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Cytokine-induced apoptosis and necrosis are preceded by disruption of the mitochondrial membrane potential (Δ ψ m ) in pancreatic RINm5F cells: prevention by Bcl-2

The mechanisms of cytokine-induced β-cell death are poorly characterised. In rat insulin-producing RINm5F cells, the combination of interleukin-1β, interferon-γ and tumour necrosis factor-α presently induced disruption of the mitochondrial membrane potential (Δ ψ m ) as demonstrated by reduced JC-1 fluorescence. The reduction of Δ ψ 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 Δ ψ 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 Δ ψ m and that this may be a necessary event for both β-cell apoptosis and necrosis. Bcl-2 may prevent β-cell death by counteracting mitochondrial permeability transition. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular and Cellular Endocrinology Elsevier
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