Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 정동탁 | - |
dc.date.accessioned | 2021-08-27T06:26:42Z | - |
dc.date.available | 2021-08-27T06:26:42Z | - |
dc.date.issued | 2020-09 | - |
dc.identifier.citation | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, v. 24, Issue. 20, Page. 11768-11778 | en_US |
dc.identifier.issn | 1582-1838 | - |
dc.identifier.issn | 1582-4934 | - |
dc.identifier.uri | https://onlinelibrary.wiley.com/doi/10.1111/jcmm.15789 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/164645 | - |
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. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | WILEY | en_US |
dc.title | The matricellular protein CCN5 prevents adverse atrial structural and electrical remodelling | en_US |
dc.type | Article | en_US |
dc.relation.no | 20 | - |
dc.relation.volume | 24 | - |
dc.identifier.doi | 10.1111/jcmm.15789 | - |
dc.relation.page | 11768-11778 | - |
dc.relation.journal | JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | - |
dc.contributor.googleauthor | Lee, Min-Ah | - |
dc.contributor.googleauthor | Raad, Nour | - |
dc.contributor.googleauthor | Song, Min Ho | - |
dc.contributor.googleauthor | Yoo, Jimeen | - |
dc.contributor.googleauthor | Lee, Miyoung | - |
dc.contributor.googleauthor | Jang, Seung Pil | - |
dc.contributor.googleauthor | Kwak, Tae Hwan | - |
dc.contributor.googleauthor | Kook, Hyun | - |
dc.contributor.googleauthor | Choi, Eun-Kyoung | - |
dc.contributor.googleauthor | Cha, Tae-Joon | - |
dc.contributor.googleauthor | Jeong, Dongtak | - |
dc.relation.code | 2020051693 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF SCIENCE AND CONVERGENCE TECHNOLOGY[E] | - |
dc.sector.department | DEPARTMENT OF MOLECULAR AND LIFE SCIENCE | - |
dc.identifier.pid | cooljdt | - |
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