Source:http://linkedlifedata.com/resource/pubmed/id/20807727
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2010-10-11
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| pubmed:abstractText |
Type 1 diabetes mellitus is characterized by a progressive autoimmune destruction of insulin-producing ? 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 ? cell death. ? 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 ? 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 ? 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 ? cells and the manifestation of insulin-dependent diabetes mellitus.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Peroxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxiredoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Streptozocin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1479-6805
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
207
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
163-75
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| pubmed:meshHeading |
pubmed-meshheading:20807727-Animals,
pubmed-meshheading:20807727-Apoptosis,
pubmed-meshheading:20807727-Caspase 3,
pubmed-meshheading:20807727-Caspase 9,
pubmed-meshheading:20807727-Cell Line,
pubmed-meshheading:20807727-Cytokines,
pubmed-meshheading:20807727-Female,
pubmed-meshheading:20807727-Gene Expression Regulation,
pubmed-meshheading:20807727-Hydrogen Peroxide,
pubmed-meshheading:20807727-Insulin-Secreting Cells,
pubmed-meshheading:20807727-Insulinoma,
pubmed-meshheading:20807727-Male,
pubmed-meshheading:20807727-Mice,
pubmed-meshheading:20807727-Mice, Inbred BALB C,
pubmed-meshheading:20807727-Mice, Inbred C57BL,
pubmed-meshheading:20807727-Nitric Oxide Synthase Type II,
pubmed-meshheading:20807727-Pancreas,
pubmed-meshheading:20807727-Peroxiredoxins,
pubmed-meshheading:20807727-Rats,
pubmed-meshheading:20807727-Streptozocin
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| pubmed:year |
2010
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| pubmed:articleTitle |
Peroxiredoxin III protects pancreatic ß cells from apoptosis.
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| pubmed:affiliation |
Department of Medical Biochemistry and Molecular Biology, University of Greifswald, Klinikum, Sauerbruchstrasse, D-17487 Greifswald, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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