Zafeiriou, Maria Patapia

[["dc.bibliographiccitation.firstpage","361"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids"],["dc.bibliographiccitation.lastpage","369"],["dc.bibliographiccitation.volume","1811"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Nigam, Santosh"],["dc.contributor.author","Siafaka-Kapadai, Athanassia"],["dc.date.accessioned","2018-11-07T08:55:31Z"],["dc.date.available","2018-11-07T08:55:31Z"],["dc.date.issued","2011"],["dc.description.abstract","Pancreatic beta-cells have a deficit of scavenging enzymes such as catalase (Cat) and glutathione peroxidase (GPx) and therefore are susceptible to oxidative stress and apoptosis. Our previous work showed that, in the absence of cytosolic GPx in insulinoma RINm5F cells, an intrinsic activity of 12 lipoxygenase (12(S)-LOX) converts 12S-hydroperoxyeicosatetraenoic acid (12(S)-HpETE) to the bioactive epoxide hepoxilin A(3) (HXA(3)). The aim of the present study was to investigate the effect of HXA(3) on apoptosis as compared to its precursor 12(S)-HpETE and shed light upon the underlying pathways. In contrast to 12(S)-HpETE, which induced apoptosis via the extrinsic pathway, we found HXA(3) not only to prevent it but also to promote cell proliferation. In particular, HXA3 suppressed the pro-apoptotic BAX and upregulated the anti-apoptotic Bcl-2. Moreover, HXA(3) induced the anti-apoptotic 12(S)-LOX by recruiting heat shock protein 90 (HSP90), another anti-apoptotic protein. Finally, a co-chaperone protein of HSP90, protein phosphatase 5 (PP5), was upregulated by HXA(3), which counteracted oxidative stress-induced apoptosis by dephosphorylating and thus inactivating apoptosis signal-regulating kinase 1 (ASK1). Taken together, these findings suggest that HXA(3) protects insulinoma cells from oxidative stress and, via multiple signaling pathways, prevents them from undergoing apoptosis. (C) 2011 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft, Bonn [Ni242/27-1]"],["dc.identifier.doi","10.1016/j.bbalip.2011.03.002"],["dc.identifier.isi","000291192600001"],["dc.identifier.pmid","21420506"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22928"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1388-1981"],["dc.title","Hepoxilin A(3) protects beta-cells from apoptosis in contrast to its precursor, 12-hydroperoxyeicosatetraenoic acid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Dietz, Rainer"],["dc.contributor.author","Schaeffer, Hans-Joerg"],["dc.contributor.author","Bergmann, Martin"],["dc.contributor.author","Zelarayan, Laura"],["dc.date.accessioned","2018-11-07T08:49:44Z"],["dc.date.available","2018-11-07T08:49:44Z"],["dc.date.issued","2011"],["dc.identifier.isi","000299738706353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21532"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0009-7322"],["dc.title","Interaction of Krueppel-Like Factor (klf) 15 and Wnt-Signaling Pathway and its Role in Adult Cardiac Precursor Cell Regulation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.contributor.author","Rathjens, Franziska S."],["dc.contributor.author","Blenkle, Alica"],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Syeda, Fahima"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Jungmann, Andreas"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zafeiriou, Maria Patapia"],["dc.date.accessioned","2021-06-01T10:51:17Z"],["dc.date.available","2021-06-01T10:51:17Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Aims  Arrhythmias and sudden cardiac death (SCD) occur commonly in patients with heart failure. We found T-box 5 (TBX5) dysregulated in ventricular myocardium from heart failure patients and thus we hypothesized that TBX5 reduction contributes to arrhythmia development in these patients. To understand the underlying mechanisms, we aimed to reveal the ventricular TBX5-dependent transcriptional network and further test the therapeutic potential of TBX5 level normalization in mice with documented arrhythmias. Methods and results  We used a mouse model of TBX5 conditional deletion in ventricular cardiomyocytes. Ventricular (v) TBX5 loss in mice resulted in mild cardiac dysfunction and arrhythmias and was associated with a high mortality rate (60%) due to SCD. Upon angiotensin stimulation, vTbx5KO mice showed exacerbated cardiac remodelling and dysfunction suggesting a cardioprotective role of TBX5. RNA-sequencing of a ventricular-specific TBX5KO mouse and TBX5 chromatin immunoprecipitation was used to dissect TBX5 transcriptional network in cardiac ventricular tissue. Overall, we identified 47 transcripts expressed under the control of TBX5, which may have contributed to the fatal arrhythmias in vTbx5KO mice. These included transcripts encoding for proteins implicated in cardiac conduction and contraction (Gja1, Kcnj5, Kcng2, Cacna1g, Chrm2), in cytoskeleton organization (Fstl4, Pdlim4, Emilin2, Cmya5), and cardiac protection upon stress (Fhl2, Gpr22, Fgf16). Interestingly, after TBX5 loss