Eschenhagen, Thomas

[["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","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"]]