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PubMed1991

Shedding of human neuroblastoma gangliosides.

Gangliosides shed by tumor cells are implicated in modulating tumor formation. For example, rapid progression of human neuroblastoma tumors is associated with high circulating levels of shed GD2 ganglioside. To elucidate the kinetic and qualitative characteristics of tumor cell ganglioside shedding, which is difficult to accomplish in vivo, we examined this process in LAN-5 human neuroblastoma cells in vitro. Three major gangliosides, GD2, GM2 and GT1b, comprise 82% of the mean total of 38 nmol LBSA/10(8) cells. These molecules are shed very rapidly (1-3 pmol/10(6) cells per h, or approx. 0.5% of the total cell gangliosides per h). Quantitative and qualitative characteristics of ganglioside shedding are remarkably constant over a 40-fold range of cell density. Not only GD2, but every major carbohydrate species is shed, in proportion to its concentration in the cell, with slightly greater shedding of ceramide subspecies containing shorter chain fatty acids. These findings were confirmed in three other neuroblastoma cell lines, LAN-1, IMR and KCNR. We suggest that the high expression and rapid generalized shedding of human neuroblastoma tumor gangliosides results in significant in vivo accumulation of these biologically active molecules during tumor growth.

Animals↗
PubMed1992

Generation of one set of monoclonal antibodies specific for b-pathway ganglio-series gangliosides.

We established six murine monoclonal antibodies (MAbs) specific for b-pathway ganglio-series gangliosides by immunizing C3H/HeN mice with these purified gangliosides adsorbed to Salmonella minnesota mutant R595. The binding specificities of these MAbs were determined by an enzyme-linked immunosorbent assay and immunostaining on thin-layer chromatogram. These six MAbs, designated GGB19, GMR2, GMR7, GGR12, GMR5, and GGR13 reacted strongly with the gangliosides GD3, O-Ac-GD3, GD2, GD1b, GT1b, and GQ1b, respectively, that were used as immunogens. All these MAbs except GGB19 showed highly restricted binding specificities, reacting only with the immunizing ganglioside. None of other various authentic gangliosides or neutral glycolipids were recognized. On the other hand, MAb GGB19 exhibited a broader specificity, cross-reacting weakly with O-Ac-GD3, GQ1b, and GT1a, but not with other gangliosides or neutral glycolipids. Using these MAbs, we determined the expression of these gangliosides, especially GD1b, GT1b, and GQ1b on mouse, rat, and human leukemia cells. GD1b was expressed on rat leukemia cells, but not on mouse and human leukemia cells tested. Neither GT1b nor GQ1b was detected in these cell lines.

Animals↗
PubMed1993

Biosynthesis and shedding of murine lymphoma gangliosides.

Ganglioside biosynthesis and subsequent shedding are a potential mechanism contributing to tumor cell escape from the host immune response. As a first step in identifying active molecular species, structural characterization and quantification of the purified individual cellular and shed gangliosides of YAC-1 murine lymphoma cells were undertaken. These studies uncovered three striking changes in ganglioside metabolism in cells passaged in vivo, compared with cells cultured in vitro. (i) Marked inhibition of GalNAcGM1b synthesis: GM1b was present in an equal proportion to its biosynthetic product GalNAcGM1b in vitro, but was present in a 6-fold higher concentration in vivo. (ii) Marked inhibition of NeuGc synthesis: NeuGc, present in vitro in an up to 7-fold higher concentration than its biosynthetic precursor NeuAc, was decreased in relative concentration in vivo (1:1). (iii) Selectivity of shedding: ganglioside shedding in vitro was generalized with respect to both carbohydrate structure and ceramide structure (mainly d18:1-C24:1 and d18:1-C16:0), while in vivo, there was selective shedding of gangliosides containing NeuGc and the shorter chain fatty acid. The reduced synthesis of NeuGc and of GalNAcGM1b in vivo, and the selective shedding of more polar ganglioside species, also in vivo, show that the extracellular environment can markedly affect cellular ganglioside metabolism.

Animals↗
PubMed1984

Inhibition of interleukin-2-dependent cytotoxic T-lymphocyte growth by gangliosides.

