Publikation: Oligodendrocyte cell death induced by Disialoganglioside GD3
Dateien
Datum
Autor:innen
Herausgeber:innen
ISSN der Zeitschrift
Electronic ISSN
ISBN
Bibliografische Daten
Verlag
Schriftenreihe
Auflagebezeichnung
URI (zitierfähiger Link)
Internationale Patentnummer
Link zur Lizenz
Angaben zur Forschungsförderung
Projekt
Open Access-Veröffentlichung
Sammlungen
Core Facility der Universität Konstanz
Titel in einer weiteren Sprache
Publikationstyp
Publikationsstatus
Erschienen in
Zusammenfassung
Oligodendrocytes are target of an autoimmune attack in demyelinating diseases. The crucial mediator causing oligodendrocyte loss and myelin degradation has not yet been defined. In order to investigate degeneration of murine oligodendrocytes in vitro, a culture enriched in oligodendrocytes was established. 30 of all cells developed to mature oligodendrocytes, expressing myelin oligodendrocyte glycoprotein. In this culture, no sensitivity of oligodendrocytes to inflammatory cytokines or to stimulation of CD95 was observed. Inhibition of transcription or translation did not sensitise oligodendrocytes for cytokines or CD95-ligation. This result finds correlates and contrary examples in the literature and indicates that these stimuli are not the only ones involved in oligodendrocyte damage in vivo.
Althoug ganglioside levels are alterated in demyelination, gangliosides have not been studied before with regard to demyelination. Disialoganglioside GD3, but no structurally similar ganglioside, damaged oligodendrocytes with high cell type specificity. Parallel evaluation of chemically synthesised and bovine brain-derived GD3 ensured the purity of the effect excluding toxcitiy caused by contamination.
GD3 induced apoptotic cell death in oligodendrocytes, causing chromatin condensation, phosphatidylserine exposure, cytochrome c release, activation of caspase-3 and maintenance of cellular integrity. The involvement of caspases seemed to be of minor importance in GD3 induced oligodendrocyte death, as their inhibition did not prevent cell death. GD3-caused oligodendrocyte death was inhibited in cells overexpressing human bcl-2. We conclude that mitochondria play an essential role in GD3 triggered apoptosis.
That microglia synthesises GD3 in vivo was observed before. This study shows that microglia is able to release GD3 into the culture medium upon activation by inflammatory stimuli. This provides evidence for GD3 as a microglia-derived mediator during inflammation.
Zusammenfassung in einer weiteren Sprache
Fachgebiet (DDC)
Schlagwörter
Konferenz
Rezension
Zitieren
ISO 690
SIMON, Bernadett, 2000. Oligodendrocyte cell death induced by Disialoganglioside GD3 [Dissertation]. Konstanz: University of KonstanzBibTex
@phdthesis{Simon2000Oligo-8568, year={2000}, title={Oligodendrocyte cell death induced by Disialoganglioside GD3}, author={Simon, Bernadett}, address={Konstanz}, school={Universität Konstanz} }
RDF
<rdf:RDF xmlns:dcterms="http://purl.org/dc/terms/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:void="http://rdfs.org/ns/void#" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/server/rdf/resource/123456789/8568"> <dcterms:title>Oligodendrocyte cell death induced by Disialoganglioside GD3</dcterms:title> <dcterms:issued>2000</dcterms:issued> <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/> <dcterms:alternative>Oligodendrozyten-Zelltod induziert durch Disialogangliosid GD3</dcterms:alternative> <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/> <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/8568"/> <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/8568/1/BernaDissertationInternet.pdf"/> <dcterms:abstract xml:lang="eng">Oligodendrocytes are target of an autoimmune attack in demyelinating diseases. The crucial mediator causing oligodendrocyte loss and myelin degradation has not yet been defined. In order to investigate degeneration of murine oligodendrocytes in vitro, a culture enriched in oligodendrocytes was established. 30 of all cells developed to mature oligodendrocytes, expressing myelin oligodendrocyte glycoprotein. In this culture, no sensitivity of oligodendrocytes to inflammatory cytokines or to stimulation of CD95 was observed. Inhibition of transcription or translation did not sensitise oligodendrocytes for cytokines or CD95-ligation. This result finds correlates and contrary examples in the literature and indicates that these stimuli are not the only ones involved in oligodendrocyte damage in vivo.<br />Althoug ganglioside levels are alterated in demyelination, gangliosides have not been studied before with regard to demyelination. Disialoganglioside GD3, but no structurally similar ganglioside, damaged oligodendrocytes with high cell type specificity. Parallel evaluation of chemically synthesised and bovine brain-derived GD3 ensured the purity of the effect excluding toxcitiy caused by contamination.<br />GD3 induced apoptotic cell death in oligodendrocytes, causing chromatin condensation, phosphatidylserine exposure, cytochrome c release, activation of caspase-3 and maintenance of cellular integrity. The involvement of caspases seemed to be of minor importance in GD3 induced oligodendrocyte death, as their inhibition did not prevent cell death. GD3-caused oligodendrocyte death was inhibited in cells overexpressing human bcl-2. We conclude that mitochondria play an essential role in GD3 triggered apoptosis.<br />That microglia synthesises GD3 in vivo was observed before. This study shows that microglia is able to release GD3 into the culture medium upon activation by inflammatory stimuli. This provides evidence for GD3 as a microglia-derived mediator during inflammation.</dcterms:abstract> <dc:format>application/pdf</dc:format> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/> <dc:rights>terms-of-use</dc:rights> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:44:45Z</dc:date> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:44:45Z</dcterms:available> <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/8568/1/BernaDissertationInternet.pdf"/> <foaf:homepage rdf:resource="http://localhost:8080/"/> <dc:language>eng</dc:language> <dc:contributor>Simon, Bernadett</dc:contributor> <dc:creator>Simon, Bernadett</dc:creator> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> </rdf:Description> </rdf:RDF>