Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Cleavage of Bid may amplify caspase-8-induced neuronal death following focally evoked limbic seizures
Autore:
Henshall, DC; Bonislawski, DP; Skradski, SL; Lan, JQ; Meller, R; Simon, RP;
Indirizzi:
Legacy Clin Res & Technol Ctr, Robert S Dow Neurobiol Labs, Portland, OR 97232 USA Legacy Clin Res & Technol Ctr Portland OR USA 97232 ortland, OR 97232 USA
Titolo Testata:
NEUROBIOLOGY OF DISEASE
fascicolo: 4, volume: 8, anno: 2001,
pagine: 568 - 580
SICI:
0969-9961(200108)8:4<568:COBMAC>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
TEMPORAL-LOBE EPILEPSY; CYTOCHROME-C RELEASE; CELL-DEATH; DNA FRAGMENTATION; HIPPOCAMPAL-NEURONS; CASPASE ACTIVATION; BRAIN-DAMAGE; IN-VITRO; APOPTOSIS; RECEPTORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Henshall, DC Legacy Clin Res & Technol Ctr, Robert S Dow Neurobiol Labs, 1225 NE 2nd Ave, Portland, OR 97232 USA Legacy Clin Res & Technol Ctr 1225 NE 2nd Ave Portland OR USA 97232
Citazione:
D.C. Henshall et al., "Cleavage of Bid may amplify caspase-8-induced neuronal death following focally evoked limbic seizures", NEUROBIOL D, 8(4), 2001, pp. 568-580

Abstract

The mechanism by which seizures induce neuronal death is not completely understood. Caspase-8 is a key initiator of apoptosis via extrinsic, death receptor-mediated pathways; we therefore investigated its role in mediating seizure-induced neuronal death evoked by unilateral kainic acid injection into the amygdala of the rat, terminated after 40 min by diazepam. We demonstrate that cleaved (P18) caspase-8 was detectable immediately following seizure termination coincident with an increase in cleavage of the substrate lie-Glu-Thr-Asp (IETD)-p-nitroanilide and the appearance of cleaved (p15) Bid. Expression of Fas and FADD, components of death receptor signaling, was increased following seizures. In vivo intracerebroventricular z-IETD-fluoromethyl ketone administration significantly reduced seizure-induced activities of caspases 8, 9, and 3 as well as reducing Bid and caspase-9 cleavage, cytochrome c release, DNA fragmentation, and neuronal death. These data suggest that intervention in caspase-8 and/or death receptor signaling may confer protection on the brain from the injurious effects of seizures. (C) 2001Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 03:20:43