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dc.contributor.authorChang, Shih-Linen_US
dc.contributor.authorHsiao, Ya-Wenen_US
dc.contributor.authorTsai, Yung-Nanen_US
dc.contributor.authorLin, Shien-Fongen_US
dc.contributor.authorLiu, Shuen-Hsinen_US
dc.contributor.authorLin, Yenn-Jiangen_US
dc.contributor.authorLo, Li-Weien_US
dc.contributor.authorChung, Fa-Poen_US
dc.contributor.authorChao, Tze-Fanen_US
dc.contributor.authorHu, Yu-Fengen_US
dc.contributor.authorTuan, Ta-Chuanen_US
dc.contributor.authorLiao, Nanen_US
dc.contributor.authorHsieh, Yu-Chengen_US
dc.contributor.authorWu, Tsu-Jueyen_US
dc.contributor.authorHiga, Satoshien_US
dc.contributor.authorChen, Shih-Annen_US
dc.date.accessioned2019-04-02T06:00:53Z-
dc.date.available2019-04-02T06:00:53Z-
dc.date.issued2018-09-01en_US
dc.identifier.issn0022-2828en_US
dc.identifier.urihttp://dx.doi.org/10.1016/j.yjmcc.2018.08.005en_US
dc.identifier.urihttp://hdl.handle.net/11536/148197-
dc.description.abstractBackground: We aimed to investigate the impact of interleukin (IL)-17 on ventricular remodeling and the genesis of ventricular arrhythmia (VA) in an ischemic heart failure (HF) model. The expression of the proinflammatory cytokine IL-17 is upregulated during myocardial ischemia and plays a fundamental role in post-infarct inflammation. However, the influence of IL-17 on the genesis of VA has not yet been studied. Methods and results: The level of inflammation and Th17 cell (CD4(+)IL-17(+)) expression in the rabbit model of ischemic HF were studied by flow cytometry, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA). The effect of IL-17 on VA induction following acute and chronic administration of IL-17 was determined using electrophysiological techniques and optical mapping. The expression of IL-17 target genes and related cytokines and chemokines in vivo and in vitro were measured using qPCR, ELISA, and immunoblotting. Th17 cells were markedly increased in the ischemic HF rabbit model. IL-17 directly induced VA in vivo and in vitro in a dose-dependent manner. IL-17 decreased conduction velocity, lengthened action potential duration, and increased the slope of the left ventricle (LV) restitution curve. IL-17 treatment led to fibrosis, collagen production and apoptosis in the LV. Furthermore, increased IL-17 signaling activated mitogen-activated protein kinase and increased the expression of downstream target genes, IL-6, TNF, CCL20, and CXCL1. An anti IL -17 neutralizing antibody abolished the effects of IL-17. Conclusions: The expression of IL-17 and its downstream target genes may play fundamental roles in inducing VA in ischemic HF.en_US
dc.language.isoen_USen_US
dc.subjectVentricular arrhythmiasen_US
dc.subjectInflammationen_US
dc.subjectIL-17en_US
dc.subjectMAPKen_US
dc.titleInterleukin-17 enhances cardiac ventricular remodeling via activating MAPK pathway in ischemic heart failureen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.yjmcc.2018.08.005en_US
dc.identifier.journalJOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGYen_US
dc.citation.volume122en_US
dc.citation.spage69en_US
dc.citation.epage79en_US
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000445321700007en_US
dc.citation.woscount2en_US
Appears in Collections:Articles