skin or rat glioma cells.
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PMID:Glucocorticoid-mediated establishment of an antiviral state coincident with other glucocorticoid-induced biochemical activities in L929 cells. 286 88

A cell clone--A15 A5--derived from an N-ethyl-N-nitrosourea (ENU)-induced glioma in a BDIX rat has been maintained in vitro for over 50 passages. These cells, which produce tumours when injected intracerebrally into syngeneic rats, possess several features of neoplastic astrocytes. In the present study A15 A5 cells were found to express both glial fibrillary acidic protein and glutamine synthetase, thus confirming their astrocytic nature.
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PMID:Cloned neoplastic cells from a chemically-induced rat glioma: immunocytochemical characterization. 286 65


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