and arrhythmia development in vTbx5KO mice, TBX5 protein-level normalization by systemic adeno-associated-virus (AAV) 9 application, re-established TBX5-dependent transcriptome. Consequently, cardiac dysfunction was ameliorated and the propensity of arrhythmia occurrence was reduced. Conclusions  This study uncovers a novel cardioprotective role of TBX5 in the adult heart and provides preclinical evidence for the therapeutic value of TBX5 protein normalization in the control of arrhythmia."],["dc.identifier.doi","10.1093/cvr/cvaa239"],["dc.identifier.pmid","32777030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86956"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/211"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/380"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["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.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.relation.workinggroup","RG Zafeiriou (3D Electrically Excitable Cell Networks – Brain and Heart)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY-NC 4.0"],["dc.title","Preclinical evidence for the therapeutic value of TBX5 normalization in arrhythmia control"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","992"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1007"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Schaeffer, Hans-Joerg"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Pavlova, Elena"],["dc.contributor.author","Dietz, Rainer"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Bergmann, Martin W."],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2017-09-07T11:48:25Z"],["dc.date.available","2017-09-07T11:48:25Z"],["dc.date.issued","2012"],["dc.description.abstract","Wnt/beta-catenin signalling controls adult heart remodelling in part via regulation of cardiac progenitor cell (CPC) differentiation. An enhanced understanding of mechanisms controlling CPC biology might facilitate the development of new therapeutic strategies in heart failure. We identified and characterized a novel cardiac interaction between Krueppel-like factor 15 and components of the Wnt/beta-catenin pathway leading to inhibition of transcription. In vitro mutation, reporter assays and co-localization analyses revealed that KLF15 requires both the C-terminus, necessary for nuclear localization, and a minimal N-terminal regulatory region to inhibit transcription. In line with this, functional Klf15 knock-out mice exhibited cardiac beta-catenin transcriptional activation along with functional cardiac deterioration in normal homeostasis and upon hypertrophy. We further provide in vivo and in vitro evidences for preferential endothelial lineage differentiation of CPCs upon KLF15 deletion. Via inhibition of beta-catenin transcription, KLF15 controls CPC homeostasis in the adult heart similar to embryonic cardiogenesis. This knowledge may provide a tool for reactivation of this apparently dormant CPC population in the adult heart and thus be an attractive approach to enhance endogenous cardiac repair."],["dc.identifier.doi","10.1002/emmm.201101043"],["dc.identifier.gro","3142470"],["dc.identifier.isi","000308302900015"],["dc.identifier.pmid","22767436"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8640"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Deutsche Forschungsgemeinschaft (DFG); Juergen Manchot Foundation"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1757-4676"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Krueppel-like factor 15 regulates Wnt/ss-catenin transcription and controls cardiac progenitor cell fate in the postnatal heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","928"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stem Cells"],["dc.bibliographiccitation.lastpage","940"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Pavlova, Elena"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Sharkova, Krasimira"],["dc.contributor.author","Bergmann, Martin W."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayán, Laura C."],["dc.date.accessioned","2017-09-07T11:47:43Z"],["dc.date.available","2017-09-07T11:47:43Z"],["dc.date.issued","2013"],["dc.description.abstract","The multiphasic regulation of the Wnt/beta-catenin canonical pathway is essential for cardiogenesis in vivo and in vitro. To achieve tight regulation of the Wnt/b-catenin signaling, tissue- and cell-specific coactivators and repressors need to be recruited. The identification of such factors may help to elucidate mechanisms leading to enhanced cardiac differentiation efficiency in vitro as well as promote regeneration in vivo. Using a yeast-two-hybrid screen, we identified four-and-a-half-LIM-domain 2 (FHL2) as a cardiac-specific beta-catenin interaction partner and activator of Wnt/beta-catenin-dependent transcription. We analyzed the role of this interaction for early cardiogenesis in an in vitro model by making use of embryoid body cultures from mouse embryonic stem cells (ESCs). In