Rebs, Sabine

[["dc.bibliographiccitation.artnumber","13"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Haupt, Luis Peter"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Maurer, Wiebke"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Maus, Andreas"],["dc.contributor.author","Köhne, Steffen"],["dc.contributor.author","Tappu, Rewati"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2022-04-01T10:01:09Z"],["dc.date.available","2022-04-01T10:01:09Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Cancer therapies with anthracyclines have been shown to induce cardiovascular complications. The aims of this study were to establish an in vitro induced pluripotent stem cell model (iPSC) of anthracycline-induced cardiotoxicity (ACT) from patients with an aggressive form of B-cell lymphoma and to examine whether doxorubicin (DOX)-treated ACT-iPSC cardiomyocytes (CM) can recapitulate the clinical features exhibited by patients, and thus help uncover a DOX-dependent pathomechanism. ACT-iPSC CM generated from individuals with CD20 + B-cell lymphoma who had received high doses of DOX and suffered cardiac dysfunction were studied and compared to control-iPSC CM from cancer survivors without cardiac symptoms. In cellular studies, ACT-iPSC CM were persistently more susceptible to DOX toxicity including augmented disorganized myofilament structure, changed mitochondrial shape, and increased apoptotic events. Consistently, ACT-iPSC CM and cardiac fibroblasts isolated from fibrotic human ACT myocardium exhibited higher DOX-dependent reactive oxygen species. In functional studies, Ca 2+ transient amplitude of ACT-iPSC CM was reduced compared to control cells, and diastolic sarcoplasmic reticulum Ca 2+ leak was DOX-dependently increased. This could be explained by overactive CaMKIIδ in ACT CM. Together with DOX-dependent augmented proarrhythmic cellular triggers and prolonged action potentials in ACT CM, this suggests a cellular link to arrhythmogenic events and contractile dysfunction especially found in ACT engineered human myocardium. CamKIIδ inhibition prevented proarrhythmic triggers in ACT. In contrast, control CM upregulated SERCA2a expression in a DOX-dependent manner, possibly to avoid heart failure conditions. In conclusion, we developed the first human patient-specific stem cell model of DOX-induced cardiac dysfunction from patients with B-cell lymphoma. Our results suggest that DOX-induced stress resulted in arrhythmogenic events associated with contractile dysfunction and finally in heart failure after persistent stress activation in ACT patients."],["dc.identifier.doi","10.1007/s00395-022-00918-7"],["dc.identifier.pii","918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105613"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1435-1803"],["dc.relation.issn","0300-8428"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Doxorubicin induces cardiotoxicity in a pluripotent stem cell model of aggressive B cell lymphoma cancer patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","S2666166721008236"],["dc.bibliographiccitation.firstpage","101117"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","STAR Protocols"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Buchwald, Tjark Alexander"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2022-04-01T10:02:33Z"],["dc.date.available","2022-04-01T10:02:33Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/j.xpro.2021.101117"],["dc.identifier.pii","S2666166721008236"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105942"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.issn","2666-1667"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","A quantitative RT-PCR protocol to adapt and quantify RBM20-dependent exon splicing of targets at the human locus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","101746"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Maurer, Wiebke"],["dc.contributor.author","Ghadri, Jelena R."],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Templin, Christian"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2020-12-10T15:21:15Z"],["dc.date.available","2020-12-10T15:21:15Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.scr.2020.101746"],["dc.identifier.issn","1873-5061"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72964"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Generation of iPSC-lines from two independent Takotsubo syndrome patients with recurrent Takotsubo events"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","136"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","147"],["dc.bibliographiccitation.volume","164"],["dc.contributor.author","Emanuelli, Giulia"],["dc.contributor.author","Zoccarato, Anna"],["dc.contributor.author","Reumiller, Christina M."],["dc.contributor.author","Papadopoulos, Angelos"],["dc.contributor.author","Chong, Mei"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Betteridge, Kai"],["dc.contributor.author","Beretta, Matteo"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Shah, Ajay M."],["dc.date.accessioned","2022-06-01T09:39:03Z"],["dc.date.available","2022-06-01T09:39:03Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/j.yjmcc.2021.12.001"],["dc.identifier.pii","S0022282821002285"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108375"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.issn","0022-2828"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","A roadmap for the characterization of energy metabolism in human cardiomyocytes derived from induced pluripotent stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","101901"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Sedaghat-Hamedani, Farbod"],["dc.contributor.author","Kayvanpour, Elham"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2021-04-14T08:24:33Z"],["dc.date.available","2021-04-14T08:24:33Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.scr.2020.101901"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81329"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","1873-5061"],["dc.title","Generation of pluripotent stem cell lines and CRISPR/Cas9 modified