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Titolo:
Temporospatial sequence of cellular events associated with etoposide-induced neuronal cell death: Role of antiapoptotic protein Bcl-X-L
Autore:
Kim, JE; Han, BS; Choi, WS; Eom, DS; Lee, EH; Oh, TH; Markelonis, GJ; Saido, TC; Lee, GE; Chung, IK; Oh, YJ;
Indirizzi:
Yonsei Univ, Coll Sci, Dept Biol, Seoul 120749, South Korea Yonsei Univ Seoul South Korea 120749 ept Biol, Seoul 120749, South Korea Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 & Neurobiol, Baltimore, MD 21201 USA RIKEN, Brain Sci Inst, Lab Proteolyt Neurosci, Saitama, Japan RIKEN Saitama Japan in Sci Inst, Lab Proteolyt Neurosci, Saitama, Japan
Titolo Testata:
JOURNAL OF NEUROSCIENCE RESEARCH
fascicolo: 6, volume: 66, anno: 2001,
pagine: 1074 - 1082
SICI:
0360-4012(200112)66:6<1074:TSOCEA>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
DRUG-INDUCED APOPTOSIS; CYTOCHROME-C; POLY(ADP-RIBOSE) POLYMERASE; TOPOISOMERASE-II; NERVOUS-SYSTEM; DEPENDENT ACTIVATION; HL-60 CELLS; CLEAVAGE; CASPASE; CALPAIN;
Keywords:
cell death; caspase; calpain; Bcl-X-L; MN9D; etoposide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Oh, YJ Yonsei Univ, Coll Sci, Dept Biol, 134 Shinchondong Seodaemoonku, Seoul 120749, South Korea Yonsei Univ 134 Shinchondong Seodaemoonku Seoul South Korea 120749
Citazione:
J.E. Kim et al., "Temporospatial sequence of cellular events associated with etoposide-induced neuronal cell death: Role of antiapoptotic protein Bcl-X-L", J NEUROSC R, 66(6), 2001, pp. 1074-1082

Abstract

Etoposide-induced death comprises such nuclear events as the formation of topoisomerase II-DNA cleavable complex and cytosolic events including caspase activation. By first establishing the temporospatial death sequence triggered by etoposide in a neuronal cell line, MN9D overexpressing Bcl-X-L (MN9D/Bcl-X-L) or control vector (MN9D/Neo), we examined whether formation of this complex is primarily responsible for cell death and at which strategicpoints and how Bcl-X-L blocks etoposide-induced neuronal death. Etoposide induced death that was dependent on caspase, cycloheximide, and calpain in MN9D/Neo cells. Etoposide also induced death in enucleated MN9D/Neo cells, although this was less severe. The level of topoisomerase II-DNA cleavable complex reached at a maximum of 2 hr after etoposide treatment was identical in MN9D/Neo and MN9D/Bcl-X-L cells. In MN9D/Neo cells, cytochrome c release into the cytosol and caspase activation occurred as early as 2 hr and 3-6 hr after etoposide treatment, respectively. Etoposide-induced DNA laddering potentially via caspase appeared as early as 12 hr after drug treatment,followed by nuclear swelling in MN9D/Neo cells (> 18-20 hr). Subsequently,nuclear condensation started by 24-28 hr and became apparent thereafter. All of these events except for nuclear swelling were substantially blocked in MN9D/Bcl-X-L. At the later stage of cell death (< 32-36 hr), a specific cleavage of Bax and fodrin appeared that was completely blocked by calpain inhibitor or by Bcl-X-L. Taken together, our data suggest that BCl-X-L prevents etoposide-induced neuronal death by exerting its anticaspase and anticalpain effect on cellular events after the formation of topoisomerase II-DNAcleavable complex that may not be a major contributor to cell death. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 12:50:01