Zimmermann, Wolfram-Hubertus

[["dc.bibliographiccitation.firstpage","975"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","991"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Guessoum, Celina I."],["dc.contributor.author","Lam, Tuan-Dinh D."],["dc.contributor.author","Ghadri, Jelena R."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Huber, Mia A."],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Lüscher, Thomas F."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Templin, Christian"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2018-04-23T11:48:11Z"],["dc.date.available","2018-04-23T11:48:11Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Takotsubo syndrome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life-threating complications in the acute phase. The underlying disease mechanism in TTS is still unknown. A genetic basis has been suggested to be involved in the pathogenesis. Objectives The aims of the study were to establish an in vitro induced pluripotent stem cell (iPSC) model of TTS, to test the hypothesis of altered β-adrenergic signaling in TTS iPSC-cardiomyocytes (CMs), and to explore whether genetic susceptibility underlies the pathophysiology of TTS. Methods Somatic cells of patients with TTS and control subjects were reprogrammed to iPSCs and differentiated into CMs. Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overstimulation. We investigated β-adrenergic signaling and TTS cardiomyocyte function. Results Enhanced β-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the cardiac stress marker NR4A1; cyclic adenosine monophosphate levels; and cyclic adenosine monophosphate–dependent protein kinase A–mediated hyperphosphorylation of RYR2-S2808, PLN-S16, TNI-S23/24, and Cav1.2-S1928, and leads to a reduced calcium time to transient 50% decay. These cellular catecholamine-dependent responses were mainly mediated by β1-adrenoceptor signaling in TTS. Engineered heart muscles from TTS-iPSC-CMs showed an impaired force of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control subjects. In addition, altered electrical activity and increased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed by differentially expressed lipid transporters CD36 and CPT1C. Furthermore, we uncovered genetic variants in different key regulators of cardiac function. Conclusions Enhanced β-adrenergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechanisms associated with the TTS phenotype."],["dc.identifier.doi","10.1016/j.jacc.2017.06.061"],["dc.identifier.gro","3142333"],["dc.identifier.pmid","28818208"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13468"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/204"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Catecholamine-Dependent β-Adrenergic Signaling in a Pluripotent Stem Cell Model of Takotsubo Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Stem Cells International"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","2018"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Sattler, Katherine"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:37:41Z"],["dc.date.available","2020-12-10T18:37:41Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1155/2018/6067096"],["dc.identifier.pmid","29535773"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77065"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/325"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ion Channel Expression and Characterization in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1410"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","1421"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Albers, Sebastian"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Xu, Qiang"],["dc.contributor.author","Kleinsorge, Mandy"],["dc.contributor.author","Huang, Mengying"],["dc.contributor.author","Liao, Zhenxing"],["dc.contributor.author","Zhong, Rujia"],["dc.contributor.author","Rudic, Boris"],["dc.contributor.author","Müller, Jonas"],["dc.contributor.author","Dinkel, Hendrik"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Diecke, Sebastian"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:19:09Z"],["dc.date.available","2020-12-10T18:19:09Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1093/europace/euz122"],["dc.identifier.pmid","31106349"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75142"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/328"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","A cellular model of Brugada syndrome with SCN10A variants using human-induced pluripotent stem cell-derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","Suppl. 1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Springer, R."],["dc.contributor.author","Seibertz, F."],["dc.contributor.author","Solano, R. A."],["dc.contributor.author","Rubio, T."],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Voigt, Niels"],["dc.date.accessioned","2022-05-17T07:38:45Z"],["dc.date.available","2022-05-17T07:38:45Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1093/eurheartj/ehz748.0193"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107983"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/316"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A13: Bedeutung einer gestörten zytosolischen Calciumpufferung bei der atrialen Arrhythmogenese bei Patienten mit Herzinsuffizienz (HF)"],["dc.relation.conference","ESC Congress 2019 together with World Congress of Cardiology"],["dc.relation.eventend","2019-09-04"],["dc.relation.eventlocation","Paris"],["dc.relation.eventstart","2019-08-31"],["dc.relation.issn","0195-668X"],["dc.relation.issn","1522-9645"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Voigt (Molecular Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","P1235Acetylcholine-activated inward-rectifier potassium currents in atrial cardiomyocytes derived from induced pluripotent stem cells and atrial