DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wang, Jie | ko |
dc.contributor.author | Song, Mi-Young | ko |
dc.contributor.author | Lee, Joo Young | ko |
dc.contributor.author | Kwon, Keun Sang | ko |
dc.contributor.author | Park, Byung-Hyun | ko |
dc.date.accessioned | 2024-03-22T07:00:46Z | - |
dc.date.available | 2024-03-22T07:00:46Z | - |
dc.date.created | 2024-03-21 | - |
dc.date.issued | 2015-10 | - |
dc.identifier.citation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.466, no.3, pp.300 - 305 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | http://hdl.handle.net/10203/318778 | - |
dc.description.abstract | Uncontrolled endoplasmic reticulum (ER) stress activates members of the NOD-like receptor family, which are involved in the pyrin domain containing 3 (NLRP3) inflammasome pathway. This pathway has been proposed to contribute to beta-cell dysfunction and death. However, the connection between ER stress and NLRP3 inflammasome activation remains controversial. Here we generated Akita/KO (Ins2(+/C96Y); NLRP3(-/-)) mice by crossing Akita (Ins2(+/C96Y); NLRP3(+/+)) mice with NLRP3 KO (Ins2(+/+); NLRP3(-/-)) mice. We then compared the metabolic phenotypes of the different strains. Knockout of the NLRP3 inflammasome did not affect the onset or the severity of diabetes in Akita/KO mice at any point of the study. Histological observations of pancreatic islets supported these findings. Tunicamycin-exposed islets from NLRP3 KO mice exhibited similar levels of ER stress and apoptosis induction as islets from WT (Ins2(+/+); NLRP3(+/+)) mice. Furthermore, NLRP3 deletion did not prevent tunicamycin-mediated reduction of glucose-stimulated insulin secretion. In conclusion, deletion of the NLRP3 inflammasome did not protect against ER stress-induced diabetes development or beta-cell damage, indicating that beta cell death in Akita mice is not mediated via activation of the NLRP3 inflammasome. (C) 2015 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.title | The NLRP3 inflammasome is dispensable for ER stress-induced pancreatic β-cell damage in Akita mice | - |
dc.type | Article | - |
dc.identifier.wosid | 000363094400004 | - |
dc.identifier.scopusid | 2-s2.0-84943365756 | - |
dc.type.rims | ART | - |
dc.citation.volume | 466 | - |
dc.citation.issue | 3 | - |
dc.citation.beginningpage | 300 | - |
dc.citation.endingpage | 305 | - |
dc.citation.publicationname | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.identifier.doi | 10.1016/j.bbrc.2015.09.009 | - |
dc.contributor.localauthor | Park, Byung-Hyun | - |
dc.contributor.nonIdAuthor | Wang, Jie | - |
dc.contributor.nonIdAuthor | Song, Mi-Young | - |
dc.contributor.nonIdAuthor | Lee, Joo Young | - |
dc.contributor.nonIdAuthor | Kwon, Keun Sang | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | NLRP3 inflammasome | - |
dc.subject.keywordAuthor | Akita | - |
dc.subject.keywordAuthor | ER stress | - |
dc.subject.keywordAuthor | Islets | - |
dc.subject.keywordAuthor | Tunicamycin | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | THIOREDOXIN-INTERACTING PROTEIN | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | IL-1-BETA | - |
dc.subject.keywordPlus | PUMA | - |
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