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dc.contributor.authorWolf, G.
dc.contributor.authorAumann, N.
dc.contributor.authorMichalska, M.
dc.contributor.authorBast, A.
dc.contributor.authorSonnemann, J.
dc.contributor.authorBeck, J.
dc.contributor.authorLendeckel, U.
dc.contributor.authorNewsholme, Philip
dc.contributor.authorWalther, R.
dc.date.accessioned2017-01-30T11:34:13Z
dc.date.available2017-01-30T11:34:13Z
dc.date.created2016-09-12T08:36:25Z
dc.date.issued2010
dc.date.submitted2016-09-12
dc.identifier.citationWolf, 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.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/13012
dc.identifier.doi10.1677/JOE-09-0455
dc.description.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.

dc.publisherBioScientifica
dc.titlePeroxiredoxin III protects pancreatic ß cells from apoptosis
dc.typeJournal Article
dcterms.dateSubmitted2016-09-12
dcterms.source.volume207
dcterms.source.number2
dcterms.source.startPage163
dcterms.source.endPage175
dcterms.source.issn0022-0795
dcterms.source.titleJournal of Endocrinology
curtin.digitool.pid242621
curtin.pubStatusPublished
curtin.refereedTRUE
curtin.departmentSchool of Biomedical Sciences
curtin.identifier.scriptidPUB-HEA-SBS-PN-15933
curtin.identifier.elementsidELEMENTS-63983
curtin.accessStatusOpen access via publisher


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