Cited 32 times in
sRAGE attenuates angiotensin II-induced cardiomyocyte hypertrophy by inhibiting RAGE-NFκB-NLRP3 activation.
DC Field | Value | Language |
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dc.contributor.author | 박성하 | - |
dc.date.accessioned | 2018-09-28T08:49:35Z | - |
dc.date.available | 2018-09-28T08:49:35Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 1023-3830 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/163124 | - |
dc.description.abstract | OBJECTIVE AND DESIGN: The receptor for advanced glycation endproducts (RAGE) is an innate immunity receptor that has been implicated in the pathogenesis of atherosclerotic cardiovascular disease. However, the possibility that RAGE-mediated signaling is involved in angiotensin II (Ang II)-induced cardiac left ventricular hypertrophy has yet to be investigated. We therefore determined whether RAGE has a role in regulating pathological cardiac hypertrophy. MATERIALS AND SUBJECTS: Protein abundance was estimated using Western blotting and intracellular ROS level and phospho-p65 were detected using fluorescence microscopy. Enzyme-linked immunosorbent assay was used to detect HMGB1 and IL-1β. All in vitro experiments were performed using H9C2 cells. TREATMENTS: To induce cardiomyocyte hypertrophy, 300 nM Ang II was treated for 48 h and 2 µg/ml sRAGE was treated 1 h prior to addition of Ang II. RESULTS: sRAGE attenuated Ang II-induced cardiomyocyte hypertrophy by downregulating RAGE and angiotensin II type 1 receptor expression. Secretion levels of high motility group box 1 and interleukin-1β, estimated from a cell culture medium, were significantly reduced by sRAGE. Activated PKCs and ERK1/2, important signals in left ventricular hypertrophy (LVH) development, were downregulated by sRAGE treatment. Furthermore, we found that nuclear factor-κB and NOD-like receptor protein 3 (NLRP3) were associated with RAGE-mediated cardiomyocyte hypertrophy. CONCLUSIONS: In the context of these results, we conclude that RAGE induces cardiac hypertrophy through the activation of the PKCs-ERK1/2 and NF-κB-NLRP3-IL1β signaling pathway, and suggest that RAGE-NLRP3 may be an important mediator of Ang II-induced cardiomyocyte hypertrophy. In addition, we determined that inhibition of RAGE activation with soluble RAGE (sRAGE) has a protective effect on Ang II-induced cardiomyocyte hypertrophy. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Birkhäuser | - |
dc.relation.isPartOf | INFLAMMATION RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | sRAGE attenuates angiotensin II-induced cardiomyocyte hypertrophy by inhibiting RAGE-NFκB-NLRP3 activation. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Internal Medicine | - |
dc.contributor.googleauthor | Soyeon Lim | - |
dc.contributor.googleauthor | Myung Eun Lee | - |
dc.contributor.googleauthor | Jisu Jeong | - |
dc.contributor.googleauthor | Jiye Lee | - |
dc.contributor.googleauthor | Soyoung Cho | - |
dc.contributor.googleauthor | Miran Seo | - |
dc.contributor.googleauthor | Sungha Park | - |
dc.identifier.doi | 10.1007/s00011-018-1160-9 | - |
dc.contributor.localId | A01512 | - |
dc.relation.journalcode | J01059 | - |
dc.identifier.eissn | 1420-908X | - |
dc.identifier.pmid | 29796842 | - |
dc.identifier.url | https://link.springer.com/article/10.1007%2Fs00011-018-1160-9 | - |
dc.subject.keyword | Cardiac hypertrophy | - |
dc.subject.keyword | NLRP3 | - |
dc.subject.keyword | RAGE | - |
dc.subject.keyword | Soluble RAGE | - |
dc.contributor.alternativeName | Park, Sung Ha | - |
dc.contributor.affiliatedAuthor | Park, Sung Ha | - |
dc.citation.volume | 67 | - |
dc.citation.number | 8 | - |
dc.citation.startPage | 691 | - |
dc.citation.endPage | 701 | - |
dc.identifier.bibliographicCitation | INFLAMMATION RESEARCH, Vol.67(8) : 691-701, 2018 | - |
dc.identifier.rimsid | 58395 | - |
dc.type.rims | ART | - |
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