The matricellular protein CCN5 prevents adverse atrial structural and electrical remodelling
DC Field | Value | Language |
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dc.contributor.author | Lee, Min-Ah | - |
dc.contributor.author | Raad, Nour | - |
dc.contributor.author | Song, Min Ho | - |
dc.contributor.author | Yoo, Jimeen | - |
dc.contributor.author | Lee, Miyoung | - |
dc.contributor.author | Jang, Seung Pil | - |
dc.contributor.author | Kwak, Tae Hwan | - |
dc.contributor.author | Kook, Hyun | - |
dc.contributor.author | Choi, Eun-Kyoung | - |
dc.contributor.author | Cha, Tae-Joon | - |
dc.contributor.author | Hajjar, Roger J. | - |
dc.contributor.author | Jeong, Dongtak | - |
dc.contributor.author | Park, Woo Jin | - |
dc.date.accessioned | 2021-06-22T05:59:16Z | - |
dc.date.available | 2021-06-22T05:59:16Z | - |
dc.date.created | 2021-01-21 | - |
dc.date.issued | 2020-10 | - |
dc.identifier.issn | 1582-1838 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/834 | - |
dc.description.abstract | Atrial structural remodelling including atrial hypertrophy and fibrosis is a key mediator of atrial fibrillation (AF). We previously demonstrated that the matricellular protein CCN5 elicits anti-fibrotic and anti-hypertrophic effects in left ventricles under pressure overload. We here determined the utility of CCN5 in ameliorating adverse atrial remodelling and arrhythmias in a murine model of angiotensin II (AngII) infusion. Advanced atrial structural remodelling was induced by AngII infusion in control mice and mice overexpressing CCN5 either through transgenesis (CCN5 Tg) or AAV9-mediated gene transfer (AAV9-CCN5). The mRNA levels of pro-fibrotic and pro-inflammatory genes were markedly up-regulated by AngII infusion, which was significantly normalized by CCN5 overexpression. In vitro studies in isolated atrial fibroblasts demonstrated a marked reduction in AngII-induced fibroblast trans-differentiation in CCN5-treated atria. Moreover, while AngII increased the expression of phosphorylated CaMKII and ryanodine receptor 2 levels in HL-1 cells, these molecular features of AF were prevented by CCN5. Electrophysiological studies in ex vivo perfused hearts revealed a blunted susceptibility of the AAV9-CCN5-treated hearts to rapid atrial pacing-induced arrhythmias and concomitant reversal in AngII-induced atrial action potential prolongation. These data demonstrate the utility of a gene transfer approach targeting CCN5 for reversal of adverse atrial structural and electrophysiological remodelling. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.title | The matricellular protein CCN5 prevents adverse atrial structural and electrical remodelling | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Jeong, Dongtak | - |
dc.identifier.doi | 10.1111/jcmm.15789 | - |
dc.identifier.scopusid | 2-s2.0-85090138392 | - |
dc.identifier.wosid | 000565648800001 | - |
dc.identifier.bibliographicCitation | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, v.24, no.20, pp.11768 - 11778 | - |
dc.relation.isPartOf | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | - |
dc.citation.title | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | - |
dc.citation.volume | 24 | - |
dc.citation.number | 20 | - |
dc.citation.startPage | 11768 | - |
dc.citation.endPage | 11778 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.subject.keywordPlus | FIBRILLATION | - |
dc.subject.keywordPlus | FIBROSIS | - |
dc.subject.keywordPlus | AAV1/SERCA2A | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | MYOCYTES | - |
dc.subject.keywordPlus | INSIGHTS | - |
dc.subject.keywordPlus | DESIGN | - |
dc.subject.keywordPlus | BURDEN | - |
dc.subject.keywordPlus | CAMKII | - |
dc.subject.keywordPlus | TRIAL | - |
dc.subject.keywordAuthor | atrial fibrillation | - |
dc.subject.keywordAuthor | atrial fibrosis | - |
dc.subject.keywordAuthor | CaMKII | - |
dc.subject.keywordAuthor | CCN5 | - |
dc.identifier.url | https://onlinelibrary.wiley.com/doi/10.1111/jcmm.15789 | - |
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