Metabolism of cholesterol, phosphatidylethanolamine and stearylamine analogues of GM1 ganglioside by rat glioma C6 cells
Autor: | Peter H. Fishman, Tadeusz Pacuszka |
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Rok vydání: | 1991 |
Předmět: |
Molecular Sequence Data
Biophysics G(M1) Ganglioside Biology medicine.disease_cause Biochemistry chemistry.chemical_compound symbols.namesake Endocrinology Glycolipid Tumor Cells Cultured medicine Animals Amines Monensin Phosphatidylethanolamine chemistry.chemical_classification Ganglioside Phosphatidylethanolamines Cholera toxin Chloroquine Glioma Metabolism Golgi apparatus Oligosaccharide Rats Cholesterol Carbohydrate Sequence chemistry Cell culture symbols |
Zdroj: | Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism. 1083:153-160 |
ISSN: | 0005-2760 |
DOI: | 10.1016/0005-2760(91)90036-h |
Popis: | Tritium-labeled neoglycolipids consisting of the oligosaccharide of ganglioside GM1 attached to cholesterol (GM1OSNH-X-CHOL), phosphatidylethanolamine (GM1OS-PE) and stearylamine (GM1OSNHC18) were synthesized and their uptake and metabolism by GM1-deficient rat glioma C6 cells were determined. When the neoglycolipids were added to serum-free culture medium, all three were rapidly taken up by the cells and initially inserted into the plasma membrane based on their resistance to trypsia and their ability to bind cholera toxin. With time, the neoglycolipids underwent internalization as the ratio of cell-associated radioactivity to cell surface toxin binding increased; this process was slow for GM1OSNH-X-CHOL and GM1OS-PE and rapid for GM1OSNHC18. Analysis of lipids extracted from the cells indicated that the neoglycolipids also underwent metabolism to GDtaOS-based analogues. In addition, GM1OSNH-X-CHOL and GM1OSNHC18 were degraded to their GM2OS-based analogues, whereas GM2OS-PE was not detected. In contrast, large amounts of 3H were recovered in the medium from cells treated with GM1OS-PE and the label was associated with material that behaved neither as an oligosaccharide or a neoglycolipid. In the presence of monensin or chloroquine, metabolism of the three neoglycolipids was inhibited. Thus, GM1OS-based neoglycolipids were taken up by the cells, internalized and sorted both to the Golgi apparatus (sialylated to GD1aOS-based analogues) and to lysosomes (hydrolyzed to GM2OS-based analogues). The rate and extent of these processes, however, were strongly influenced by the nature of lipid moiety. |
Databáze: | OpenAIRE |
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