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

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Abstract

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

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

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