Chitinase-3-like protein 1 ameliorates atherosclerotic responses via PPAR delta-mediated suppression of inflammation and ER stress
DC Field | Value | Language |
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dc.contributor.author | Jung, Tae Woo | - |
dc.contributor.author | Park, Hyung Sub | - |
dc.contributor.author | Choi, Geum Hee | - |
dc.contributor.author | Kim, Daehwan | - |
dc.contributor.author | Jeong, Ji Hoon | - |
dc.contributor.author | Lee, Taeseung | - |
dc.date.available | 2019-03-07T04:35:18Z | - |
dc.date.issued | 2018-08 | - |
dc.identifier.issn | 0730-2312 | - |
dc.identifier.issn | 1097-4644 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1897 | - |
dc.description.abstract | Chitinase 3-like protein 1 (CHI3L1) is a novel biomarker of systemic inflammation. However, the effects of CHI3L1 on the progression of atherosclerosis remain to be explored. In the current study, we found that CHI3L1 induces peroxisome proliferator-activated receptor delta (PPAR) expression, leading to a dose-dependent increase in oxygen-regulated protein 150 (ORP150) expression. We demonstrated that CHI3L1 suppresses atherosclerotic reactions caused by LPS treatment via a PPAR-dependent pathway. Treatment of HUVECs and THP-1 cells with CHI3L1 suppressed LPS-induced phosphorylation of nuclear factor kappa B (NFB) and secretion of proinflammatory cytokines such as TNF and MCP-1. In HUVECs, expression of adhesion molecules and LPS-stimulated adhesion of THP-1 cells to the endothelium were significantly reduced after CHI3L1 treatment. Furthermore, LPS-induced endoplasmic reticulum (ER) stress and cell apoptosis were significantly ameliorated after treatment of HUVECs with CHI3L1. Particularly, all of the pro-atherosclerotic effects were significantly mitigated by treatment with small interfering (si) RNA for PPAR. In conclusion, CHI3L1 ameliorates LPS-induced atherosclerotic reactions via PPAR-mediated suppression of inflammation and ER stress. | - |
dc.format.extent | 11 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY | - |
dc.title | Chitinase-3-like protein 1 ameliorates atherosclerotic responses via PPAR delta-mediated suppression of inflammation and ER stress | - |
dc.type | Article | - |
dc.identifier.doi | 10.1002/jcb.26873 | - |
dc.identifier.bibliographicCitation | JOURNAL OF CELLULAR BIOCHEMISTRY, v.119, no.8, pp 6795 - 6805 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000436542900048 | - |
dc.identifier.scopusid | 2-s2.0-85046536014 | - |
dc.citation.endPage | 6805 | - |
dc.citation.number | 8 | - |
dc.citation.startPage | 6795 | - |
dc.citation.title | JOURNAL OF CELLULAR BIOCHEMISTRY | - |
dc.citation.volume | 119 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | chitinase 3-like protein 1 | - |
dc.subject.keywordAuthor | HUVECs | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | oxygen-regulated protein 150 | - |
dc.subject.keywordAuthor | peroxisome proliferator-activated receptor delta | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | FOLLISTATIN-LIKE 1 | - |
dc.subject.keywordPlus | ACUTE CORONARY SYNDROME | - |
dc.subject.keywordPlus | HUMAN CARTILAGE GP-39 | - |
dc.subject.keywordPlus | SMOOTH-MUSCLE CELLS | - |
dc.subject.keywordPlus | LDLR-/-MICE | - |
dc.subject.keywordPlus | ENDOTHELIAL-CELLS | - |
dc.subject.keywordPlus | REDUCES ATHEROSCLEROSIS | - |
dc.subject.keywordPlus | MYOCARDIAL-INFARCTION | - |
dc.subject.keywordPlus | ADHESION MOLECULES | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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