Calpain inhibitors prevent nitric oxidetriggered excitotoxic apoptosis

Volbracht, Christiane; Fava, Eugenio; Leist, Marcel; Nicotera, Pierluigi

Calpain inhibitors prevent nitric oxidetriggered excitotoxic apoptosis

Dateien

cv_calpain_2001.pdfGröße: 463.96 KBDownloads: 616

Datum

2001

Autor:innen

Volbracht, Christiane

Fava, Eugenio

Leist, Marcel

Nicotera, Pierluigi

URI (zitierfähiger Link)

http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-81813

Link zur Lizenz

Urheberrechtlich geschützt

Open Access-Veröffentlichung

Open Access Green

Sammlungen

Biologie

Publikationstyp

Zeitschriftenartikel

Publikationsstatus

Published

Erschienen in

NeuroReport. 2001, 12(17), pp. 3645-3648

Zusammenfassung

The pathogenesis of some neurodegenerative disorders has been linked to excitotoxicity, excess generation of nitric oxide (NO) and apoptosis. Here, we used a model of NO-triggered neuronal apoptosis that was strictly dependent on autocrine NMDA receptor (NMDA-R) activation and intracellular Ca2 increase. We investigated the efficiency and potentially beneficial effects of calpain inhibition. Three calpain inhibitors that prevented intracellular fodrin proteolysis also blocked apoptotic features such as decrease in mitochondrial membrane potential, chromatin breakdown, and subsequent death of cerebellar granule neurons exposed to NO donors (S-nitroso- L-glutathione, S-nitroso-N-acetyl D,L-penicillamine, and diethylamino- diazenolate-2-oxide). Since inhibitors did not interfere with NMDA-R activation, we suggest that block of calpains blunts NO-triggered neuronal apoptosis by stopping the cascade downstream of primary autocrine excitotoxic events.

Fachgebiet (DDC)

570 Biowissenschaften, Biologie

Schlagwörter

Apoptosis, Calpains, Excitotoxicity, Mitochondria, Nitric oxide

Zitieren

ISO 690

VOLBRACHT, Christiane, Eugenio FAVA, Marcel LEIST, Pierluigi NICOTERA, 2001. Calpain inhibitors prevent nitric oxidetriggered excitotoxic apoptosis. In: NeuroReport. 2001, 12(17), pp. 3645-3648

BibTex

@article{Volbracht2001Calpa-7742,
  year={2001},
  title={Calpain inhibitors prevent nitric oxidetriggered excitotoxic apoptosis},
  number={17},
  volume={12},
  journal={NeuroReport},
  pages={3645--3648},
  author={Volbracht, Christiane and Fava, Eugenio and Leist, Marcel 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/123456789/7742">
    <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:creator>Nicotera, Pierluigi</dc:creator>
    <dc:rights>terms-of-use</dc:rights>
    <dcterms:title>Calpain inhibitors prevent nitric oxidetriggered excitotoxic apoptosis</dcterms:title>
    <dc:language>eng</dc:language>
    <dcterms:bibliographicCitation>First publ. in: NeuroReport 12 (2001), 17, pp. 3645-3648</dcterms:bibliographicCitation>
    <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/>
    <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/7742/1/cv_calpain_2001.pdf"/>
    <dc:contributor>Nicotera, Pierluigi</dc:contributor>
    <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:37:12Z</dcterms:available>
    <dcterms:issued>2001</dcterms:issued>
    <dc:creator>Fava, Eugenio</dc:creator>
    <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/server/rdf/resource/123456789/28"/>
    <dc:contributor>Leist, Marcel</dc:contributor>
    <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/7742"/>
    <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/>
    <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/7742/1/cv_calpain_2001.pdf"/>
    <dc:creator>Volbracht, Christiane</dc:creator>
    <dc:creator>Leist, Marcel</dc:creator>
    <dc:contributor>Volbracht, Christiane</dc:contributor>
    <foaf:homepage rdf:resource="http://localhost:8080/"/>
    <dc:contributor>Fava, Eugenio</dc:contributor>
    <dc:format>application/pdf</dc:format>
    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:37:12Z</dc:date>
    <dcterms:abstract xml:lang="eng">The pathogenesis of some neurodegenerative disorders has been linked to excitotoxicity, excess generation of nitric oxide (NO) and apoptosis. Here, we used a model of NO-triggered neuronal apoptosis that was strictly dependent on autocrine NMDA receptor (NMDA-R) activation and intracellular Ca2  increase. We investigated the efficiency and potentially beneficial effects of calpain inhibition. Three calpain inhibitors that prevented intracellular fodrin proteolysis also blocked apoptotic features such as decrease in mitochondrial membrane potential, chromatin breakdown, and subsequent death of cerebellar granule neurons exposed to NO donors (S-nitroso- L-glutathione, S-nitroso-N-acetyl D,L-penicillamine, and diethylamino- diazenolate-2-oxide). Since inhibitors did not interfere with NMDA-R activation, we suggest that block of calpains blunts NO-triggered neuronal apoptosis by stopping the cascade downstream of primary autocrine excitotoxic events.</dcterms:abstract>
  </rdf:Description>
</rdf:RDF>

Universitätsbibliographie

Nein