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Titolo:
Caspase inhibition extends the commitment to neuronal death beyond cytochrome c release to the point of mitochondrial depolarization
Autore:
Deshmukh, M; Kuida, K; Johnson, EM;
Indirizzi:
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, Dept Neurol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Neurol, St Louis, MO 63110 USA Vertex Pharmaceut, Cambridge, MA 02139 USA Vertex Pharmaceut Cambridge MAUSA 02139 rmaceut, Cambridge, MA 02139 USA
Titolo Testata:
JOURNAL OF CELL BIOLOGY
fascicolo: 1, volume: 150, anno: 2000,
pagine: 131 - 143
SICI:
0021-9525(20000710)150:1<131:CIETCT>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; DEPRIVED SYMPATHETIC NEURONS; PROGRAMMED CELL-DEATH; ICE FAMILY PROTEASES; PERMEABILITY TRANSITION; FACTOR DEPRIVATION; FACTOR WITHDRAWAL; NUCLEAR-CHANGES; OUTER-MEMBRANE; APOPTOSIS;
Keywords:
apoptosis; caspase-9; bax; sympathetic neurons; NGF;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Johnson, EM Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis,MO 63110 USA Washington Univ St Louis MO USA 63110 St Louis, MO 63110 USA
Citazione:
M. Deshmukh et al., "Caspase inhibition extends the commitment to neuronal death beyond cytochrome c release to the point of mitochondrial depolarization", J CELL BIOL, 150(1), 2000, pp. 131-143

Abstract

Nerve growth factor (NGF) deprivation induces a Bar-dependent, caspase-dependent programmed cell death in sympathetic neurons. We examined whether the release of cytochrome c was accompanied by the loss of mitochondrial membrane potential during sympathetic neuronal death. NGF-deprived, caspase inhibitor-treated mouse sympathetic neurons maintained mitochondrial membrane potential for 25-30 h after releasing cytochrome c. NGF-deprived sympathetic neurons became committed to die, as measured by the inability of cells tobe rescued by NGF readdition, at the time of cytochrome c release. In the presence of caspase inhibitor, however, this commitment to death was extended beyond the point of cytochrome c release, but only up to the subsequent point of mitochondrial membrane potential loss. Caspase-9 deficiency also arrested NGF-deprived sympathetic neurons after release of cytochrome c, andpermitted these neurons to be rescued with NGF readdition. Commitment to death in the NGF-deprived, caspase-9-deficient sympathetic neurons was also coincident with the loss of mitochondrial membrane potential. Thus, caspaseinhibition extended commitment to death in trophic factor-deprived sympathetic neurons and allowed recovery of neurons arrested after the loss of cytochrome c, but not beyond the subsequent loss of mitochondrial membrane potential.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 07:55:19