Eschenhagen, Thomas

[["dc.bibliographiccitation.firstpage","452"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Nixdorff, U"],["dc.contributor.author","Hess, Andreas"],["dc.contributor.author","Budinsky, L."],["dc.contributor.author","Brune, K"],["dc.contributor.author","Michaelis, B."],["dc.contributor.author","Dhein, S."],["dc.contributor.author","Schwoerer, Alexander Peter"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:53:08Z"],["dc.date.available","2017-09-07T11:53:08Z"],["dc.date.issued","2006"],["dc.description.abstract","The concept of regenerating diseased myocardium by implantation of tissue-engineered heart muscle is intriguing, but convincing evidence is lacking that heart tissues can be generated at a size and with contractile properties that would lend considerable support to failing hearts. Here we created large (thickness/ diameter, 1-4 mm/15 mm), force-generating engineered heart tissue from neonatal rat heart cells. Engineered heart tissue formed thick cardiac muscle layers when implanted on myocardial infarcts in immune-suppressed rats. When evaluated 28 d later, engineered heart tissue showed undelayed electrical coupling to the native myocardium without evidence of arrhythmia induction. Moreover, engineered heart tissue prevented further dilation, induced systolic wall thickening of infarcted myocardial segments and improved fractional area shortening of infarcted hearts compared to controls (sham operation and noncontractile constructs). Thus, our study provides evidence that large contractile cardiac tissue grafts can be constructed in vitro, can survive after implantation and can support contractile function of infarcted hearts."],["dc.identifier.doi","10.1038/nm1394"],["dc.identifier.gro","3143714"],["dc.identifier.isi","000236581300035"],["dc.identifier.pmid","16582915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1259"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Engineered heart tissue grafts improve systolic and diastolic function in infarcted rat hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e14263"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Schwoerer, Alexander Peter"],["dc.contributor.author","Neuber, Christiane"],["dc.contributor.author","Emmons, Julius"],["dc.contributor.author","Biermann, Daniel"],["dc.contributor.author","Christalla, Thomas"],["dc.contributor.author","Grundhoff, Adam"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ehmke, Heimo"],["dc.date.accessioned","2017-09-07T11:45:09Z"],["dc.date.available","2017-09-07T11:45:09Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Mechanical overload leads to cardiac hypertrophy and mechanical unloading to cardiac atrophy. Both conditions produce similar transcriptional changes including a re-expression of fetal genes, despite obvious differences in phenotype. MicroRNAs (miRNAs) are discussed as superordinate regulators of global gene networks acting mainly at the translational level. Here, we hypothesized that defined sets of miRNAs may determine the direction of cardiomyocyte plasticity responses. Methodology/Principal Findings: We employed ascending aortic stenosis (AS) and heterotopic heart transplantation (HTX) in syngenic Lewis rats to induce mechanical overloading and unloading, respectively. Heart weight was 26 +/- 3% higher in AS (n = 7) and 33 +/- 2% lower in HTX (n = 7) as compared to sham-operated (n = 6) and healthy controls (n = 7). Small RNAs were enriched from the left ventricles and subjected to quantitative stem-loop specific RT-PCR targeting a panel of 351 miRNAs. In total, 153 miRNAs could be unambiguously detected. Out of 72 miRNAs previously implicated in the cardiovascular system, 40 miRNAs were regulated in AS and/or HTX. Overall, HTX displayed a slightly broader activation pattern for moderately regulated miRNAs. Surprisingly, however, the regulation of individual miRNA expression was strikingly similar in direction and amplitude in AS and HTX with no miRNA being regulated in opposite direction. In contrast, fetal hearts from Lewis rats at embryonic day 18 exhibited an entirely different miRNA expression pattern. Conclusions: Taken together, our findings demonstrate that opposite changes in cardiac workload induce a common miRNA expression pattern which is markedly different from the fetal miRNA expression pattern. The direction of postnatal adaptive cardiac growth does, therefore, not appear to be determined at the level of single miRNAs or a specific set of miRNAs. Moreover, miRNAs themselves are not reprogrammed to a fetal program in response to changes in hemodynamic load."],["dc.identifier.doi","10.1371/journal.pone.0014263"],["dc.identifier.gro","3142819"],["dc.identifier.isi","000285135800004"],["dc.identifier.pmid","21151612"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6919"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/265"],["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.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Common MicroRNA Signatures in Cardiac Hypertrophic and Atrophic Remodeling Induced by Changes in Hemodynamic Load"],["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","1285"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","1298"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Christalla, Peter"],["dc.contributor.author","Rubart, Michael"],["dc.contributor.author","Muppala, Vijayakumar"],["dc.contributor.author","Doeker, Stephan"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Rau, Thomas"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Schwoerer, Alexander Peter"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Schumacher, Udo"],["dc.contributor.author","Fuchs, Sigrid"],["dc.contributor.author","Lange, Claudia"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Tao, Wen"],["dc.contributor.author","Scherschel, John A."],["dc.contributor.author","Soonpaa, Mark H."],["dc.contributor.author","Yang, Tao"],["dc.contributor.author","Lin, Qiong"],["dc.contributor.author","Zenke, Martin"],["dc.contributor.author","Han, Dong-Wook"],["dc.contributor.author","Schoeler, Hans R."],["dc.contributor.author","Rudolph, Cornelia"],["dc.contributor.author","Steinemann, Doris"],["dc.contributor.author","Schlegelberger, Brigitte"],["dc.contributor.author","Kattman, Steve"],["dc.contributor.author","Witty, Alec"],["dc.contributor.author","Keller, Gordon"],["dc.contributor.author","Field, Loren J."