isogenic controls from a patient with dilated cardiomyopathy harboring a RBM20 p.R634W mutation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Kokot, Karoline E."],["dc.contributor.author","Kneuer, Jasmin M."],["dc.contributor.author","John, David"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Möbius-Winkler, Maximilian N."],["dc.contributor.author","Erbe, Stephan"],["dc.contributor.author","Müller, Marion"],["dc.contributor.author","Andritschke, Michael"],["dc.contributor.author","Gaul, Susanne"],["dc.contributor.author","Sheikh, Bilal N."],["dc.contributor.author","Boeckel, Jes-Niels"],["dc.date.accessioned","2022-07-01T07:35:35Z"],["dc.date.available","2022-07-01T07:35:35Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Alterations of RNA editing that affect the secondary structure of RNAs can cause human diseases. We therefore studied RNA editing in failing human hearts. Transcriptome sequencing showed that adenosine-to-inosine (A-to-I) RNA editing was responsible for 80% of the editing events in the myocardium. Failing human hearts were characterized by reduced RNA editing. This was primarily attributable to Alu elements in introns of protein-coding genes. In the failing left ventricle, 166 circRNAs were upregulated and 7 circRNAs were downregulated compared to non-failing controls. Most of the upregulated circRNAs were associated with reduced RNA editing in the host gene. ADAR2, which binds to RNA regions that are edited from A-to-I, was decreased in failing human hearts. In vitro , reduction of ADAR2 increased circRNA levels suggesting a causal effect of reduced ADAR2 levels on increased circRNAs in the failing human heart. To gain mechanistic insight, one of the identified upregulated circRNAs with a high reduction of editing in heart failure, AKAP13, was further characterized. ADAR2 reduced the formation of double-stranded structures in AKAP13 pre-mRNA, thereby reducing the stability of Alu elements and the circularization of the resulting circRNA. Overexpression of circAKAP13 impaired the sarcomere regularity of human induced pluripotent stem cell-derived cardiomyocytes. These data show that ADAR2 mediates A-to-I RNA editing in the human heart. A-to-I RNA editing represses the formation of dsRNA structures of Alu elements favoring canonical linear mRNA splicing and inhibiting the formation of circRNAs. The findings are relevant to diseases with reduced RNA editing and increased circRNA levels and provide insights into the human-specific regulation of circRNA formation."],["dc.description.sponsorship"," Deutsche Gesellschaft für Kardiologie-Herz und Kreislaufforschung. http://dx.doi.org/10.13039/501100010578"],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship"," Universität Leipzig 501100008678"],["dc.identifier.doi","10.1007/s00395-022-00940-9"],["dc.identifier.pii","940"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112209"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","1435-1803"],["dc.relation.issn","0300-8428"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Reduction of A-to-I RNA editing in the failing human heart regulates formation of circular RNAs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1357"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","JACC: Clinical Electrophysiology"],["dc.bibliographiccitation.lastpage","1366"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Körtl, Thomas"],["dc.contributor.author","Stehle, Thea"],["dc.contributor.author","Riedl, Dominic"],["dc.contributor.author","Trausel, Johanna"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Paulus, Michael"],["dc.contributor.author","Holzamer, Andreas"],["dc.contributor.author","Marrouche, Nassir"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2022-12-01T08:30:38Z"],["dc.date.available","2022-12-01T08:30:38Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/j.jacep.2022.07.016"],["dc.identifier.pii","S2405500X22006466"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/117940"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.issn","2405-500X"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Atrial Fibrillation Burden Specifically Determines Human Ventricular Cellular Remodeling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","129"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Genomics, Proteomics & Bioinformatics"],["dc.bibliographiccitation.lastpage","146"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Boeckel, Jes-Niels"],["dc.contributor.author","Möbius-Winkler, Maximilian"],["dc.contributor.author","Müller, Marion"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Eger, Nicole"],["dc.contributor.author","Schoppe, Laura"],["dc.contributor.author","Tappu, Rewati"],["dc.contributor.author","Kokot, Karoline E."],["dc.contributor.author","Kneuer, Jasmin M."],["dc.contributor.author","Gaul, Susanne"],["dc.contributor.author","Meder, Benjamin"],["dc.date.accessioned","2022-12-01T08:30:36Z"],["dc.date.available","2022-12-01T08:30:36Z"],["dc.date.issued","2022"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/501100003042 Else Kroner-Fresenius-Stiftung"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/501100004937 BMBF Berlin"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/501100005970 Deutsche Stiftung für Herzforschung"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/501100007316 Klaus Tschira Foundation"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/501100013811 University of Leipzig Faculty of Medicine"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/100010447 DZHK"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/100011272 European Commission Seventh Framework Programme for Research and Technological Development Health"],["dc.identifier.doi","10.1016/j.gpb.2021.01.006"],["dc.identifier.pii","S1672022921001467"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/117929"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.issn","1672-0229"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","SLM2 Is A Novel Cardiac Splicing Factor Involved in Heart Failure due to Dilated Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]