Previous work has shown that exogenous gangliosides suppress lectin-induced T-lymphocyte mitogenesis in mixed populations of immune cells. As one potential cellular site of this inhibition, the influence of gangliosides on interleukin-2-dependent T-cell proliferation was tested, using cultures of cytotoxic T cells (strain CT-6). Incubation of CT-6 cells with mixed bovine brain gangliosides resulted in a dose-dependent inhibition of cell proliferation. Cell viability was unaffected by gangliosides, and the inhibition was totally reversed when the gangliosides were removed. Individual purified gangliosides were tested and GM2 was most inhibitory (I50 = 15 microM). GD1a and GT1b were somewhat less potent, whereas GM1 and GM3 were only weakly inhibitory. Various nonpolar lipids, sulfatides, and sialic acid did not inhibit CT-6 cell growth. The results suggest that a primary mechanism whereby gangliosides inhibit lectin-induced lymphocyte mitogenesis is by inhibition of the interleukin-2-stimulated proliferation of T cells in these cultures.

Animals↗
PubMed1996

Gangliosides in phospholipid bilayer membranes: interaction with tetanus toxin.

The interaction between tetanus toxin and its fragments with gangliosides and negatively charged phosphatidylglycerols has been studied in phosphatidylcholine host membranes by protein circular dichroism measurement, calorimetry to determine lipid phase transitions, and by fluorescence spectroscopy to follow the toxin-induced pore formation by measuring the release of intravesicular entrapped dye. CD-spectroscopic secondary structure analysis showed conformational change of the toxin only in the presence of GT1b clearly demonstrating the involvement of the ganglioside headgroups for this lipid-protein-interaction. In a dot-blot analysis we showed that fragment C binds to GT1b in reconstituted vesicles and that this fragment is then accessible to a fragment C specific antibody which is only possible if fragment C is exposed at least partially on the surface of the vesicle. Our calorimetric study demonstrates the preferential binding of tetanus toxin to ganglioside GT1b. However, this protein is also able to bind to other gangliosides and also to negatively charged phospholipids causing phase separation due to electrostatic interaction. Since tetanus toxin preferentially binds short chain phosphatidylglycerol, we conclude that the protein adopts lipids with respect to charge, head group structure and chain length from the bulk phase. One consequence of this lipid-protein interaction is the ability of tetanus toxin to permeabilize lipid vesicles. Pore formation is favoured in the presence of GT1b in phosphatidylcholine membranes but only at a sufficiently high enough ganglioside content. Gangliosides others than GT1b are less effective in pore formation. In the presence of negatively charged phosphatidylglycerol tetanus toxin causes a dye release which in contrast to GT1b-containing vesicles is not saturable. We conclude that tetanus toxin acts in combination with a given number of GT1b molecules. Twenty ganglioside molecules are found to be necessary to form the stable pore. Other negatively charged lipids also cause the toxin to intercalate into the membrane but in this case the release velocity is determined by the formation of membrane defects.

Circular Dichroism↗
PubMed1987

Ganglioside abnormalities associated with failed neural differentiation in a T-locus mutant mouse embryo.

The T-locus on mouse chromosome 17 contains a number of mutations that disrupt cellular differentiation and embryonic development. Because of their purported role in neuronal differentiation and brain development, gangliosides were studied in mouse embryos homozygous for two T-locus mutations: T and twl. Mice homozygous for the dominant T mutation die from failed mesodermal differentiation in the notochord, whereas mice homozygous for the recessive twl mutation die from failed neural differentiation in the ventral portion of the neural tube. No major ganglioside abnormalities were found in T/T mutant embryos at Embryonic Day 10 (E-10). In contrast, E-11 twl/twl mutants expressed a marked deficiency of the tetrasialoganglioside GQ1. Since this ganglioside migrates with GQ1b in three different thin-layer solvent systems, it may have the same structure as GQ1b. To gain insight into regional distribution, gangliosides were examined in head regions and body regions of normal (+/+) E-11 embryos. The ganglioside composition of these regions was the same as that of the whole embryo, with GM3 and GD3 comprising about 75% of the total ganglioside distribution. Moreover, N-acetylneuraminic acid was the only sialic acid species detectable in the E-10 and the E-11 embryos. These findings indicate that N-acetylneuraminic acid-containing gangliosides are synthesized actively in E-10 and E-11 mouse embryos and also suggest that the GQ1 deficiency in the twl/twl mutants is closely associated with failed neural differentiation.

