Nucleotide-binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions

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dc.contributor.authorM Y Kwon-
dc.contributor.authorN Hwang-
dc.contributor.authorS H Back-
dc.contributor.authorSeon-Jin Lee-
dc.contributor.authorM A Perrella-
dc.contributor.authorS W Chung-
dc.date.accessioned2020-10-27T03:19:13Z-
dc.date.available2020-10-27T03:19:13Z-
dc.date.issued2020-
dc.identifier.issn1742464X-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/22985-
dc.description.abstractEndoplasmic reticulum (ER) stress-induced cell death of vascular smooth muscle cells (VSMCs) is extensively involved in atherosclerotic plaque stabilization. We previously reported that nucleotide-binding oligomerization domain protein 2 (NOD2) participated in vascular homeostasis and tissue injury. However, the role and underlying mechanisms of NOD2 remain unknown in ER stress-induced cell death of VSMC during vascular diseases, including advanced atherosclerosis. Here, we report that NOD2 specifically interacted with ER stress sensor activating transcription factor 6 (ATF6) and suppressed the expression of proapoptotic transcription factor CHOP (C/EBP homologous protein) during ER stress. CHOP-positive cells were increased in neointimal lesions after femoral artery injury in NOD2-deficient mice. In particular, a NOD2 ligand, MDP, and overexpression of NOD2 decreased CHOP expression in wild-type VSMCs. NOD2 interacted with an ER stress sensor molecule, ATF6, and acted as a negative regulator for ATF6 activation and its downstream target molecule, CHOP, that regulates ER stress-induced apoptosis. Moreover, NOD2 deficiency promoted disruption of advanced atherosclerotic lesions and CHOP expression in NOD2-/- ApoE-/- mice. Our findings indicate an unsuspected critical role for NOD2 in ER stress-induced cell death.-
dc.publisherWiley-
dc.titleNucleotide-binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions-
dc.title.alternativeNucleotide-binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions-
dc.typeArticle-
dc.citation.titleFEBS Journal-
dc.citation.number10-
dc.citation.endPage2069-
dc.citation.startPage2055-
dc.citation.volume287-
dc.contributor.affiliatedAuthorSeon-Jin Lee-
dc.contributor.alternativeName권민영-
dc.contributor.alternativeName황나래-
dc.contributor.alternativeName박성훈-
dc.contributor.alternativeName이선진-
dc.contributor.alternativeNamePerrella-
dc.contributor.alternativeName정수월-
dc.identifier.bibliographicCitationFEBS Journal, vol. 287, no. 10, pp. 2055-2069-
dc.identifier.doi10.1111/febs.15294-
dc.subject.keywordATF6-
dc.subject.keywordcell death-
dc.subject.keywordCHOP-
dc.subject.keywordER stress-
dc.subject.keywordNOD2-
dc.subject.localATF6-
dc.subject.localcell death-
dc.subject.localCell death-
dc.subject.localCHOP-
dc.subject.localER stress-
dc.subject.localNOD2-
dc.description.journalClassY-
Appears in Collections:
Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
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