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Titolo:
Functional role and therapeutic implications of neuronal caspase-1 and-3 in a mouse model of traumatic spinal cord injury
Autore:
Li, M; Ona, VO; Chen, M; Kaul, M; Tenneti, L; Zhang, X; Stieg, PE; Lipton, SA; Friedlander, RM;
Indirizzi:
Harvard Univ, Sch Med, Brigham & Womens Hosp, Neuroapoptosis Lab, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Neuroapoptosis Lab, Boston, MA 02115 USA Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Cardiovasc Div, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Med,Cardiovasc Div, Boston, MA 02115 USA Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Surg,Neurosurg Serv, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 urg,Neurosurg Serv, Boston, MA 02115 USA Harvard Univ, Sch Med, Brigham & Womens Hosp, Cerebrovasc & Neurosci Res Inst, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Neurosci Res Inst, Boston, MA 02115 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 2, volume: 99, anno: 2000,
pagine: 333 - 342
SICI:
0306-4522(2000)99:2<333:FRATIO>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERLEUKIN-1-BETA CONVERTING-ENZYME; TROPHIC FACTOR WITHDRAWAL; DOMINANT-NEGATIVE MUTANT; CELL-DEATH; IL-1-BETA-CONVERTING ENZYME; BRAIN INJURY; CYSTEINE PROTEASE; FAMILY PROTEASES; CONTUSION INJURY; MICE DEFICIENT;
Keywords:
apoptosis; ICE; zVAD-fmk; interleukin-1 beta; neuroprotection;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Friedlander, RM Harvard Univ, Sch Med, Brigham & Womens Hosp, Neuroapoptosis Lab, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 ab, Boston, MA 02115 USA
Citazione:
M. Li et al., "Functional role and therapeutic implications of neuronal caspase-1 and-3 in a mouse model of traumatic spinal cord injury", NEUROSCIENC, 99(2), 2000, pp. 333-342

Abstract

Evidence indicates that both necrotic and apoptotic cell death contribute to tissue injury and neurological dysfunction following spinal cord injury. Caspases have been implicated as important mediators of apoptosis following acute central nervous system insults. We investigated whether caspase-1 and caspase-3 are involved in spinal cord injury-mediated cell death, and whether caspase inhibition may reduce tissue damage and improve outcome following spinal cord injury. We demonstrate a 17-fold increase in caspase-1 activity in traumatized spinal cord samples when compared with samples from sham-operated mice. Caspase-1 and caspase-3 activation were also detected by western blot following spinal cord injury, which was significantly inhibited by the broad caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone. By immunofluorescence or in situ fluorogenic substrate assay, caspase-1 and caspase-3 expression were detected in neuronal and non-neuronal cells following spinal cord injury. N-Benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone treated mice, and transgenic mice expressing a caspase-1 dominant negative mutant, demonstrated a significant improvement of motor function and a reduction of lesion size compared with vehicle-treated mice. Our results demonstrate for the first time that both caspase-1 and caspase-3 are activated in neurons following spinal cord injury, and that caspase inhibition reduces post-traumatic lesion size and improves motor performance. Caspase inhibitors may be one of the agents to be used for the treatmentof spinal cord injury. (C) 2000 IBRO. Published by Elsevier Science Ltd. All rights reserved.

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Documento generato il 10/07/20 alle ore 03:08:16