Morphological and Biochemical Effects of Gangliosides in Neuroblastoma Cells

Leon, Alberta; Facci, Laura; Benvegnù, D.; Toffano, G.

doi:10.1159/000112666

Cited by 122 publications

(45 citation statements)

References 15 publications

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“…It is generally accepted that exogenous gangliosides can induce a variety of cellular modifications: differentiation (Dimpfel et al, 1980;Leon et al, 1982;Roison et al, 1981), membrane dynamics by modifications of the Na+,K ÷ ATPase activity (Leon et al, 1981), adenylate cyclase activity (Partington & Daly, 1979), cell surface sialylation-desialylation processes (Hakomori et al, 1980) and nerve sprouting (Gorio et al, 1980). Thus, in our experiments, gangliosides might have acted through an indirect effect on the cell membrane.…”

Section: Gm3mentioning

confidence: 57%

Involvement of Gangliosides in Rabies Virus Infection

Superti

Hauttecoeur

Morelec

et al. 1986

Journal of General Virology

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SUMMARYThe role of gangliosides in rabies virus infection of chick embryo-related (CER) cells was investigated. Cultured cells were pretreated with neuraminidase to render the cells transiently non-susceptible to viral infection. Incubation of these desialylated cells with gangliosides allowed them to incorporate exogenous gangliosides and they recovered their susceptibility to rabies virus infection. Infection of CER cells was monitored by specific fluorescence 24 h after virus inoculation. The use of individual purified gangliosides or mixtures of two gangliosides to restore cellular susceptibility to viral infection showed that GTlb and GQlb were the most effective. The disialogangliosides were also active, principally GD 1 b, whereas GM 1, GM3 were poorly active and GD3 inactive. Incubation of rabies virus with gangliosides prior to virus infection reduced the percentage of infected cells. The results indicate that highly sialylated gangliosides are part of the cellular membrane receptor structure for the attachment of infective rabies virus. However, it is possible that other glycoconjugates such as glycoproteins or glycolipids also participate as components of a receptor structure for rabies virus.

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Section: Gm3mentioning

confidence: 57%

Involvement of Gangliosides in Rabies Virus Infection

Superti

Hauttecoeur

Morelec

et al. 1986

Journal of General Virology

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“…Many neuronal cell types respond to exogenous gangliosides with concomitant sprouting and extension of net&es, including neuroblastoma cell lines Neuro2A (Dimpfel et al, 198 1;Roisen et al, 198 1;Leon et al, 1982;Byrne et al, 1983;Spoerri, 1983) SB21Bl (Rybak et al, 1983) GOTO, and NB-1 (Tsuji et al, 1983); neuronal cell lines B103 and 104 (Morgan and Seifert, 1979); pheochromocytoma PC1 2 cells (Ferrari et al, 1983;Katoh-Semba et al, 1984); and primary cultures of dorsal root ganglia (Roisen et al, 1981) spinal root ganglia (Hauw et al, 1981) and cerebrum (Dreyfus et al, 1984). Exogenous gangliosides have important effects on the regulation of neural differentiation, not only in tissue culture systems, but there is no doubt that they facilitate regeneration of damaged PNS and CNS neurons (reviewed in Ledeen, 1985).…”

mentioning

confidence: 99%

Interaction of ganglioside GM1 with the B subunit of cholera toxin modulates growth and differentiation of neuroblastoma N18 cells

1991

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The present study uses the B subunit of cholera toxin, a protein that binds specifically to ganglioside GM1, to examine the role of endogenous GM1 in the process of growth and differentiation of mouse neuroblastoma N18 cells. Binding of the B subunit to neuroblastoma N18 cells inhibited DNA synthesis with concomitant induction of differentiation. The B subunit induced pronounced morphological changes: an increase in neurite outgrowth with branched neurites and spinelike processes. The distinct morphological alterations and neuritogenesis in response to the B subunit were also revealed by immunofluorescence with fluorescein-labeled B subunit. The mechanism of the B subunit-induced differentiation is different than that of spontaneous differentiation. Thrombin, a serine protease present in normal serum, inhibits neurite outgrowth induced by the removal of serum from the medium. In contrast, thrombin did not cause retraction of the neurites induced by the B subunit. Thus, thrombin or a thrombin- like protease is not involved in the process of neurite outgrowth mediated through endogenous GM1. The biological effects of the B subunit are due to the binding of the B subunit to ganglioside GM1 and not due to changes in cAMP levels resulting from contaminating A subunit. We used highly purified cloned B subunit that cannot contain any A subunit because it was isolated from a Vibrio cholerae mutant that only expresses the B subunit. Neither the cloned nor commercial preparations of the B subunit induced increases of cAMP in these cells. There was a good correlation between the amount of B subunit bound to the cells and the biological effect. Finally, treatment with neuraminidase, which caused a fourfold increase in the level of membrane GM1 as determined by iodinated cholera toxin binding, enhanced the biological effect of the B subunit. However, neuraminidase treatment alone did not have significant effects, either on DNA synthesis or on morphology of the cells, indicating that elevations in the level of GM1 per se are not sufficient by themselves to cause significant changes in cell growth or differentiation. It seems most likely that the aggregation of endogenous GM1 on the cell surface by the B subunit is responsible for these effects on mouse neuroblastoma N18 cells.

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“…It is generally accepted that exogenous gangliosides can induce a variety of cellular modifications, such as alterations in differentiation (Dimpfel et al, 1980;Leon et al, 1982;Roison et al, 198 I), membrane dynamics, by modifications of Na ÷-, K+-ATPase activity (Leon et al, 1981), adenylate cyclase activity (Partington & Daly, 1979), cell surface sialylation-desialylation processes (Hakomori et al, 1980) and nerve sprouting (Gorio et al, 1980). Thus, in our experiments gangliosides might have acted through an indirect effect on the cell membrane.…”

Section: Discussionmentioning

confidence: 99%

Gangliosides as binding sites in SA-11 rotavirus infection of LLC-MK2 cells

Superti

Donelli

1991

Journal of General Virology

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The chemical nature of receptors involved in the attachment of simian rotavirus (SA-11) to a monkey kidney cell line (LLC-MK2) was investigated. Enzymic treatment of cells before virus infection indicated that membrane proteins and phospholipids are not involved in virus attachment, whereas sialic acid and galactose participate in the receptor structure to differing extents. Incubation ofSA-11 with bovine brain gangliosides before infection strongly reduced its ability to bind to cell membranes. Similar experiments with individual purified gangliosides from bovine brain showed that virus infection was prevented by preincubation with GM1. Moreover, desialylated cells regained susceptibility to virus infection when coated with whole gangliosides or GM1 immediately after Clostridium perfringens neuraminidase treatment. The binding of SA-11 to whole gangliosides or GM1 was quantified by an ELISA procedure. The results suggest that gangliosides, mainly GM 1, are part of the receptor structure for SA-I 1 of susceptible LLC-MK2 cells.

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Morphological and Biochemical Effects of Gangliosides in Neuroblastoma Cells

Cited by 122 publications

References 15 publications

Involvement of Gangliosides in Rabies Virus Infection

Involvement of Gangliosides in Rabies Virus Infection

Interaction of ganglioside GM1 with the B subunit of cholera toxin modulates growth and differentiation of neuroblastoma N18 cells

Gangliosides as binding sites in SA-11 rotavirus infection of LLC-MK2 cells

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