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dc.contributor.authorSchimmel, Katharina
dc.contributor.authorStojanović, Stevan D.
dc.contributor.authorHuang, Cheng Kai
dc.contributor.authorJung, Mira
dc.contributor.authorMeyer, Martin H.
dc.contributor.authorXiao, Ke
dc.contributor.authorGrote-Levi, Lea
dc.contributor.authorBär, Christian
dc.contributor.authorPfanne, Angelika
dc.contributor.authorMitzka, Saskia
dc.contributor.authorJust, Annette
dc.contributor.authorGeffers, Robert
dc.contributor.authorBock, Katharina
dc.contributor.authorKenneweg, Franziska
dc.contributor.authorKleemiß, Felix
dc.contributor.authorFalk, Christine S.
dc.contributor.authorFiedler, Jan
dc.contributor.authorThum, Thomas
dc.date.accessioned2020-11-18T12:28:18Z
dc.date.available2020-11-18T12:28:18Z
dc.date.issued2021-01-01
dc.identifier.citationJ Mol Cell Cardiol. 2020 Oct 28;150:91-100. doi: 10.1016/j.yjmcc.2020.10.008. Epub ahead of print.en_US
dc.identifier.issn00222828
dc.identifier.pmid33127387en
dc.identifier.doi10.1016/j.yjmcc.2020.10.008
dc.identifier.urihttp://hdl.handle.net/10033/622594
dc.description.abstractBackground: Myocardial fibrosis is a hallmark of the failing heart, contributing to the most common causes of deaths worldwide. Several microRNAs (miRNAs, miRs) controlling cardiac fibrosis were identified in recent years; however, a more global approach to identify miRNAs involved in fibrosis is missing. Methods and results: Functional miRNA mimic library screens were applied in human cardiac fibroblasts (HCFs) to identify annotated miRNAs inducing proliferation. In parallel, miRNA deep sequencing was performed after subjecting HCFs to proliferating and resting stimuli, additionally enabling discovery of novel miRNAs. In-depth in vitro analysis confirmed the pro-fibrotic nature of selected, highly conserved miRNAs miR-20a-5p and miR-132-3p. To determine downstream cellular pathways and their role in the fibrotic response, targets of the annotated miRNA candidates were modulated by synthetic siRNA. We here provide evidence that repression of autophagy and detoxification of reactive oxygen species by miR-20a-5p and miR-132-3p explain some of their pro-fibrotic nature on a mechanistic level. Conclusion: We here identified both miR-20a-5p and miR-132-3p as crucial regulators of fibrotic pathways in an in vitro model of human cardiac fibroblast biology.en_US
dc.description.sponsorshipEuropean Research Councilen_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectAutophagyen_US
dc.subjectCardiac fibrosisen_US
dc.subjectmiR-132en_US
dc.subjectMiR-20a-5pen_US
dc.subjectNovel miRsen_US
dc.subjectReactive oxygen speciesen_US
dc.titleCombined high-throughput library screening and next generation RNA sequencing uncover microRNAs controlling human cardiac fibroblast biologyen_US
dc.typeArticleen_US
dc.identifier.eissn10958584
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalJournal of Molecular and Cellular Cardiologyen_US
dc.identifier.eid2-s2.0-85094615995
dc.identifier.scopusidSCOPUS_ID:85094615995
dc.identifier.piiS0022282820303035
dc.source.volume150
dc.source.beginpage91
dc.source.endpage100
refterms.dateFOA2020-11-18T12:28:19Z
dc.source.journaltitleJournal of Molecular and Cellular Cardiology


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