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Titolo:
Chloroquine-induced neuronal cell death is p53 and Bcl-2 family-dependent but caspase-independent
Autore:
Zaidi, AU; McDonough, JS; Klocke, BJ; Latham, CB; Korsmeyer, SJ; Flavell, RA; Schmidt, RE; Roth, KA;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol & Immunol, Div Neuropathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Neuropathol, St Louis, MO 63110 USA Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pathol,Howard Hughes Med Inst, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 rd Hughes Med Inst, Boston, MA 02115 USA Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med,Howard Hughes Med Inst, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 rd Hughes Med Inst, Boston, MA 02115 USA Yale Univ, Sch Med, Howard Hughes Med Inst, Immunol Sect, New Haven, CT 06510 USA Yale Univ New Haven CT USA 06510 t, Immunol Sect, New Haven, CT 06510 USA
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 10, volume: 60, anno: 2001,
pagine: 937 - 945
SICI:
0022-3069(200110)60:10<937:CNCDIP>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
MITOCHONDRIAL PERMEABILITY TRANSITION; X-DEFICIENT MICE; ALZHEIMERS-DISEASE; PROTEIN-DEGRADATION; CATHEPSIN-D; HUNTINGTIN EXPRESSION; LYSOSOMAL SYSTEM; UP-REGULATION; IN-VITRO; APOPTOSIS;
Keywords:
apoptosis; autophagy; caspase-3; lysosome; telencephalon;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med, Dept Pathol & Immunol, Div Neuropathol,660 S Euclid Ave,Box 8118, St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave,Box 8118 St Louis MO USA 63110 A
Citazione:
A.U. Zaidi et al., "Chloroquine-induced neuronal cell death is p53 and Bcl-2 family-dependent but caspase-independent", J NE EXP NE, 60(10), 2001, pp. 937-945

Abstract

Chloroquine is a lysosomotropic agent that causes marked changes in intracellular protein processing and trafficking and extensive autophagic vacuoleformation. Chloroquine may be cytotoxic and has been used as a model of lysosomal-dependent cell death. Recent studies indicate that autophagic cell death may involve Bcl-2 family members and share some features with caspase-dependent apoptotic death. To determine the molecular pathway of chloroquine-induced neuronal cell death, we examined the effects of chloroquine on primary telencephalic neuronal cultures derived from mice with targeted genedisruptions in p53, and various caspase and bcl-2 family members. In wild-type neurons, chloroquine produced concentration- and time-dependent accumulation of autophagosomes, caspase-3 activation, and cell death. Cell death was inhibited by 3-methyladenine, an inhibitor of autophagic vacuole formation, but not by Boc-Asp-FMK (BAF), a broad caspase inhibitor. Targeted genedisruptions of b53 and bax inhibited and bcl-x potentiated chloroquine-induced neuron death. Caspase-9- and caspase-3-deficient neurons were not protected from chloroquine cytotoxicity. These studies indicate that chloroquine activates a regulated cell death pathway that partially overlaps with theapoptotic cascade.

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Documento generato il 11/07/20 alle ore 02:42:36