Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
IL-1 receptor antagonist prevents apoptosis and caspase-3 activation afterspinal cord injury
Autore:
Nesic, O; Xu, GY; McAdoo, D; High, KW; Hulsebosch, C; Perez-Polo, R;
Indirizzi:
Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 l Chem & Genet, Galveston, TX 77555 USA Univ Texas, Med Branch, Inst Marine Biomed, Galveston, TX 77550 USA Univ Texas Galveston TX USA 77550 Marine Biomed, Galveston, TX 77550 USA Univ Texas, Med Branch, Dept Anat & Neurosci, Galveston, TX 77550 USA UnivTexas Galveston TX USA 77550 nat & Neurosci, Galveston, TX 77550 USA
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 9, volume: 18, anno: 2001,
pagine: 947 - 956
SICI:
0897-7151(200109)18:9<947:IRAPAA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERLEUKIN-1-BETA CONVERTING-ENZYME; EXPERIMENTAL TRAUMATIC INJURY; FOCAL CEREBRAL-ISCHEMIA; NEURONAL CELL-DEATH; MESSENGER-RNA; POSSIBLE INVOLVEMENT; ALZHEIMER-DISEASE; CONTUSION INJURY; GENE-EXPRESSION; TRANSGENIC MICE;
Keywords:
apoptosis; caspase-3; Il-1 beta; IL-1 receptor antagonist; spinal cord injury;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Nesic, O Univ Texas, Med Branch, Dept Human Biol Chem & Genet, 301 Univ Blvd, Galveston, TX 77555 USA Univ Texas 301 Univ Blvd Galveston TX USA 77555ton, TX 77555 USA
Citazione:
O. Nesic et al., "IL-1 receptor antagonist prevents apoptosis and caspase-3 activation afterspinal cord injury", J NEUROTRAU, 18(9), 2001, pp. 947-956

Abstract

One of the consequences of cytokine-orchestrated inflammation after CNS trauma is apoptosis. Our hypothesis is that cell death in the spinal cord after injury results in part from increased synthesis and release of IL-1 beta. Using a ribonuclease protection assay, we demonstrated that there is increased transient expression of IL-1 beta mRNA and, by using IL-1 beta protein ELISA assay, that there are increased IL-1 beta protein levels in the contused rat spinal cord, initially localized to the impact region of the spinal cord (segment T8). Using an ELISA cell death assay, we showed that thereis apoptosis in the spinal cord 72 h after injury, a finding that was confirmed by measuring caspase-3 activity, which also significantly increased at the site of injury 72 h after trauma. Treatment of the contused spinal cord at the site of injury with the IL-1 receptor antagonist (rmIL-1ra, 750 ng/mL) for 72 h using an osmotic minipump completely abolished the increasesin contusion-induced apoptosis and caspase-3 activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 22:24:20