this model, stable FHL2 gain-of-function promoted mesodermal cell formation and cell proliferation while arresting cardiac differentiation in an early cardiogenic mesodermal progenitor state. Mechanistically, FHL2 overexpression enhanced nuclear accumulation of beta-catenin and activated Wnt/beta-catenin-dependent transcription leading to sustained upregulation of the early cardiogenic gene Igfbp5. In an alternative P19 cell model, transient FHL2 overexpression led to early activation of Wnt/beta-catenin-dependent transcription, but not sustained high-level of Igfbp5 expression. This resulted in enhanced cardiogenesis. We propose that early Wnt/beta-catenin-dependent transcriptional activation mediated by FHL2 is important for the transition to and expansion of early cardiogenic mesodermal cells. Collectively, our findings offer mechanistic insight into the early cardiogenic code and may be further exploited to enhance cardiac progenitor cell activity in vitro and in vivo. STEM CELLS 2013;31:928-940"],["dc.identifier.doi","10.1002/stem.1332"],["dc.identifier.gro","3142355"],["dc.identifier.isi","000318014100010"],["dc.identifier.pmid","23341242"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10650"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7364"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/49"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.issn","1066-5099"],["dc.relation.issn","1549-4918"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The Four and a Half LIM-Domain 2 Controls Early Cardiac Cell Commitment and Expansion Via Regulating β-Catenin-Dependent Transcription"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2018-11-07T09:54:34Z"],["dc.date.available","2018-11-07T09:54:34Z"],["dc.date.issued","2015"],["dc.identifier.isi","000374552800252"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36562"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Loss of Krueppel-like Factor 15 (KLF15) Leads to Altered Wnt-dependent Gene Regulation in Hearts With Systolic Dysfunction"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","387"],["dc.contributor.author","Pavlova, Elena"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayan, Laura"],["dc.date.accessioned","2018-11-07T09:44:50Z"],["dc.date.available","2018-11-07T09:44:50Z"],["dc.date.issued","2014"],["dc.format.extent","S74"],["dc.identifier.isi","000359538500300"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34482"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","Basic leucine zipper and W2 domain is a novel Wnt component with a potential role in cardiogenesis and cardiac remodeling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2480"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","STEM CELLS"],["dc.bibliographiccitation.lastpage","2491"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Zafiriou, Maria Patapia"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Pavlova, Elena"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Bergmann, Martin W."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2017-09-07T11:45:36Z"],["dc.date.available","2017-09-07T11:45:36Z"],["dc.date.issued","2014"],["dc.description.abstract","The role of erythropoietin (Epo) in myocardial repair after infarction remains inconclusive. We observed high Epo receptor (EPOR) expression in cardiac progenitor cells (CPCs). Therefore, we aimed to characterize these cells and elucidate their contribution to myocardial regeneration on Epo stimulation. High EPOR expression was detected during murine embryonic heart development followed by a marked decrease until adulthood. EPOR-positive cells in the adult heart were identified in a CPC-enriched cell population and showed coexpression of stem, mesenchymal, endothelial, and cardiomyogenic cell markers. We focused on the population coexpressing early (TBX5, NKX2.5) and definitive (myosin heavy chain [MHC], cardiac Troponin T [cTNT]) cardiomyocyte markers. Epo increased their proliferation and thus were designated as Epo-responsive MHC expressing cells (EMCs). In vitro, EMCs proliferated and partially differentiated toward cardiomyocyte-like cells. Repetitive Epo administration in mice with myocardial infarction (cumulative dose 4 IU/g) resulted in an increase in cardiac EMCs and cTNT-positive cells in the infarcted area. This was further accompanied by a significant preservation of cardiac function when compared with control mice. Our study characterized an EPO-responsive MHC-expressing cell population in the adult heart. Repetitive, moderate-dose Epo treatment enhanced the proliferation of EMCs resulting in preservation of post-ischemic cardiac function."],["dc.identifier.doi","10.1002/stem.1741"],["dc.identifier.gro","3142066"],["dc.identifier.isi","000341294500017"],["dc.identifier.pmid","24806289"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12130"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4167"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/77"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1549-4918"],["dc.relation.issn","1066-5099"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Erythropoietin