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Titolo:
Death commitment point is advanced by axotomy in sympathetic neurons
Autore:
Fletcher, GC; Xue, LZ; Passingham, SK; Tolkovsky, AM;
Indirizzi:
Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England Univ Cambridge Cambridge England CB2 1QW hem, Cambridge CB2 1QW, England
Titolo Testata:
JOURNAL OF CELL BIOLOGY
fascicolo: 4, volume: 150, anno: 2000,
pagine: 741 - 754
SICI:
0021-9525(20000821)150:4<741:DCPIAB>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; PROGRAMMED CELL-DEATH; MITOCHONDRIAL PERMEABILITY TRANSITION; CYTOCHROME-C; PHOSPHATIDYLINOSITOL 3-KINASE; CASPASE ACTIVATION; FAMILY PROTEASES; BRAIN INJURY; BAX DELETION; CYCLIC-AMP;
Keywords:
apoptosis; caspases; mitochondria; NGF; survival signaling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Tolkovsky, AM Univ Cambridge, Dept Biochem, Bldg 0,Downing Site, CambridgeCB2 1QW, England Univ Cambridge Bldg 0,Downing Site Cambridge England CB21QW
Citazione:
G.C. Fletcher et al., "Death commitment point is advanced by axotomy in sympathetic neurons", J CELL BIOL, 150(4), 2000, pp. 741-754

Abstract

Axotomized neurons have several characteristics that are different from intact neurons. Here we show that, unlike established cultures, the axotomized sympathetic neurons deprived of NGF become committed to die before caspase activation, since the same proportion of NGF-deprived neurons are rescuedby NGF regardless of whether caspases are inhibited by the pan-caspase inhibitor Boc-Asp(O-methyl)-CH2F (BAF). Despite prolonged Akt and ERK signaling induced by NGF after BAF treatment has prevented death, the neurons fail to increase protein synthesis, recover ATP levels, or grow. Within 3 d, allthe mitochondria disappear without apparent removal of any other organelles or loss of membrane integrity. Although NGF does rescue intact BAF-treated 6-d cultures after NGF deprivation, rescue by NGF fails when these neurons are axotomized before NGF deprivation and BAF treatment. Moreover, cytosolic cytochrome c rapidly kills axotomized neurons. We propose that axotomy induces signals that make sympathetic neurons competent to die prematurely. NGF cannot repair these NGF-deprived, BAF-treated neurons because receptorsignaling (which is normal) is uncoupled from protein renewal, and the mitochondria (which are damaged) go on to be eliminated. Hence, the order of steps underlying neuronal death commitment is mutable and open to regulation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/08/20 alle ore 11:36:03