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Titolo:
BAX contributes to apoptotic-like death following neonatal hypoxia-ischemia: Evidence for distinct apoptosis pathways
Autore:
Gibson, ME; Han, BH; Choi, JJ; Knudson, CM; Korsmeyer, SJ; Parsadanian, M; Holtzman, DM;
Indirizzi:
Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Neurol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 & Pharmacol, St Louis, MO 63110 USA Washington Univ, Sch Med, Ctr Study Nervous Syst Injury, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Syst Injury, St Louis, MO 63110 USA Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA Univ Iowa Iowa City IA USA 52242 wa, Dept Pathol, Iowa City, IA 52242 USA Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pathol & Med, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Dept Pathol & Med, Boston, MA 02115 USA
Titolo Testata:
MOLECULAR MEDICINE
fascicolo: 9, volume: 7, anno: 2001,
pagine: 644 - 655
SICI:
1076-1551(200109)7:9<644:BCTADF>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYTOCHROME-C RELEASE; TRANSIENT FOREBRAIN ISCHEMIA; IN-SITU IMMUNODETECTION; PERINATAL BRAIN INJURY; DEVELOPING RAT-BRAIN; CELL-DEATH; CEREBRAL-ISCHEMIA; NEURONAL DEATH; NERVOUS-SYSTEM; CASPASE-3 ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
78
Recensione:
Indirizzi per estratti:
Indirizzo: Holtzman, DM Washington Univ, Sch Med, Dept Neurol, 660 S Euclid Ave,Box 8111, St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave,Box 8111 St Louis MO USA 63110
Citazione:
M.E. Gibson et al., "BAX contributes to apoptotic-like death following neonatal hypoxia-ischemia: Evidence for distinct apoptosis pathways", MOL MED, 7(9), 2001, pp. 644-655

Abstract

Background: Hypoxic-ischemic (H-I) injury to the neonatal brain has been shown to result in rapid cell death with features of acute excitotoxicity/necrosis as well as prominent delayed cell death with features of apoptosis such as marked caspase-3 activation. BAX, a pro-apoptotic molecule, has beenshown to be required for apoptotic neuronal cell death during normal development but the contribution of endogenous BAX in cell death pathways following H-I injury to the developing or adult brain has not been studied. Materials and Methods: Bax +/+, +/-, and -/- mice at post-natal day 7 weresubjected to unilateral carotid ligation followed by exposure to 45 minutes of 8% oxygen. At different timepoints following H-I, brain tissue was studied by conventional histology, immunohistochemistry, immunofluorescence, Western blotting, and enzymatic assay to determine the extent and type of cell injury as well as the amount of caspase activation. Results: We found that bax -/- mice had significantly less (38%) hippocampal tissue loss than mice expressing bax. Some of the remaining cell death in bax -/- mice, however, still had features of apoptosis including evidenceof nuclear shrinkage and caspase-3 activation. Though bax -/- mice had significantly decreased caspase-3 activation as compared to bax expressing mice following H-I, the density of cells with activated caspase-8 in the CA3 region of the hippocampus did not differ between bax +/- and bax -/- mice. Conclusions: These findings demonstrate that endogenous BAX plays a role in regulating cell death in the central nervous system (CNS) following neonatal H-I. a model of cerebral palsy. in addition, while BAX appears to modulate the caspase-3 activation following neonatal H-I, caspase-8 which is linked to death receptor activation, may contribute to apoptotic-like neuronaldeath in a BAX-independent manner.

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Documento generato il 02/04/20 alle ore 02:50:32