Responsive Cardiomyogenic Cells Contribute to Heart Repair Post Myocardial Infarction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1804"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","1819"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Schoger, Eric"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Woelfer, Monique"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Milting, Hendrik"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Streckfuss-Boemeke, Katrin"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayán, Laura C."],["dc.date.accessioned","2020-12-10T14:24:44Z"],["dc.date.available","2020-12-10T14:24:44Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.jacc.2019.07.076"],["dc.identifier.pmid","31582141"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72339"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/283"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["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 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["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","KLF15-Wnt–Dependent Cardiac Reprogramming Up-Regulates SHISA3 in the Mammalian Heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2850"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","2867"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Iyer, Lavanya M"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Woelfer, Monique"],["dc.contributor.author","Schoger, Eric"],["dc.contributor.author","Khadjeh, Sara"],["dc.contributor.author","Zafiriou, Maria Patapia"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Herting, Jonas"],["dc.contributor.author","Pang, Sze Ting"],["dc.contributor.author","Weber, Tobias"],["dc.contributor.author","Rathjens, Franziska S."],["dc.contributor.author","Fischer, Thomas H."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Zelarayán, Laura C."],["dc.date.accessioned","2018-04-23T11:47:57Z"],["dc.date.available","2018-04-23T11:47:57Z"],["dc.date.issued","2018"],["dc.description.abstract","Chromatin remodelling precedes transcriptional and structural changes in heart failure. A body of work suggests roles for the developmental Wnt signalling pathway in cardiac remodelling. Hitherto, there is no evidence supporting a direct role of Wnt nuclear components in regulating chromatin landscapes in this process. We show that transcriptionally active, nuclear, phosphorylated(p)Ser675-β-catenin and TCF7L2 are upregulated in diseased murine and human cardiac ventricles. We report that inducible cardiomyocytes (CM)-specific pSer675-β-catenin accumulation mimics the disease situation by triggering TCF7L2 expression. This enhances active chromatin, characterized by increased H3K27ac and TCF7L2 occupancies to cardiac developmental and remodelling genes in vivo. Accordingly, transcriptomic analysis of β-catenin stabilized hearts shows a strong recapitulation of cardiac developmental processes like cell cycling and cytoskeletal remodelling. Mechanistically, TCF7L2 co-occupies distal genomic regions with cardiac transcription factors NKX2–5 and GATA4 in stabilized-β-catenin hearts. Validation assays revealed a previously unrecognized function of GATA4 as a cardiac repressor of the TCF7L2/β-catenin complex in vivo, thereby defining a transcriptional switch controlling disease progression. Conversely, preventing β-catenin activation post-pressure-overload results in a downregulation of these novel TCF7L2-targets and rescues cardiac function. Thus, we present a novel role for TCF7L2/β-catenin in CMs-specific chromatin modulation, which could be exploited for manipulating the ubiquitous Wnt pathway."],["dc.description.sponsorship","Open-Access-Publikatinsfonds 2018"],["dc.identifier.doi","10.1093/nar/gky049"],["dc.identifier.gro","3142314"],["dc.identifier.pmid","29394407"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13447"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/201"],["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 | A11: Absolute Arrhythmie bei Vorhofflimmern - ein neuer Mechanismus, der zu einer Störung von Ca2+-Homöostase und elektrischer Stabilität in der Transition zur Herzinsuffizienz führt"],["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 | S02: Hochauflösende Fluoreszenzmikroskopie und integrative Datenanalyse"],["dc.relation","SFB 1002 | INF: Unterstützung der SFB 1002 Forschungsdatenintegration, -visualisierung und -nachnutzung"],["dc.relation.issn","0305-1048"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG T. Fischer"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","A context-specific cardiac β-catenin and GATA4 interaction influences TCF7L2 occupancy and remodels chromatin driving disease progression in the adult heart"],["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"]]