Animals↗
PubMed1985

Complement-dependent immune damage to liposomes containing gangliosides.

Rabbit antiserum against mixed beef brain gangliosides served as an excellent source of antibodies to gangliosides GM1, GM3, GD1a, GD1b, and GT1b. Immune potency of antiserum was determined by complement-dependent damage to liposomes containing gangliosides as antigens. Antibody levels in antiserum to mixed gangliosides, when tested against individual gangliosides, were equivalent or superior to the levels obtained by immunization of rabbits with purified individual gangliosides. Naturally occurring antibodies to GM1, GD1b, and GM3 were observed in preimmunization sera. The levels of these natural antibodies, although easily high enough to serve as antiserum sources for liposome assay, were increased substantially following immunization. High titers of antibodies to GM1 and GD1b were observed in certain individual guinea pig sera, and selection of individual non-reacting guinea pig sera was necessary in order to obtain suitable complement sources when testing rabbit antibodies to liposomal GM1 and GD1b. The maximum plateau level of trapped glucose release from liposomes in the presence of saturating levels of antigen, antiserum, and complement was influenced strongly both by the method of removing untrapped glucose during liposome preparation and by the type of ganglioside incorporated into the lipid bilayer.

Animals↗
PubMed1991

Age-related alteration of brain gangliosides in senescence-accelerated mouse (SAM)-P/8.

The senescence-accelerated mouse (SAM)-P/8 was examined with respect to changes in the content and composition of brain gangliosides during aging from juvenile to senescence. The gangliosides were compared with those of control mice, senescence-accelerated resistant mouse (SAM)-R/1. The ganglioside contents in the whole brains of SAM-P/8 and -R/1 were at almost constant level from 0.5 to 6 months, but decreased thereafter until senescence to about 80% of the levels reached at the younger ages. Upon aging, the ganglioside compositions changed with an increase of GM1, and decreases of GD1a, GD1b and GT1b in both strains (GT1b greater than GD1a greater than GD1b). A minor component, GM3 was two to four fold higher in the molecular distributions of the whole brain gangliosides of SAM-P/8 than those of -R/1 at any age examined throughout the life span. The regional gangliosides in olfactory bulb, cerebral cortex, hippocampus, hypothalamus, cerebellum, corpora quadrigemina region, brain stem and medulla oblongata were compared between the two strains at the age of three months. The ganglioside contents in the brain stem and medulla oblongata were lower in SAM-P/8 than -R/1, but there was no significant difference between the two strains in the other regions. As a minor component, GM3 was found to occur in a higher concentration in SAM-P/8 than -R/1 in all brain regions examined, except in the olfactory bulb where GM3 was detected as a major component with no difference in the distribution level between the two strains.

Aging↗
PubMed1989

Modulation of human macrophage functions by gangliosides.

In human tumors of neuroectodermal origin cell surface expression of individual gangliosides is either increased or decreased relative to comparable normal cells. We have previously shown that gangliosides shed from melanoma cells can immunomodulate T cell activity. Monocytes/macrophages (m/m) are known to play an important role as accessory and effector cells in immune responses. We therefore investigated the effect of exogenous gangliosides derived from melanoma on m/m functions in vitro. Gangliosides commonly expressed on human melanoma such as GM3, GD3, GM2, and GD2 were investigated, as well as GM1, a major component of human neural tissue. Monocytes were isolated from human peripheral blood mononuclear cell populations, treated with gangliosides in vitro, and evaluated in several functional assays. Treatment of m/m with GM2 and GM3 gave the greatest inhibition of Fc receptor expression. GM1 and GD3 on the other hand most inhibited the production of interleukin-1 (IL-1) by m/m. Production of tumor necrosis factor (TNF) like monocytoxin was not affected by incubation with individual gangliosides. These studies suggest that individual melanoma gangliosides have different regulatory effects on m/m functions.

Gangliosides↗
PubMed1982

Development changes and regional variation in the ganglioside composition of the rat hippocampus.

