Cytokine-induced apoptosis and necrosis are preceded by disruption of the mitochondrial membrane potential (Deltapsi(m)) in pancreatic RINm5F cells: prevention by Bcl-2.
Mol Cell Endocrinol
; 190(1-2): 75-82, 2002 Apr 25.
Article
en En
| MEDLINE
| ID: mdl-11997180
The mechanisms of cytokine-induced beta-cell death are poorly characterised. In rat insulin-producing RINm5F cells, the combination of interleukin-1beta, interferon-gamma and tumour necrosis factor-alpha presently induced disruption of the mitochondrial membrane potential (Deltapsi(m)) as demonstrated by reduced JC-1 fluorescence. The reduction of Deltapsi(m) was maximal after 8 h and was preceded by increased formation of reactive oxygen species (ROS), as assessed by dichlorofluorescein-diacetate (DCFH-DA) fluorescence. A nitric oxide synthase-, but not a ROS-inhibitor, prevented cytokine-induced loss of Deltapsi(m). Overexpression of the anti-apoptotic protein Bcl-2 increased both JC-1 and DCFH-DA fluorescence, which was paralleled by protection against cytokine-induced apoptosis and necrosis. It is concluded that cytokines induce a nitric oxide-dependent disruption of Deltapsi(m) and that this may be a necessary event for both beta-cell apoptosis and necrosis. Bcl-2 may prevent beta-cell death by counteracting mitochondrial permeability transition.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Interferón gamma
/
Interleucina-1
/
Factor de Necrosis Tumoral alfa
/
Apoptosis
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Proteínas Proto-Oncogénicas c-bcl-2
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Potenciales de la Membrana
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Mitocondrias
/
Necrosis
Límite:
Animals
Idioma:
En
Revista:
Mol Cell Endocrinol
Año:
2002
Tipo del documento:
Article
País de afiliación:
Suecia
Pais de publicación:
Irlanda