engineered heart muscle preparations"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2935"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2018-04-23T11:49:22Z"],["dc.date.available","2018-04-23T11:49:22Z"],["dc.date.issued","2017"],["dc.description.abstract","Severe infections like sepsis lead frequently to cardiomyopathy. The mechanisms are unclear and an optimal therapy for septic cardiomyopathy still lacks. The aim of this study is to establish an endotoxin-induced inflammatory model using human induced pluripotent stem cell (hiPSC) derived cardiomyocytes (hiPSC-CMs) for mechanistic and therapeutic studies. hiPSC-CMs were treated by lipopolysaccharide (LPS) in different concentrations for different times. ELISA, FACS, qPCR, and patch-clamp techniques were used for the study. TLR4 (Toll-like receptor 4) and its associated proteins, CD14, LBP (lipopolysaccharide binding protein), TIRAP (toll-interleukin 1 receptor domain containing adaptor protein), Ly96 (lymphocyte antigen 96) and nuclear factor kappa B as well as some pro-and anti-inflammatory factors are expressed in hiPSC-CMs. LPS-treatment for 6 hours increased the expression levels of pro-inflammatory and chemotactic cytokines (TNF-a, IL-1ß, IL-6, CCL2, CCL5, IL-8), whereas 48 hour-treatment elevated the expression of anti-inflammatory factors (IL-10 and IL-6). LPS led to cell injury resulting from exaggerated cell apoptosis and necrosis. Finally, LPS inhibited small conductance Ca2+-activated K+ channel currents, enhanced Na+/Ca2+-exchanger currents, prolonged action potential duration, suggesting cellular electrical dysfunctions. Our data demonstrate that hiPSC-CMs possess the functional reaction system involved in endotoxin-induced inflammation and can model some bacterium-induced inflammatory responses in cardiac myocytes."],["dc.identifier.doi","10.1038/s41598-017-03147-4"],["dc.identifier.gro","3142526"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14783"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13682"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Lipopolysaccharides induced inflammatory responses and electrophysiological dysfunctions in human-induced pluripotent stem cell derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","S1873506121003202"],["dc.bibliographiccitation.firstpage","102473"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Schoger, Eric"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zelarayán, Laura Cecilia"],["dc.date.accessioned","2021-08-12T07:44:46Z"],["dc.date.available","2021-08-12T07:44:46Z"],["dc.date.issued","2021"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1016/j.scr.2021.102473"],["dc.identifier.pii","S1873506121003202"],["dc.identifier.pmid","34343828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88289"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/333"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/400"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation","SFB 1002 | INF: Unterstützung der SFB 1002 Forschungsdatenintegration, -visualisierung und -nachnutzung"],["dc.relation.issn","1873-5061"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Establishment of two homozygous CRISPR interference (CRISPRi) knock-in human induced pluripotent stem cell (hiPSC) lines for titratable endogenous gene repression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e99941"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","JCI Insight"],["dc.bibliographiccitation.lastpage","17"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Sekeres, Karolina"],["dc.contributor.author","Gerstenberg, Kathleen"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Henze, Sarah"],["dc.contributor.author","Stauske, Michael"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.date.accessioned","2019-02-04T14:06:58Z"],["dc.date.available","2019-02-04T14:06:58Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1172/jci.insight.99941"],["dc.identifier.pmid","29925689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57518"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/214"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A04: Patienten-spezifische induzierte pluripotente Stammzellen zur funktionellen Untersuchung von Ryanodinrezeptor-Mutationen"],["dc.relation","SFB 1002 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Lenz"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Deep phenotyping of human induced pluripotent stem cell–derived atrial and ventricular cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Müller, Jonas"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Zhong, Rujia"],["dc.contributor.author","Zhang, Feng"],["dc.contributor.author","Kleinsorge, Mandy"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Xu, Qiang"],["dc.contributor.author","Huang, Mengying"],["dc.contributor.author","Liao, Zhenxing"],["dc.contributor.author","Moscu-Gregor, Alexander"],["dc.contributor.author","Albers, Sebastian"],["dc.contributor.author","Dinkel, Hendrik"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Diecke, Sebastian"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiaobo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:44:21Z"],["dc.date.available","2020-12-10T18:44:21Z"],["dc.date.issued","2019"],["dc.description.abstract","Background Among rare channelopathies BrS patients are at high risk of sudden cardiac death (SCD). SCN5A mutations are found in a quarter of patients. Other rare gene mutations including SCN1B have been implicated to BrS. Studying the human cellular phenotype of BrS associated with rare gene mutation remains lacking. Objectives We sought to study the cellular phenotype of BrS with the SCN1B gene variants using human-induced pluripotent stem cell (hiPSCs)–derived cardiomyocytes (hiPSC-CMs). Methods and Results A BrS patient suffering from recurrent syncope harboring a two variants (c.629T \\u0026gt; C and c.637C \\u0026gt; A) in SCN1B, which encodes the function-modifying sodium channel beta1 subunit, and three independent healthy subjects were recruited and their skin biopsies were used to generate hiPSCs, which were differentiated into cardiomyocytes (hiPSC-CMs) for studying the cellular electrophysiology. A significantly reduced peak and late sodium channel current (INa) and a shift of activation curve to more positive potential as well as a shift of inactivation curve to more negative potential were detected in hiPSC-CMs of the BrS patient, indicating that the SCN1B variants impact the function of sodium channels in cardiomyocytes. The reduced INa led to a reduction of amplitude (APA) and upstroke velocity (Vmax) of action potentials. Ajmaline, a sodium channel blocker, showed a stronger effect on APA and Vmax in BrS cells as compared to cells from healthy donors. Furthermore, carbachol was able to increase arrhythmia events and the beating frequency in BrS. Conclusion Our hiPSC-CMs from a BrS-patient with two variants in SCN1B recapitulated some key phenotypic features of BrS and can provide a platform for studies on BrS with SCN1B variants."],["dc.identifier.doi","10.3389/fcell.2019.00261"],["dc.identifier.eissn","2296-634X"],["dc.identifier.pmid","31737628"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17195"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78416"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2296-634X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Studying Brugada Syndrome With an SCN1B Variants in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","195"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","202"],["dc.bibliographiccitation.volume","254"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Schünemann, Jan-Dierk"],["dc.contributor.author","Sattler, Katherine"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Patocskai, Bence"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Yücel, Gökhan"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Nowak, Daniel"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Bieback, Karen"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ravens, Ursula"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2018-04-23T11:49:14Z"],["dc.date.available","2018-04-23T11:49:14Z"],["dc.date.issued","2018"],["dc.description.abstract","Background and purpose Previous studies revealed that Takotsubo cardiomyopathy (TTC), a transient disorder of ventricular dysfunction affecting predominantly postmenopausal women, is associated with acquired long QT syndrome and arrhythmias, but the exact pathophysiologic mechanism is unknown. Our aim is to investigate the electrophysiological mechanism for QT-prolongation in TTC-patients by using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Methods hiPSC-CMs, which were generated from human skin fibroblasts of three healthy donors, were treated by estradiol (10 μM for one week) and a toxic concentration of isoprenaline (Iso, 1 mM for 2 h). Patch clamp techniques, qPCR and fluorescence-activated cell sorting (FACS) were employed for the study. Key results Iso enhanced late INa and suppressed Ito and thus prolonged the action potential duration (APD), suggesting possible reasons for arrhythmias in TTC. Iso elevated the production of reactive oxygen species (ROS). N-acetylcystein (1 mM), a ROS-blocker, abolished the effects of Iso on late INa and Ito. H2O2 (100 μM) mimicked Iso effects on late INa and Ito. These data indicate that the effects of Iso were mediated by ROS. Metoprolol (1 mM), a beta-blocker, prevented the effects of Iso on late INa and APD, confirming the adrenoceptor-dependent effects of Iso. Estradiol treatment prevented the APD-prolongation, attenuated the enhancement of INa, diminished the reduction of Ito, suppressed ROS-production induced by Iso and reduced the expression levels of adrenoceptors, suggesting protective effects of estragon against toxic effects of catecholamine. Conclusions Estradiol has protective effects against catecholamine excess and hence reduction in estrogen level may increase the risk of acquired long QT syndrome in TTC."],["dc.identifier.doi","10.1016/j.ijcard.2017.11.007"],["dc.identifier.gro","3142511"],["dc.identifier.pmid","29407091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13665"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/324"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0167-5273"],["dc.title","Estradiol protection against toxic effects of catecholamine on electrical properties in human-induced pluripotent stem cell derived cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","f46"],["dc.bibliographiccitation.issue","FI1"],["dc.bibliographiccitation.journal","Europace"],["dc.bibliographiccitation.lastpage","f56"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","El-Battrawy, Ibrahim"],["dc.contributor.author","Zhao, Zhihan"],["dc.contributor.author","Lan, Huan"],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Tombers, Christoph"],["dc.contributor.author","Li, Xin"],["dc.contributor.author","Buljubasic, Fanis"],["dc.contributor.author","Lang, Siegfried"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Utikal, Jochen"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Borggrefe, Martin"],["dc.contributor.author","Zhou, Xiao-Bo"],["dc.contributor.author","Akin, Ibrahim"],["dc.date.accessioned","2020-12-10T18:19:08Z"],["dc.date.available","2020-12-10T18:19:08Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1093/europace/euy042"],["dc.identifier.pmid","29566126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75139"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/271"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Electrical dysfunctions in human-induced pluripotent stem cell-derived cardiomyocytes from a patient with an arrhythmogenic right ventricular cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]