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:47:47Z"],["dc.date.available","2017-09-07T11:47:47Z"],["dc.date.issued","2013"],["dc.description.abstract","Uniparental parthenotes are considered an unwanted byproduct of in vitro fertilization. In utero parthenote development is severely compromised by defective organogenesis and in particular by defective cardiogenesis. Although developmentally compromised, apparently pluripotent stem cells can be derived from parthenogenetic blastocysts. Here we hypothesized that nonembryonic parthenogenetic stem cells (PSCs) can be directed toward the cardiac lineage and applied to tissue-engineered heart repair. We first confirmed similar fundamental properties in murine PSCs and embryonic stem cells (ESCs), despite notable differences in genetic (allelic variability) and epigenetic (differential imprinting) characteristics. Haploidentity of major histocompatibility complexes (MHCs) in PSCs is particularly attractive for allogeneic cell-based therapies. Accordingly, we confirmed acceptance of PSCs in MHC-matched allotransplantation. Cardiomyocyte derivation from PSCs and ESCs was equally effective. The use of cardiomyocyte-restricted GFP enabled cell sorting and documentation of advanced structural and functional maturation in vitro and in vivo. This included seamless electrical integration of PSC-derived cardiomyocytes into recipient myocardium. Finally, we enriched cardiomyocytes to facilitate engineering of force-generating myocardium and demonstrated the utility of this technique in enhancing regional myocardial function after myocardial infarction. Collectively, our data demonstrate pluripotency, with unrestricted cardiogenicity in PSCs, and introduce this unique cell type as an attractive source for tissue-engineered heart repair."],["dc.identifier.doi","10.1172/JCI66854"],["dc.identifier.gro","3142382"],["dc.identifier.isi","000315749400038"],["dc.identifier.pmid","23434590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7663"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/10"],["dc.notes.intern","WoS Import 2017-03-10"],["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","0021-9738"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Parthenogenetic stem cells for tissue-engineered heart repair"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","470"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","474"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Rudolph, Volker"],["dc.contributor.author","Andrié, René P."],["dc.contributor.author","Rudolph, Tanja K."],["dc.contributor.author","Friedrichs, Kai"],["dc.contributor.author","Klinke, Anna"],["dc.contributor.author","Hirsch-Hoffmann, Birgit"],["dc.contributor.author","Schwoerer, Alexander P."],["dc.contributor.author","Lau, Denise"],["dc.contributor.author","Fu, XiaoMing"],["dc.contributor.author","Klingel, Karin"],["dc.contributor.author","Sydow, Karsten"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Seniuk, Anika"],["dc.contributor.author","von Leitner, Eike-Christin"],["dc.contributor.author","Szoecs, Katalin"],["dc.contributor.author","Schrickel, Jan W."],["dc.contributor.author","Treede, Hendrik"],["dc.contributor.author","Wenzel, Ulrich"],["dc.contributor.author","Lewalter, Thorsten"],["dc.contributor.author","Nickenig, Georg"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Meinertz, Thomas"],["dc.contributor.author","Böger, Rainer H."],["dc.contributor.author","Reichenspurner, Hermann"],["dc.contributor.author","Freeman, Bruce A."],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Hazen, Stanley L."],["dc.contributor.author","Willems, Stephan"],["dc.contributor.author","Baldus, Stephan"],["dc.date.accessioned","2017-09-07T11:46:08Z"],["dc.date.available","2017-09-07T11:46:08Z"],["dc.date.issued","2010"],["dc.description.abstract","Observational clinical and ex vivo studies have established a strong association between atrial fibrillation and inflammation(1). However, whether inflammation is the cause or the consequence of atrial fibrillation and which specific inflammatory mediators may increase the atria's susceptibility to fibrillation remain elusive. Here we provide experimental and clinical evidence for the mechanistic involvement of myeloperoxidase (MPO), a heme enzyme abundantly expressed by neutrophils, in the pathophysiology of atrial fibrillation. MPO-deficient mice pretreated with angiotensin II (AngII) to provoke leukocyte activation showed lower atrial tissue abundance of the MPO product 3-chlorotyrosine, reduced activity of matrix metalloproteinases and blunted atrial fibrosis as compared to wild-type mice. Upon right atrial electrophysiological stimulation, MPO-deficient mice were protected from atrial fibrillation, which was reversed when MPO was restored. Humans with atrial fibrillation had higher plasma concentrations of MPO and a larger MPO burden in right atrial tissue as compared to individuals devoid of atrial fibrillation. In the atria, MPO colocalized with markedly increased formation of 3-chlorotyrosine. Our data demonstrate that MPO is a crucial prerequisite for structural remodeling of the myocardium, leading to an increased vulnerability to atrial fibrillation."],["dc.identifier.doi","10.1038/nm.2124"],["dc.identifier.gro","3142946"],["dc.identifier.isi","000276446800053"],["dc.identifier.pmid","20305660"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6269"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/406"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10. FU_Med"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1078-8956"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]