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Neurodegeneration caused by microtubule disruption. Caspase-dependent and -independent mechanisms

Neurodegeneration caused by microtubule disruption. Caspase-dependent and -independent mechanisms

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VOLBRACHT, Christiane, 2000. Neurodegeneration caused by microtubule disruption. Caspase-dependent and -independent mechanisms

@phdthesis{Volbracht2000Neuro-7723, title={Neurodegeneration caused by microtubule disruption. Caspase-dependent and -independent mechanisms}, year={2000}, author={Volbracht, Christiane}, address={Konstanz}, school={Universität Konstanz} }

<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/7723"> <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/7723"/> <dcterms:abstract xml:lang="eng">In cerebellar granule cells, microtubule disassembling by colchicine induced degeneration of the axodendritic network followed by apoptotic demise of neuronal somata. Colchicine-induced apoptosis was accompanied by mitochondrial cytochrome c release, activation of execution caspase-3, advanced chromatin condensation, oligonucleosomal DNA fragmentation, and phosphatidylserine translocation to the outer surface of the plasma membrane. In the presence of peptide caspase inhibitors, apoptotic changes were prevented, although cytochrome c was released from mitochondria and the axodendritic network was still destroyed. Depletion of intracellular ATP blocked caspase activation, nuclear apoptotic features, and phosphatidylserine exposure, while the primary effect of microtubule disruption and neurite loss still occurred. Conversely, repletion of intracellular ATP restored all apoptotic features. Thus, sufficient ATP is required for the execution of neuronal apoptosis and energy deficiency may lead to the persistence of degenerating and dysfunctional neurons. Neither caspase inhibition by ATP depletion or pharmacological agents nor antiapoptotic Bcl-2 prevented microtubule breakdown or neurite loss. But neuronal somata were protected from apoptosis under these conditions. However, after a lag period caspase-inhibited as well as Bcl-2 overexpressing neurons underwent delayed cell death. This implies that death programs for neurite degeneration and apoptosis can occur independently from each other and that block of caspases may not rescue neurons from demise under degenerative conditions. The delayed caspase-independent death was characterized by partial chromatin condensation, large scale DNA fragmentation and phosphatidylserine exposure. Inhibitors of the proteasome reduced caspase-independent apoptosis, implying that noncaspase proteases can take over execution of apoptosis in neurons.</dcterms:abstract> <dc:creator>Volbracht, Christiane</dc:creator> <dc:contributor>Volbracht, Christiane</dc:contributor> <dc:language>eng</dc:language> <dcterms:title>Neurodegeneration caused by microtubule disruption. Caspase-dependent and -independent mechanisms</dcterms:title> <dc:rights>deposit-license</dc:rights> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:36:39Z</dcterms:available> <dcterms:rights rdf:resource="http://nbn-resolving.org/urn:nbn:de:bsz:352-20140905103416863-3868037-7"/> <dcterms:alternative>Neurodegeneration verursacht durch Zerstörung der Microtubuli. Caspase-abhängige und -unabhängige Mechanismen</dcterms:alternative> <dcterms:issued>2000</dcterms:issued> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-03-24T17:36:39Z</dc:date> <dc:format>application/pdf</dc:format> </rdf:Description> </rdf:RDF>

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