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Titolo:
Apoptosis in caspase-inhibited neurons
Autore:
Volbracht, C; Leist, M; Kolb, SA; Nicotera, P;
Indirizzi:
Univ Konstanz, Dept Biol, Chair Mol Toxicol, D-78457 Constance, Germany Univ Konstanz Constance Germany D-78457 icol, D-78457 Constance, Germany Univ Zurich Hosp, Dept Pathol, Electron Microscopy Lab, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland
Titolo Testata:
MOLECULAR MEDICINE
fascicolo: 1, volume: 7, anno: 2001,
pagine: 36 - 48
SICI:
1076-1551(200101)7:1<36:AICN>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; INTERLEUKIN-1-BETA CONVERTING-ENZYME; DEPRIVED SYMPATHETIC NEURONS; CEREBELLAR GRANULE CELLS; ICE FAMILY PROTEASES; MITOCHONDRIAL RELEASE; HUNTINGTONS-DISEASE; INDEPENDENT PATHWAY; CPP32-LIKE ACTIVITY; MEDIATED APOPTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
88
Recensione:
Indirizzi per estratti:
Indirizzo: Nicotera, P Univ Konstanz, Dept Biol, Chair Mol Toxicol, Box X911, D-78457Constance, Germany Univ Konstanz Box X911 Constance Germany D-78457 nce, Germany
Citazione:
C. Volbracht et al., "Apoptosis in caspase-inhibited neurons", MOL MED, 7(1), 2001, pp. 36-48

Abstract

Background: There is growing evidence of apoptosis in neurodegenerative disease. However, it is still unclear whether the pathological manifestationsobserved in slow neurodegenerative diseases are due to neuronal loss or whether they are related to independent degenerative events in the axodendritic network. It also remains elusive whether a single, caspase-based executing system involving caspases is responsible for neuronal loss by apoptosis. Materials and Methods: Long-term exposure to the microtubule-disassemblingagent, colchicine, was used to disrupt the axodendritic network and eventually trigger caspase-3-mediated apoptosis in cultures of cerebellar granulecells. For this model, we investigated the role of Bcl-2 and caspases in neurite degeneration and death of neuronal somata. Results: Early degeneration of the axodendritic network occurred by a Bcl-2 and caspase-independent mechanism. Conversely, apoptosis of the cell bodywas delayed by Bcl-2 and initially blocked by caspase inhibition. However,when caspase activity was entirely blocked by zVAD-fmk, colchicine-exposedneurons still underwent delayed cell death characterized by cytochrome release, chromatin condensation to irregularly shaped clumps, DNA-fragmentation, and exposure of phatidylserine. Inhibitors of the proteasome reduced these caspase-independent apoptotic-like features of the neuronal soma. Conclusion: Our data suggest that Bcl-2-dependent and caspase-mediated death programs account only partially for neurodegenerative changes in injuredneurons. Blockage of the caspase execution machinery may only temporarily rescue damaged neurons and classical apoptotic features can still appear incaspase-inhibited neurons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 09:01:48