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    Peroxiredoxin III protects pancreatic ß cells from apoptosis

    Access Status
    Open access via publisher
    Authors
    Wolf, G.
    Aumann, N.
    Michalska, M.
    Bast, A.
    Sonnemann, J.
    Beck, J.
    Lendeckel, U.
    Newsholme, Philip
    Walther, R.
    Date
    2010
    Type
    Journal Article
    
    Metadata
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    Citation
    Wolf, G. and Aumann, N. and Michalska, M. and Bast, A. and Sonnemann, J. and Beck, J. and Lendeckel, U. et al. 2010. Peroxiredoxin III protects pancreatic ß cells from apoptosis. Journal of Endocrinology. 207 (2): pp. 163-175.
    Source Title
    Journal of Endocrinology
    DOI
    10.1677/JOE-09-0455
    ISSN
    0022-0795
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/13012
    Collection
    • Curtin Research Publications
    Abstract

    Type 1 diabetes mellitus is characterized by a progressive autoimmune destruction of insulin-producing ß cells. Macrophages and T lymphocytes release cytokines, which induce the synthesis of oxygen and nitrogen radicals in the pancreatic islets. The resulting cellular and mitochondrial damage promotes ß cell death. ß cells are very sensitive to the autoimmune free radical-dependent attack due to their low content of antioxidant enzymes such as glutathione peroxidase and catalase. A focal point of ß cell protection should be the control of the mitochondrial redox status, which will result in the preservation of metabolic stimulus-secretion coupling. For this reason, there is a considerable interest in the mitochondrial peroxiredoxin III (PRX III), a thioredoxin-dependent peroxide reductase, which was shown to be able to protect against both oxidative and nitrosative stress. Using the Tet-On-system, we generated stably transfected rat insulinoma cells over- or under-expressing PRX III in a doxycyclin-dependent manner to analyze the effect of increased or decreased amounts of cellular PRX III, following treatment with several stressors. We provide evidence that PRX III protects pancreatic ß cells from cell stress induced by accumulation of hydrogen peroxide, or the induction of inducible nitric oxide synthase or caspase-9 and -3 by pro-inflammatory cytokines or streptozotocin. Basal insulin secretion was markedly decreased in cells expressing lower levels of PRX III. We suggest PRX III may be a suitable target for promoting deceleration or even prevention of stress-associated apoptosis in pancreatic ß cells and the manifestation of insulin-dependent diabetes mellitus. © 2010 Society for Endocrinology.

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