Inhibition of Mitochondrial ATP Generation by Nitric Oxide Switches Apoptosis to Necrosis

Lade...
Vorschaubild
Dateien
Zu diesem Dokument gibt es keine Dateien.
Datum
1999
Autor:innen
Single, Barbara
Fava, Eugenio
Simon, Bernadett
Herausgeber:innen
Kontakt
ISSN der Zeitschrift
Electronic ISSN
ISBN
Bibliografische Daten
Verlag
Schriftenreihe
Auflagebezeichnung
URI (zitierfähiger Link)
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
Published
Erschienen in
Experimental Cell Research. Elsevier. 1999, 249(2), pp. 396-403. ISSN 0014-4827. eISSN 1090-2422. Available under: doi: 10.1006/excr.1999.4514
Zusammenfassung

Under pathological conditions, the mode of cell death, apoptosis or necrosis, is relevant for the subsequent fate of the tissue. Cell demise may be shaped by endogenous mediators such as nitric oxide (NO) which interfere with subroutines of the death program. Here we show that apoptosis of Jurkat cells elicited by either staurosporine (STS) or anti-CD95 antibodies in glucose-free medium is converted to necrosis by NO donors. In the presence of NO, release of mitochondrial cytochrome c was delayed and activation of execution caspases was prevented. Stimulated cells died nonetheless. The switch in the mode of cell death was due to NO-dependent failure of mitochondrial energy production. Restoration of intracellular ATP by glucose supplementation recovered the cells' ability to activate caspases and undergo apoptosis. In this system, the apoptosis/necrosis conversion promoted by NO was not mediated by cyclic guanosine monophosphate-dependent mechanisms, poly-(ADP-ribose)-polymerase (PARP) activation, or inhibition of caspases due to S-nitrosylation and glutathione depletion. In contrast, depleting intracellular ATP with rotenone, an inhibitor of mitochondrial complex I mimicked the effect of NO. The findings presented here suggest that NO can decide the shape of cell death by lowering intracellular ATP below the level required to allow the coordinated execution of apoptosis.

Zusammenfassung in einer weiteren Sprache
Fachgebiet (DDC)
570 Biowissenschaften, Biologie
Schlagwörter
Konferenz
Rezension
undefined / . - undefined, undefined
Zitieren
ISO 690LEIST, Marcel, Barbara SINGLE, Heike NAUMANN, Eugenio FAVA, Bernadett SIMON, Simone KÜHNLE, Pierluigi NICOTERA, 1999. Inhibition of Mitochondrial ATP Generation by Nitric Oxide Switches Apoptosis to Necrosis. In: Experimental Cell Research. Elsevier. 1999, 249(2), pp. 396-403. ISSN 0014-4827. eISSN 1090-2422. Available under: doi: 10.1006/excr.1999.4514
BibTex
@article{Leist1999-06-15Inhib-51269,
  year={1999},
  doi={10.1006/excr.1999.4514},
  title={Inhibition of Mitochondrial ATP Generation by Nitric Oxide Switches Apoptosis to Necrosis},
  number={2},
  volume={249},
  issn={0014-4827},
  journal={Experimental Cell Research},
  pages={396--403},
  author={Leist, Marcel and Single, Barbara and Naumann, Heike and Fava, Eugenio and Simon, Bernadett and Kühnle, Simone and Nicotera, Pierluigi}
}
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/123456789/51269">
    <dc:creator>Single, Barbara</dc:creator>
    <dc:rights>terms-of-use</dc:rights>
    <dc:language>eng</dc:language>
    <dc:contributor>Single, Barbara</dc:contributor>
    <dc:contributor>Naumann, Heike</dc:contributor>
    <dc:contributor>Kühnle, Simone</dc:contributor>
    <dc:creator>Simon, Bernadett</dc:creator>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dcterms:title>Inhibition of Mitochondrial ATP Generation by Nitric Oxide Switches Apoptosis to Necrosis</dcterms:title>
    <dc:creator>Naumann, Heike</dc:creator>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-09T07:05:43Z</dc:date>
    <dc:creator>Nicotera, Pierluigi</dc:creator>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2020-10-09T07:05:43Z</dcterms:available>
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Kühnle, Simone</dc:creator>
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <dcterms:abstract xml:lang="eng">Under pathological conditions, the mode of cell death, apoptosis or necrosis, is relevant for the subsequent fate of the tissue. Cell demise may be shaped by endogenous mediators such as nitric oxide (NO) which interfere with subroutines of the death program. Here we show that apoptosis of Jurkat cells elicited by either staurosporine (STS) or anti-CD95 antibodies in glucose-free medium is converted to necrosis by NO donors. In the presence of NO, release of mitochondrial cytochrome c was delayed and activation of execution caspases was prevented. Stimulated cells died nonetheless. The switch in the mode of cell death was due to NO-dependent failure of mitochondrial energy production. Restoration of intracellular ATP by glucose supplementation recovered the cells' ability to activate caspases and undergo apoptosis. In this system, the apoptosis/necrosis conversion promoted by NO was not mediated by cyclic guanosine monophosphate-dependent mechanisms, poly-(ADP-ribose)-polymerase (PARP) activation, or inhibition of caspases due to S-nitrosylation and glutathione depletion. In contrast, depleting intracellular ATP with rotenone, an inhibitor of mitochondrial complex I mimicked the effect of NO. The findings presented here suggest that NO can decide the shape of cell death by lowering intracellular ATP below the level required to allow the coordinated execution of apoptosis.</dcterms:abstract>
    <dcterms:issued>1999-06-15</dcterms:issued>
    <dc:contributor>Simon, Bernadett</dc:contributor>
    <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/51269"/>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dc:contributor>Fava, Eugenio</dc:contributor>
    <dc:creator>Leist, Marcel</dc:creator>
    <dc:contributor>Leist, Marcel</dc:contributor>
    <dc:contributor>Nicotera, Pierluigi</dc:contributor>
    <dc:creator>Fava, Eugenio</dc:creator>
  </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
Ja