IL-1beta is recognized as an effector cytokine contributing to islet beta-cell destruction during diabetes. We have previously shown in vitro that IL-1beta induces nitric oxide (NO) and beta-cell damage. Here, we show that IL-1beta administration in vivo to Wistar rats transiently increases manganese superoxide dismutase activity, whereas inducible NO synthase is not detected, and the levels of nitrate?? do not change. Moreover, a significant decrease of mitochondrial aconitase, leading to a rise of hydroperoxides, and islet beta-cell apoptosis, involving caspase-3 and -8, is observed. Analysis of adhesion molecules in beta-cells showed that intercellular adhesion molecule-1 is highly expressed 48 h after IL-1beta administration and that this is concomitant to the fall of manganese superoxide dismutase activity. Thus, IL-1beta exerts a proapoptotic effect in vivo through mitochondrial enzyme alteration, which is not related to the inducible NO synthase pathway, and dysregulates the immune system through the up-regulation of adhesion molecules.

Todaro, M., Di Gaudio, F., Lavitrano, M., Stassi, G., & Papaccio, G. (2003). Islet beta-cell apoptosis triggered in vivo by interleukin-1 beta is not related to the inducible nitric oxide synthase pathway: Evidence for mitochondrial function impairment and lipoperoxidation. ENDOCRINOLOGY, 144(10), 4264-4271 [10.1210/en.2003-0385].

Islet beta-cell apoptosis triggered in vivo by interleukin-1 beta is not related to the inducible nitric oxide synthase pathway: Evidence for mitochondrial function impairment and lipoperoxidation

LAVITRANO, MARIALUISA;
2003-10

Abstract

IL-1beta is recognized as an effector cytokine contributing to islet beta-cell destruction during diabetes. We have previously shown in vitro that IL-1beta induces nitric oxide (NO) and beta-cell damage. Here, we show that IL-1beta administration in vivo to Wistar rats transiently increases manganese superoxide dismutase activity, whereas inducible NO synthase is not detected, and the levels of nitrate?? do not change. Moreover, a significant decrease of mitochondrial aconitase, leading to a rise of hydroperoxides, and islet beta-cell apoptosis, involving caspase-3 and -8, is observed. Analysis of adhesion molecules in beta-cells showed that intercellular adhesion molecule-1 is highly expressed 48 h after IL-1beta administration and that this is concomitant to the fall of manganese superoxide dismutase activity. Thus, IL-1beta exerts a proapoptotic effect in vivo through mitochondrial enzyme alteration, which is not related to the inducible NO synthase pathway, and dysregulates the immune system through the up-regulation of adhesion molecules.
Articolo in rivista - Articolo scientifico
Scientifica
apoptosis
English
4264
4271
Todaro, M., Di Gaudio, F., Lavitrano, M., Stassi, G., & Papaccio, G. (2003). Islet beta-cell apoptosis triggered in vivo by interleukin-1 beta is not related to the inducible nitric oxide synthase pathway: Evidence for mitochondrial function impairment and lipoperoxidation. ENDOCRINOLOGY, 144(10), 4264-4271 [10.1210/en.2003-0385].
Todaro, M; Di Gaudio, F; Lavitrano, M; Stassi, G; Papaccio, G
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10281/2994
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