Disialoganglioside GD3 is released by microglia and induces oligodendrocyte apoptosis

Lade...
Vorschaubild
Dateien
Leist_Simon_Disialoganglioside.pdf
Leist_Simon_Disialoganglioside.pdfGröße: 341.59 KBDownloads: 678
Datum
2002
Autor:innen
Simon, Bernadett
Malisan, Florence
Testi, Roberto
Herausgeber:innen
Kontakt
ISSN der Zeitschrift
Electronic ISSN
ISBN
Bibliografische Daten
Verlag
Schriftenreihe
Auflagebezeichnung
ArXiv-ID
Internationale Patentnummer
EU-Projektnummer
DFG-Projektnummer
Projekt
Open Access-Veröffentlichung
Sammlungen
Gesperrt bis
Titel in einer weiteren Sprache
Forschungsvorhaben
Organisationseinheiten
Zeitschriftenheft
Publikationstyp
Zeitschriftenartikel
Publikationsstatus
unikn.publication.listelement.citation.prefix.version.undefined
Cell Death and Differentiation. 2002, 9(7), pp. 758-767. ISSN 1350-9047. Available under: doi: 10.1038/sj.cdd.4401027
Zusammenfassung

Increased brain ganglioside levels are a hallmark of various neuroinflammatory pathologies. Here, we provide evidence that murine microglia can secrete disialoganglioside GD3 upon exposure to inflammatory stimuli. Comparison of different neural cell types revealed a particular and specific sensitivity of oligodendrocytes towards exogenous GD3. Oligodendrocyte death triggered by GD3 was preceded by degeneration of cellular processes, and associated with typical features of apoptosis, such as chromatin condensation, exposure of phosphatidylserine, release of cytochrome c from mitochondria, and loss of mitochondrial membrane potential, followed by the loss of plasma membrane integrity and detachment of disintegrated oligodendrocytes. Overexpression of bcl-2 partially protected oligodendrocytes from death. In contrast, treatment with the pan-caspase inhibitor zVAD-fmk did not prevent phosphatidylserine exposure, chromatin margination at the nuclear periphery, and death, although caspase-3 was blocked. Thus, GD3 produced by microglia under neuroinflammatory conditions may function as a novel mediator triggering mitochondria-mediated, but caspase-independent, apoptosis-like death of oligodendrocytes.

Zusammenfassung in einer weiteren Sprache
Fachgebiet (DDC)
570 Biowissenschaften, Biologie
Schlagwörter
oligodendrocyte, microglia, apoptosis, ganglioside, mitochondria, demyelination
Konferenz
Rezension
undefined / . - undefined, undefined
Zitieren
ISO 690SIMON, Bernadett, Florence MALISAN, Roberto TESTI, Pierluigi NICOTERA, Marcel LEIST, 2002. Disialoganglioside GD3 is released by microglia and induces oligodendrocyte apoptosis. In: Cell Death and Differentiation. 2002, 9(7), pp. 758-767. ISSN 1350-9047. Available under: doi: 10.1038/sj.cdd.4401027
BibTex
@article{Simon2002-07Disia-20169,
  year={2002},
  doi={10.1038/sj.cdd.4401027},
  title={Disialoganglioside GD3 is released by microglia and induces oligodendrocyte apoptosis},
  number={7},
  volume={9},
  issn={1350-9047},
  journal={Cell Death and Differentiation},
  pages={758--767},
  author={Simon, Bernadett and Malisan, Florence and Testi, Roberto and Nicotera, Pierluigi and Leist, Marcel}
}
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/123456789/20169">
    <dc:creator>Simon, Bernadett</dc:creator>
    <dcterms:bibliographicCitation>Cell Death &amp; Differentiation ; 9 (2002), 7. - S. 758-767</dcterms:bibliographicCitation>
    <dc:contributor>Simon, Bernadett</dc:contributor>
    <dcterms:title>Disialoganglioside GD3 is released by microglia and induces oligodendrocyte apoptosis</dcterms:title>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:contributor>Malisan, Florence</dc:contributor>
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <dc:language>eng</dc:language>
    <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/20169/2/Leist_Simon_Disialoganglioside.pdf"/>
    <dcterms:abstract xml:lang="eng">Increased brain ganglioside levels are a hallmark of various neuroinflammatory pathologies. Here, we provide evidence that murine microglia can secrete disialoganglioside GD3 upon exposure to inflammatory stimuli. Comparison of different neural cell types revealed a particular and specific sensitivity of oligodendrocytes towards exogenous GD3. Oligodendrocyte death triggered by GD3 was preceded by degeneration of cellular processes, and associated with typical features of apoptosis, such as chromatin condensation, exposure of phosphatidylserine, release of cytochrome c from mitochondria, and loss of mitochondrial membrane potential, followed by the loss of plasma membrane integrity and detachment of disintegrated oligodendrocytes. Overexpression of bcl-2 partially protected oligodendrocytes from death. In contrast, treatment with the pan-caspase inhibitor zVAD-fmk did not prevent phosphatidylserine exposure, chromatin margination at the nuclear periphery, and death, although caspase-3 was blocked. Thus, GD3 produced by microglia under neuroinflammatory conditions may function as a novel mediator triggering mitochondria-mediated, but caspase-independent, apoptosis-like death of oligodendrocytes.</dcterms:abstract>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:contributor>Testi, Roberto</dc:contributor>
    <dc:creator>Leist, Marcel</dc:creator>
    <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/20169"/>
    <dc:creator>Nicotera, Pierluigi</dc:creator>
    <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/20169/2/Leist_Simon_Disialoganglioside.pdf"/>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-08-21T09:52:11Z</dc:date>
    <dc:creator>Testi, Roberto</dc:creator>
    <dc:creator>Malisan, Florence</dc:creator>
    <dc:rights>terms-of-use</dc:rights>
    <dc:contributor>Nicotera, Pierluigi</dc:contributor>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dcterms:issued>2002-07</dcterms:issued>
    <dc:contributor>Leist, Marcel</dc:contributor>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-08-21T09:52:11Z</dcterms:available>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
  </rdf:Description>
</rdf:RDF>
Interner Vermerk
xmlui.Submission.submit.DescribeStep.inputForms.label.kops_note_fromSubmitter
Kontakt
URL der Originalveröffentl.
Prüfdatum der URL
Prüfungsdatum der Dissertation
Finanzierungsart
Kommentar zur Publikation
Allianzlizenz
Corresponding Authors der Uni Konstanz vorhanden
Internationale Co-Autor:innen
Universitätsbibliographie
Nein
Begutachtet