GT3 and its O-acetylated derivative are the principal A2B5-reactive gangliosides in cultured O2A lineage cells and are down-regulated along with O-acetyl GD3 during differentiation to oligodendrocytes
Among the developmentally regulated antigens expressed on the surface of bipotential glial precursors isolated from neonatal rat brain are the gangliosides recognized by the monoclonal antibody A2B5. Immunostaining of thin layer chromatograms showed that oligodendrocyte‐type 2 astrocyte (O2A) progen...
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Veröffentlicht in: | Journal of neuroscience research 1999-08, Vol.57 (3), p.371-380 |
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Zusammenfassung: | Among the developmentally regulated antigens expressed on the surface of bipotential glial precursors isolated from neonatal rat brain are the gangliosides recognized by the monoclonal antibody A2B5. Immunostaining of thin layer chromatograms showed that oligodendrocyte‐type 2 astrocyte (O2A) progenitors in culture express two ganglioside antigens that react strongly with the A2B5 antibody. Both ganglioside antigens are down‐regulated as the cells differentiate to oligodendrocytes, corresponding to the disappearance of cell surface immunostaining by A2B5 in mature oligodendrocytes. By contrast, both gangliosides continue to be expressed when the cells differentiate to type‐2 astrocytes. These two A2B5‐reactive gangliosides in O2A lineage cells were identified as GT3 and O‐acetyl GT3 by using the monoclonal antibody 18B8 that recognizes GT3 and an influenza C virus esterase that specifically removes O‐acetyl moieties from sialic acids. Thin‐layer chromatographic immunostaining with the JONES monoclonal antibody demonstrated that the progenitor cells in culture also express O‐acetyl GD3, which is similarly down‐regulated in oligodendrocytes, but retained in type‐2 astrocytes. The 18B8 and JONES antibodies also immunostained the surface of O2A progenitors. Therefore, expression of GT3 and O‐acetylation of GT3 and GD3 occur during the proliferative and migratory stages of glial cell development. J. Neurosci. Res. 57:371–380, 1999. Published 1999 Wiley‐Liss, Inc. |
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ISSN: | 0360-4012 1097-4547 |
DOI: | 10.1002/(SICI)1097-4547(19990801)57:3<371::AID-JNR9>3.0.CO;2-O |