Zelarayan, Laura Cecilia

[["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.firstpage","127"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.lastpage","131"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Haupt, Luis Peter"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Zelarayán, Laura Cecilia"],["dc.date.accessioned","2018-04-23T11:49:22Z"],["dc.date.available","2018-04-23T11:49:22Z"],["dc.date.issued","2017"],["dc.description.abstract","Krueppel-like factor 15 (KLF15) is abundantly expressed in liver, kidney, and muscle, including myocardium. In the adult heart KLF15 is important to maintain homeostasis and to repress hypertrophic remodeling. We generated a homozygous hESC KLF15 knockout (KO) line using paired CRISPR/Cas9n. KLF15-KO cells maintained full pluripotency and differentiation potential as well as genomic integrity. We demonstrated that KLF15-KO cells can be differentiated into morphologically normal cardiomyocytes turning them into a valuable tool for studying human KLF15-mediated mechanisms resulting in human cardiac dysfunction."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1016/j.scr.2017.07.007"],["dc.identifier.gro","3142524"],["dc.identifier.pmid","28925362"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14618"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13680"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/175"],["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 | 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.issn","1873-5061"],["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","Generation of a KLF15 homozygous knockout human embryonic stem cell line using paired CRISPR/Cas9n, and human cardiomyocytes derivation"],["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.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.firstpage","6"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","24"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Schoger, Eric"],["dc.contributor.author","Carroll, Kelli J."],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","McAnally, John R."],["dc.contributor.author","Tan, Wei"],["dc.contributor.author","Liu, Ning"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Groß, Julia"],["dc.contributor.author","Herzog, Nicole"],["dc.contributor.author","Doroudgar, Shirin"],["dc.contributor.author","Bassel-Duby, Rhonda"],["dc.contributor.author","Zimmermann, Wolfram-H."],["dc.contributor.author","Zelarayán, Laura C."],["dc.date.accessioned","2020-12-10T18:38:00Z"],["dc.date.available","2020-12-10T18:38:00Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1161/CIRCRESAHA.118.314522"],["dc.identifier.pmid","31730408"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77162"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/332"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["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.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","CRISPR-Mediated Activation of Endogenous Gene Expression in the Postnatal Heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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","88"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal of Heart Failure. Supplements"],["dc.bibliographiccitation.lastpage","88"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","ZELARAYAN, L"],["dc.contributor.author","BAURAND, A"],["dc.contributor.author","VANDERNAGEL, R"],["dc.contributor.author","GEHRKE, C"],["dc.contributor.author","RENGER, A"],["dc.contributor.author","NOACK, C"],["dc.contributor.author","DIETZ, R"],["dc.contributor.author","BERGMANN, M"],["dc.date.accessioned","2022-03-01T11:45:37Z"],["dc.date.available","2022-03-01T11:45:37Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1016/S1567-4215(07)60249-5"],["dc.identifier.pii","S1567421507602495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103393"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","1567-4215"],["dc.title","381 Inhibition of beta-catenin suppresses left ventricular remodelling after infarct"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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"]]