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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2011-3-30
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pubmed:abstractText |
C/EBP homologous protein (CHOP) has been proposed as a key transcription factor for endoplasmic reticulum (ER) stress-mediated ?-cell death induced by inflammatory cytokines in vitro. However, the contribution of CHOP induction to the pathogenesis of type 1 diabetes is not yet clear. To evaluate the relevance of CHOP in the pathogenesis of type 1 diabetes in vivo, we generated CHOP-deficient non-obese diabetic (NOD.Chop (-/-)) mice. CHOP deficiency did not affect the development of insulitis and diabetes and apoptosis in ?-cells. Interestingly, NOD.Chop (-/-) mice exhibited a delayed appearance of insulin autoantibodies compared to wild-type (wt) mice. Adoptive transfer with the diabetogenic, whole or CD8(+)-depleted splenocytes induced ?-cell apoptosis and the rapid onset of diabetes in the irradiated NOD.Chop (-/-) recipients with similar kinetics as in wt mice. Expression of ER stress-associated genes was not significantly up-regulated in the islets from NOD.Chop (-/-) compared to those from wt mice or NOD-scid mice. These findings suggest that CHOP expression is independent of the development of insulitis and diabetes but might affect the early production of insulin autoantibodies in the NOD mouse.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1573-675X
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pubmed:author |
pubmed-author:AbiruNN,
pubmed-author:ArakiEE,
pubmed-author:EguchiKK,
pubmed-author:EisenbarthG SGS,
pubmed-author:KawasakiEE,
pubmed-author:KobayashiMM,
pubmed-author:KuriyaGG,
pubmed-author:MoriMM,
pubmed-author:NagayamaYY,
pubmed-author:NakamuraHH,
pubmed-author:NakamuraKK,
pubmed-author:OyadomariSS,
pubmed-author:SatohTT,
pubmed-author:YamasakiHH,
pubmed-author:YuLL,
pubmed-author:ZhouHH
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pubmed:issnType |
Electronic
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
438-48
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21274633-Adoptive Transfer,
pubmed-meshheading:21274633-Animals,
pubmed-meshheading:21274633-Apoptosis,
pubmed-meshheading:21274633-Autoantibodies,
pubmed-meshheading:21274633-CD8-Positive T-Lymphocytes,
pubmed-meshheading:21274633-Endoplasmic Reticulum,
pubmed-meshheading:21274633-Gene Deletion,
pubmed-meshheading:21274633-Gene Expression Regulation,
pubmed-meshheading:21274633-In Situ Nick-End Labeling,
pubmed-meshheading:21274633-Insulin,
pubmed-meshheading:21274633-Insulin-Secreting Cells,
pubmed-meshheading:21274633-Lymphocyte Depletion,
pubmed-meshheading:21274633-Mice,
pubmed-meshheading:21274633-Mice, Inbred NOD,
pubmed-meshheading:21274633-Peroxidase,
pubmed-meshheading:21274633-Prediabetic State,
pubmed-meshheading:21274633-Spleen,
pubmed-meshheading:21274633-Stress, Physiological,
pubmed-meshheading:21274633-Transcription Factor CHOP
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pubmed:year |
2011
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pubmed:articleTitle |
CHOP deletion does not impact the development of diabetes but suppresses the early production of insulin autoantibody in the NOD mouse.
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pubmed:affiliation |
Department of Endocrinology and Metabolism, Unit of Translational Medicine, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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