Individual gangliosides were extracted and quantified from intact and subregionally dissected hippocampal formations during the first 3 weeks of postnatal development in the rat. The 4 major gangliosides were all found to be rapidly increasing relative to brain weight prior to the onset of significant synaptogenesis, but quantitative changes in the final proportion of each ganglioside resulted from different rates of accumulation of gangliosides D1a, D1b, and T1b, beginning about the time of synaptic maturation and dendritic arborization but prior to the onset of myelination and neurophysiological activity. A ganglioside pattern difference characterized by lower levels of T1b and D1b in the area dentata of middle and dorsal aspects of the hippocampal formation coincides with developmental gradients previously observed by morphogenetic criteria for these subregions. These ganglioside differences may thus be developmentally regulated, but the persistence into adulthood of higher levels of D1a in the dentate area suggests that some ganglioside pattern differences may be intrinsic to the unique neuronal cell populations present in different areas of the hippocampus.

Animals↗
PubMed1983

Gangliosides enhance neurite outgrowth in PC12 cells.

Gangliosides are surface membrane components that have been suggested to play a significant role in the regulation of many cellular events including neuronal differentiation, growth and regeneration. We have chosen PC12 cell as a model system to study the influence of exogenously added glycosphyngolipids on in vitro differentiation and regeneration. A mixture of bovine brain gangliosides, (GM1 21%, GD1a 39.7%, GD1b 16% and GT 19%) or purified GM1 and GT respectively were added to culture media containing NGF on plating day and their effect was monitored on alternate days starting on day 5. The degree and rate of fiber outgrowth was significantly enhanced by media containing gangliosides at a concentration of 10(-6), 10(-7) M when serum was left out and 10(-3), 10(-4) M when serum was added to the culture medium. The stimulating ganglioside action required the presence of NGF to induce neurite outgrowth. However, binding studies indicated that exogenous gangliosides do not affect NGF binding to PC12 cells, therefore their stimulatory action may be separated from the interaction between NGF and its receptors. Subculturing of NGF-treated cells for 10 days demonstrated that gangliosides treatment also enhanced the NGF stimulated regeneration of neurites. Gangliosides may be incorporated at the level of cell surface, thereby affecting and facilitating membrane phenomena involved in neurite outgrowth.

Animals↗
PubMed1986

Neuritogenic and metabolic effects of individual gangliosides and their interaction with nerve growth factor in cultures of neuroblastoma and pheochromocytoma.

The 4 major ganglioside species, GM1, GD1a, GD1b and GT1b (200 micrograms/ml), were tested individually for the ability to stimulate neuronal trophic responses. The growth parameters measured were: morphologic changes, quantitated by computer-assisted morphometry of neurite length and number per soma, and metabolic changes, indicated by alterations in ornithine decarboxylase activity (ODC). In addition, the interaction of each ganglioside with nerve growth factor (NGF) was investigated with an NGF-responsive pheochromocytoma PC12 cell line and NGF-insensitive neuroblastoma Neuro-2a cultures. PC12 cells responded to gangliosides only in the presence of NGF (20 micrograms/ml): GM1 produced the greatest morphologic response, but did not alter metabolic levels; GT1b increased both parameters. The presence (5 micrograms/ml) or absence of NGF did not have an effect on the ganglioside-mediated morphologic responses of Neuro-2a cells to each species: GD1b elicited the greatest increase in neurite length, while GD1a and GT1b stimulated both length and number. In contrast, while GT1b alone was able to elevate ODC activity independently of NGF, the simultaneous exposure of Neuro-2a cultures to NGF and GM1 or GD1a resulted in a stimulation of cellular metabolism. These results indicate that each ganglioside species has a specific target action in the stimulation of different trophic responses and that performance in one category is not a predictor of the result in another. In addition, it is possible to confer a sensitivity to NGF by simultaneous treatment with specific gangliosides. This indicates that membrane gangliosides may modulate the actions of neurotrophic factors.

Animals↗
PubMed1996

Elevated GM2 ganglioside is associated with dendritic proliferation in normal developing neocortex.

