Publikation: Calpain inhibitors prevent nitric oxidetriggered excitotoxic apoptosis
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2001
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Published
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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.
Zusammenfassung in einer weiteren Sprache
Fachgebiet (DDC)
570 Biowissenschaften, Biologie
Schlagwörter
Apoptosis, Calpains, Excitotoxicity, Mitochondria, Nitric oxide
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VOLBRACHT, Christiane, Eugenio FAVA, Marcel LEIST, Pierluigi NICOTERA, 2001. Calpain inhibitors prevent nitric oxidetriggered excitotoxic apoptosis. In: NeuroReport. 2001, 12(17), pp. 3645-3648BibTex
@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}
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<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>
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