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Titolo:
Opening of the mitochondrial permeability transition pore causes matrix expansion and outer membrane rupture in Fas-mediated hepatic apoptosis in mice
Autore:
Feldmann, G; Haouzi, D; Moreau, A; Durand-Schneider, AM; Bringuier, A; Berson, A; Mansouri, A; Fau, D; Pessayre, D;
Indirizzi:
Fac Med Xavier Bichat, INSERM, U327, Biol Cellulaire Lab, F-75870 Paris 18, France Fac Med Xavier Bichat Paris France 18 aire Lab, F-75870 Paris 18, France Hop Beaujon, INSERM, U481, Clichy, France Hop Beaujon Clichy FranceHop Beaujon, INSERM, U481, Clichy, France Hop Beaujon, Ctr Claude Bernard Hepatites Virales, Clichy, France Hop Beaujon Clichy France ude Bernard Hepatites Virales, Clichy, France Univ Paris 07, Paris, France Univ Paris 07 Paris FranceUniv Paris 07, Paris, France
Titolo Testata:
HEPATOLOGY
fascicolo: 3, volume: 31, anno: 2000,
pagine: 674 - 683
SICI:
0270-9139(200003)31:3<674:OOTMPT>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; CYTOCHROME-C; NECROSIS; HEPATOCYTES; MECHANISMS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Feldmann, G Fac Med Xavier Bichat, INSERM, U327, Biol Cellulaire Lab, BP 416, F-75870 Paris 18, France Fac Med Xavier Bichat BP 416 Paris France 18 Paris 18, France
Citazione:
G. Feldmann et al., "Opening of the mitochondrial permeability transition pore causes matrix expansion and outer membrane rupture in Fas-mediated hepatic apoptosis in mice", HEPATOLOGY, 31(3), 2000, pp. 674-683

Abstract

Although Fas stimulation has been reported to cause outer mitochondrial membrane rupture in Jurkat cells, the mechanism of this effect is debated, and it is not known if outer membrane rupture also occurs in hepatocyte mitochondria, We studied the in vivo effects of Fas stimulation on ultrastructural lesions and mitochondrial function in mice. Four hours after administration of an agonistic anti-Fas antibody (8 mu g/animal), caspase activity increased 5.4-fold. Nuclear DNA showed internucleosomal fragmentation, whereassupercoiled mitochondrial DNA was replaced by circular and linear forms. Mitochondrial cytochrome c was partly released into the cytosol. Ultrastructurally, mitochondrial lesions were observed in both apoptotic hepatocytes (with nuclear chromatin condensation/fragmentation) and nonapoptotic hepatocytes (without nuclear changes). In nonapoptotic cells, outer mitochondrial membrane rupture allowed herniation of the inner membrane and matrix through the outer membrane gap. In apoptotic hepatocytes, the matrix became electron-lucent and no longer protruded through the outer membrane gap. Mitochondria clustered around the nucleus, whereas rough endoplasmic reticulum cisternae became peripheral. In liver mitochondria isolated after Fas stimulation, the membrane potential decreased, whereas basal respiration increased. Pretreatment with either z-VAD-fmk tan inhibitor of caspases) or cyclosporin A (a permeability transition inhibitor) totally or mostly prevented mitochondrial outer membrane rupture, membrane potential decrease, cytochrome c release, and apoptosis. In conclusion, in vivo Pas stimulation causes caspase activation, mitochondrial permeability transition (decreasing the membrane potential and increasing basal respiration), mitochondrial matrix expansion las shown by matrix herniation), outer mitochondrial membrane rupture, and cytochrome c release.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 00:54:54