Mature pyramidal neurons of cerebral cortex in several neuronal storage diseases elaborate ectopic dendrites. These dendrites appear specifically on pyramidal neurons containing elevated GM2 ganglioside and a variety of studies support the hypothesis that this ganglioside is responsible for inducing the new dendrite growth. To determine whether a similar association between GM2 ganglioside and dendrite growth occurs in normal neurons, we used an antibody to localize GM2 in developing cat neocortex. Our results show that GM2 ganglioside is elevated in normal cortical neurons during the period when dendritogenesis is occurring, but is greatly diminished in these cells after dendritic differentiation is complete. Elevations of GM2 occur in deep neurons earlier than in superficial ones, a sequence that corresponds closely to the inside-first, outside-last progression of cortical neuron differentiation. Ultrastructurally, GM2 immunoreactivity is found sequestered in vesicles with a distribution that coincides with sites of ganglioside synthesis and transport. The close association between elevated GM2 ganglioside and dendrite growth in cortical pyramidal neurons during normal development, coupled with a similar correlation between GM2 and ectopic dendritogenesis in neuronal storage diseases, support the view that this specific ganglioside plays a pivotal role in regulating dendritogenesis.

Age Factors↗
PubMed1989

Lack of suppression by gangliosides of humoral or cellular immunity in vivo.

Gangliosides inhibit the proliferative responses of murine and human lymphocytes in vitro, and it has been suggested that they are immunosuppressive in vivo, although no in vivo studies have been performed. In view of the use of gangliosides to treat patients with a variety of neurological disorders, experiments were undertaken to evaluate the possible immunomodulatory effects of gangliosides in vivo. BALB/c mice were injected 5 days a week with buffer, mixed brain gangliosides, or GM1 ganglioside at dosage levels of 30 mg/kg, 60 mg/kg or 90 mg/kg. After 30 days of treatment, the mice were immunized with keyhole limpet hemocyanin or pneumococcal type III polysaccharide and the ganglioside treatment was continued. No differences between treated and control groups were noted in either the magnitude or duration of the antibody response. No differences between groups were noted in the proliferative responses of splenic mononuclear cells to concanavalin A or allogeneic antigens after 9-10 weeks of treatment, nor in the generation of cytotoxic effector cells after 90 days of treatment. Thus, despite the well-documented immunosuppressive effects of gangliosides in vitro, no evidence for a suppressive effect on humoral or cellular immunity in vivo was obtained in these studies.

Animals↗
PubMed1995

The chemical constitution of gangliosides of the vertebrate nervous system.

Glycosphingolipids are uniquely distinguished amongst the glycoconjugates by the apparently systematic structuring of their ceramide-linked carbohydrate moieties. These often highly complex oligosaccharides provide a structural repertoire that may vary considerably according to cell types and animal species. However, as a possible reflection of their specific functional role in the central nervous system, the brain glycosphingolipids of all vertebrates follow the same principles of carbohydrate structuring with only minor variations: the anabolically early addition of sialic acid to lactosylceramide (Gal beta 4Glc beta Cer-->NeuAc alpha 3Gal beta 4Glc beta Cer) in central nervous tissue results in the preferential formation of 'gangliosides', i.e., sialic acid-containing glycosphingolipids. Higher gangliosides result from extensions of sialo-lactosylceramide by addition of nucleotide-activated monosaccharides. In consequence, gangliosides of the vertebrate central nervous system consist of ceramide-linked sialo-oligosaccharides of varying chain length with a ganglio-series core carbohydrate, i.e., GalNAc beta 4Gal beta 3GalNAc beta 4Gal beta 4Glc beta < 0. Substitution by mono-, bis-, or tris-sialo-groups may variably be at the galactoside- and N-acetylgalactosaminide residues in 3- and 6-positions of the ganglio-series oligosaccharides, respectively. Ganglioside, which is derived by sialylation of galactosylceramide, NeuAc alpha 3Gal beta Cer, is a characteristic constituent of glial cells. In nerve tissue, gangliosides of the lacto-(Gal beta(3GlcNAc beta 3Gal beta)n4Glc beta <) and the neolacto-series (Gal beta(4GlcNAc beta 3Gal beta)n4Glc <) are more characteristic of vertebrate peripheral nerves and neuroectoderm-derived tumours. Recent studies using monoclonal antibodies have revealed that various single ganglioside components are specifically distributed in nervous tissues. This finding adds a new dimension to the earlier notion that gangliosides are involved in membrane related phenomena including cell to cell interactions, as well as, the modulation of signalling mechanisms.

Animals↗
PubMed1988

Stimulation of platelet adhesion and activation by ganglioside GD3 adsorbed to plastic.

