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)

Medulloblastoma, a common pediatric brain tumor, is a primitive neuroectodermal tumor which often displays neuronal and/or glial characteristics. We have investigated the consequences of treating cell lines derived from a human medulloblastoma with glia maturation factor-beta (GMF-beta), a protein found in mammalian brain. GMF-beta promotes growth arrest and morphological alteration of cultured glioma and neuroblastoma cells. The proliferation of medulloblastoma cells was arrested 24-48 hr after exposure to human recombinant GMF-beta. During the same period, treated cells acquired a morphology similar to that of mature astrocytes. By 72 hr, all treated cells bound an antibody against glial fibrillary acidic protein (GFAP), a distinguishing biochemical feature of mature astrocytes. Immunoreactivity was accompanied by de novo expression of GFAP mRNA. Our observations are the first demonstration of the induction of morphological and biochemical characteristics of mature astrocytes in cultured medulloblastoma-derived cells by an exogenous factor.
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PMID:Expression of glial fibrillary acidic protein in human medulloblastoma cells treated with recombinant glia maturation factor-beta. 129 57

Mouse neuroblastoma x rat glioma hybrid NG108-15 cells form cholinergic synapses with rat or mouse muscle cells in culture. The rate of synapse formation is greatly dependent on intracellular cyclic AMP concentrations. The synapse formation is lower in the presence of glia maturation factor, a partially purified brain extract. Once the synapse between NG108-15 cells and myotubes has been formed, this synapse is stable for days. Extracellular application of serotonin, PGF2 alpha, PGD2, neurotensin and bradykinin on NG108-15 cells increases synaptic transmission. Since bradykinin increases the level of intracellular inositol 1,4,5-trisphosphate (InsP3), bradykinin-induced facilitation is due to InsP3-dependent elevation of intracellular Ca concentrations.
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PMID:Cholinergic synapse formation between NG108-15 and muscle cells and modulation of transmission. 217 13

Glia maturation factor beta (GMF-beta) is a 17-kDa acidic protein isolated from the brain. When added to cultured cells, GMF-beta promotes the phenotypic expression of glia and neurons and inhibits the proliferation of their respective tumors. Although astrocytes produce GMF-beta and store it inside the cells, they do not secrete the protein into the cultured medium. This poses a question as to how GMF-beta mediates intercellular communication. This paper provides an answer by demonstrating the presence of GMF-beta on the surface of astrocytes, using gold-labeled antibody enhanced with silver. It appears that cell-surface GMF-beta acts on the target cells at close range when cells are in direct contact. In contrast to astrocytes, we failed to detect GMF-beta on the surface of C6 glioma cells, although these cells, like astrocytes, possess endogenous intracellular GMF-beta and are also responsive to GMF-beta added to the medium. The lack of cell-surface expression of GMF-beta in C6 cells may reflect a breakdown in intercellular communication in these malignant cells.
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PMID:Cell-surface expression of glia maturation factor beta in astrocytes. 225 51

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

Changes in cytoskeletal organization in T9 anaplastic glioma cells have been examined during morphological changes induced by nerve growth factor (NGF) and by glia maturation factor (GMF). Indirect immunofluorescent labeling of cytoskeletal proteins has revealed that while neither GMF nor NGF induces expression of glial fibrillary acidic protein in this cell line, changes in cytoskeletal organization induced by these factors show some features similar to those observable during maturation of normal glial cells. Changing cell shapes induced by these factors are clearly outlined by the prominent distribution of microfilaments along cellular margins. Microtubules and intermediate filaments gradually extend during morphological changes and fill the characteristic cytoplasmic processes induced by NGF and GMF.
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PMID:Cytoskeletal reorganization induced by nerve growth factor and glia maturation factor in anaplastic glioma cells. 268 92

A protein has been isolated from bovine brains by using a modification of the procedure used to purify glia maturation factor. The method consists of ammonium sulfate precipitation, chromatography with DEAE-Sephacel, Sephadex G-75, and hydroxylapatite columns, passage through a heparin-Sepharose column, and finally fractionation by reverse-phase HPLC with a C4 column. The isolated protein reacts strongly with the mouse monoclonal antibody G2-09 and has a molecular weight of approximately 17,000 and an isoelectric point of pH 4.9. The N terminus is blocked, but tryptic digestion releases 28 peptides, 8 of which have been sequenced. The total known residues add up to more than two-thirds of the entire 140-residue protein, estimated from amino acid composition, and show no sequence homology with any known protein. Reversible thermal renaturation greatly enhances its biological activity. The purified protein stimulates differentiation of normal neurons as well as glial cells. It inhibits the proliferation of the N-18 neuroblastoma line and the C6 glioma line while promoting their phenotypic expression. We designate this protein glia maturation factor beta.
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PMID:Purification and characterization of glia maturation factor beta: a growth regulator for neurons and glia. 272 56

