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Titolo:
Involvement of mitochondrial permeability transition and caspase-9 activation in dimethyl sulfoxide-induced apoptosis of EL-4 lymphoma cells
Autore:
Liu, J; Yoshikawa, H; Nakajima, Y; Tasaka, K;
Indirizzi:
Yamanashi Med Univ, Dept Parasitol & Immunol, Yamanashi 4093898, Japan Yamanashi Med Univ Yamanashi Japan 4093898 nol, Yamanashi 4093898, Japan
Titolo Testata:
INTERNATIONAL IMMUNOPHARMACOLOGY
fascicolo: 1, volume: 1, anno: 2001,
pagine: 63 - 74
SICI:
1567-5769(200101)1:1<63:IOMPTA>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
ADENINE-NUCLEOTIDE TRANSLOCATOR; DENSITY-DEPENDENT APOPTOSIS; FAS-MEDIATED APOPTOSIS; REVERSIBLE G1 ARREST; CYTOCHROME-C; HL-60 CELLS; GROWTH ARREST; RELEASE; DIFFERENTIATION; BCL-2;
Keywords:
DMSO; apoptosis; lymphoma cell; Bcl-2; mitochondrial membrane potential; cytochrome c; caspase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Tasaka, K Yamanashi Med Univ, Dept Parasitol & Immunol, Yamanashi 4093898,Japan Yamanashi Med Univ Yamanashi Japan 4093898 ashi 4093898, Japan
Citazione:
J. Liu et al., "Involvement of mitochondrial permeability transition and caspase-9 activation in dimethyl sulfoxide-induced apoptosis of EL-4 lymphoma cells", INT IMMUNO, 1(1), 2001, pp. 63-74

Abstract

We observed that dimethyl sulfoxide (DMSO) induced apoptotic changes in the EL-4 murine lymphoma cell line and that effect was dependent on the concentration and time period. Incubating cells over a period of 18 h, 2.5% DMSOwas found to induce sub-G1 peal; in DNA histograms analyzed by flowcytometer and nucleosomal ladder formation in DNA gel electrophoresis. We also found down-regulation of Bcl-2, collapse of mitochondrial membrane potential (Delta psi (m)) occurred following DMSO treatment, and release of cytochromec from the mitochondria to cytosol. These observations suggest that DMSO converted its pro-apoptotic signal at the mitochondria. In the involvement of caspases, caspase-9 and -3, but not caspase-8, were found to be activatedresponding to DMSO treatment. Inhibitory experiments demonstrated that caspase cascade of mitochondrial apoptotic pathway was indispensable fur DMSO-induced apoptosis. In the caspase cascade, caspase-9 was an upstream initiator and its primary signal could be transduced and amplified by caspase-3, -6 and -7. Kinetic study of these data showed mitochondrial dysfunction andcaspase activation occurred at 12 h and apoptotic change of nuclear DNA at18 h, providing another support for the transduction of DMSO pro-apoptoticsignal via the mitochondrial pathway. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 07:45:33