Platelet interaction with gangliosides GD3, GM3, GM1, GD1a and GT1b has been investigated. These gangliosides were previously identified in the vessel wall and ganglioside GD3 was found to accumulate selectively in the intima of atherosclerotic vessels. Gangliosides were adsorbed to plastic and incubated with 51Cr-labeled platelets. The adhesion of gel-filtered platelets to ganglioside GD3 was 3-4 times higher than to other immobilized gangliosides and to albumin-treated plastic. As was shown by scanning electron microscopy, GD3 stimulated intensive spreading of adherent platelets and formation of surface-bound aggregates, while only single unspread platelets were present on the surfaces coated with other gangliosides. GD3 isolated from milk and from human aorta possess the same stimulating activity. Platelet adhesion to GD3 decreased significantly in the presence of the stable prostacyclin analogue, carbacyclin.

Adsorption↗
PubMed1995

Gangliosides enhance IgE receptor-dependent histamine and LTC4 release from human mast cells.

Releasability of mast cells and basophils to an IgE-dependent stimulus is regulated by extra- and intracellular factors which are only partly understood. As gangliosides are known to modulate receptor-dependent processes in various cell types, we have evaluated the effect of these molecules on mast cell mediator release. Human skin mast cells and the human mast cell line HMC1 were pretreated with the gangliosides GM2, GM3 and GD1a as well as with asialo-GM3, heparin and buffer alone (controls). After washing, the cells were stimulated with anti-IgE, calcium ionophore A 23187, N-FMLP or substance P. All gangliosides but not asialo-GM3 and heparin augmented anti-IgE-induced mediator release in a dose-dependent fashion, whereas the release to A 23187, N-FMLP and substance P remained unaffected. Only sequential but not simultaneous addition of ganglioside and anti-IgE showed an enhancement in mediator release compared to controls. Mediator release in both ganglioside-pretreated cells and controls was calcium-dependent and could be inhibited by pretreatment of cells with staurosporine or dibutyryl cAMP, indicating an unchanged signal transduction. Gangliosides appear to specifically optimize IgE-receptor-ligand interaction and alterations in cellular gangliosides could thus induce enhanced releasability as observed in atopics.

Cell Line↗
PubMed1996

Cell-specific regulation of the stably expressed serotonin 5-HT1A receptor and altered ganglioside synthesis.

Neurotransmission is dependent on the presence of neuronal receptors at the synapses, and important cell surface molecules such as gangliosides are pivotal in the maintenance of synaptic contacts. To study the interrelationship between these two classes of molecules, we achieved stable expression of the hippocampus- and CNS-localized serotonin 1A receptor (5-HT1A-R) in three 5-HT1A-R-deficient neuronal cell lines and also the control, non-neural CHO cells. A strong passage dependence of 5-HT1A-R expression, as measured by mRNA levels as well as membrane binding to the selective agonist [3H]8-OH-DPAT, was observed only in the HN2 (hippocampal) and NCB-20 (CNS) cells which are derived from tissues of natural occurrence of the 5-HT1A-R. A paradigm of stress was obtained by carrying out continuous culture of cells without feeding. During this time a dramatic increase in 5-HT1A-R mRNA and [3H]8-OH-DPAT binding was observed only in the neuronal cells after confluence and during decreased cell viability (days 10/11). This was not due to differentiation, since deliberate serum deprivation and differentiation of cells did not result in any dramatic increase in 5-HT1A-R expression. Analysis of ganglioside synthesis by pulse labeling of the transfected cells produced striking results. In the dorsal root of the ganglion (DRG) derived F-11 cells which show low but significant levels of complex gangliosides before transfection, the mere presence of the serotonin 1A receptor resulted in a dramatic increase in synthesis of gangliosides comigrating with GM2, GD1a, GD1b, and GT1b (20-fold by densitometry). In contrast, there was only a 2-fold increase in the overall content of complex gangliosides in the presence of the 5-HT1A-R. In the NCB-20 cells which contain only GD1a but no GD1b or GT1b before transfection, a decrease in GD1a synthesis was observed following transfection. Also agonist (8-OH-DPAT) binding to the serotonin 1A receptor in NCB-20 cells produced a 3-fold increase in synthesis of a ganglioside comigrating with GM3. Thus, our neuroblastoma transfectants help demonstrate stress-induced regulation of the 5-HT1A-R, which in turn exerts a strong and cell type-specific control over such essential cell-surface determinants like gangliosides.

Animals↗