Using the monoclonal antibody G2-09 raised against bovine glia maturation factor (GMF), we conducted a survey of GMF-like immunoreactivity in various cell types. Of all the normal and neoplastic cells tested, only extracts from astroblasts, gliomas, Schwann cells and schwannomas, but not their conditioned media, possessed endogenous GMF-like immunoreactivity. The presence of immunoreactive GMF correlated well with GMF bioactivity. Using the same monoclonal antibody, the GMF-like factor in astroblasts and C6 glioma cells was characterized by immunofluorescence, immunoadsorption and immunoblotting. Immunofluorescence confirmed the intracellular location of GMF. Immunoadsorption completely eliminated the GMF-like bioactivity from the cell extracts. Immunoblotting identified a protein band having a mol. wt. of 14,000 Da. Thus, the evidence strongly supports the argument that the GMF-like factor in astroblasts and C6 cells is identical with GMF from the bovine brain. In order to explain the fact that astroblasts and C6 cells are both the source and targets of GMF, we propose the hypothesis that GMF functions as an injury signal, being released from the injured glia and serving as a stimulant for gliosis in the neighboring intact glia.
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PMID:Endogenous immunoreactive glia maturation factor-like molecule in astrocytes and glioma cells. 329 57

C6 rat glioma cells respond to glia maturation factor (GMF) with characteristic morphological alterations. Observed under phase-contrast microscopy, the cells changed from a rounded morphology in random formation to a spindle-shaped appearance in parallel arrays. Observed under scanning electron microscopy, GMF led to a decrease in the number of microvilli and cell surface knobs. Transmission electron microscopy demonstrated the appearance of numerous microtubules aligned with the long axis of the cells after GMF stimulation. The change in cell shape and histotypic pattern was inhibited by vinblastin, further implicating the involvement of microtubules. Immunofluorescence using anti-alpha-tubulin revealed a well-defined cytoskeletal system in GMF-stimulated cells but not in the control cells. Finally, an increase in tubulin was confirmed with enzyme-linked immunosorbent assay (ELISA) on extracts from these cultures. The findings indicate that morphological alterations induced by GMF are associated with changes in the quantity and arrangement of microtubules.
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PMID:Induction of cytoskeletal alterations in C6 glioma by glia maturation factor. 350

Anaplastic glioma T9 cells were treated with either nerve growth factor (NGF) or glia maturation factor (GMF) or both. It was found that, when T9 cells were treated with these factors in a chemically defined medium, both NGF and GMF induced characteristic changes of cell morphology and growth pattern. Several differences in the effects of NGF and GMF were noted. NGF retarded growth rate, whereas GMF did not. The cells treated with NGF were characterized by a flattened extended cytoplasm with numerous protruding processes. The cell masses were somatically connected by cell bridges. GMF, on the other hand, produced slender cells with long, branching processes forming an interconnecting cell net. Concomitant administration of NGF and GMF retarded cell growth as was demonstrated with NGF alone and induced morphological changes predominantly attributable to GMF. The maximal effect of either NGF or GMF or both was attained after 4 days of treatment. A withdrawal of the factors from the medium following various periods of treatment revealed that the effects of GMF were readily reversible while morphological changes induced by NGF persisted in its absence.
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PMID:Modulation of growth and of morphological characteristics in glioma cells by nerve growth factor and glia maturation factor. 360 53

The effects of glia maturation factor (GMF) on cell proliferation and differentiation were investigated with 3 astroglioma cells (GE-12, C6, and GA-1), Schwannoma-like cells (354A), and mixed glioma cells (LRM-55). In the exponentially growing phase the growth rates of all glioma cells were enhanced by GMF regardless of the presence or absence of serum, but the factor failed to make the saturation density surpass the control level observed in the medium without GMF even in the chemically defined medium (N2 medium). GMF markedly lowered the saturation density of Schwannoma-like cells in N2 medium. Although GMF increased the intracellular content of S-100 protein 10-fold and 2',3'-cyclic nucleotide phosphohydrolase activity 1.5-fold in Schwannoma-like cells, GMF conversely decreased the S-100 contents and glycerol phosphate dehydrogenase activity in astroglioma cells. All the astroglioma cells secreted into the culture medium large quantities of a growth-promoting factor(s) which had similar chemical properties to those of GMF and stimulated the proliferation of normal glioblasts; but Schwannoma-like cells did not, although they produced a small amount of such a factor(s). These findings imply that astroglioma cells are deprived of the differentiation-promoting response to GMF while Schwannoma-like cells still preserve the response in addition to the proliferative response to GMF.
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PMID:The absence of differentiation-promoting response of astroglioma cells to glia maturation factor. 632 49


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