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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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Title: CHOP deletion does not impact the development of diabetes but suppresses the early production of insulin autoantibody in the NOD mouse.
Authors: Satoh, T / Abiru, Norio / Kobayashi, M / Zhou, H / Nakamura, K / Kuriya, Genpei / Nakamura, H / Nagayama, Y / Kawasaki, Eiji / Yamasaki, H / Yu, L / Eisenbarth, G S / Araki, Eiichi / Mori, M / Oyadomari, Seiichi / Eguchi, K
Issue Date: Apr-2011
Publisher: Springer
Citation: Apoptosis, 16(4), pp.438-448; 2011
Abstract: C/EBP homologous protein (CHOP) has been proposed as a key transcription factor for endoplasmic reticulum (ER) stress-mediated β-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 β-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 β-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.
Keywords: Apoptosis / Autoantibody / CHOP / ER stress / Non-obese diabetic mouse / Type 1 diabetes
URI: http://hdl.handle.net/10069/24877
ISSN: 13608185
DOI: 10.1007/s10495-011-0576-2
PubMed ID: 21274633
Rights: © Springer Science+Business Media, LLC 2011 / The original publication is available at www.springerlink.com
Type: Journal Article
Text Version: author
Appears in Collections:Articles in academic journal

Citable URI : http://hdl.handle.net/10069/24877

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