Becker, Alexander

[["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Rokita, Adam G."],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Preuss, Lena"],["dc.contributor.author","Gupta, Shamindra N."],["dc.contributor.author","Schmidt, Kathie"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zhu, W."],["dc.contributor.author","Reuter, Sean P."],["dc.contributor.author","Field, Loren J."],["dc.contributor.author","Kararigas, Georgios"],["dc.contributor.author","Regitz-Zagrosek, Vera"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Krueger, Martina"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Backs, Johannes"],["dc.date.accessioned","2018-11-07T08:56:56Z"],["dc.date.available","2018-11-07T08:56:56Z"],["dc.date.issued","2011"],["dc.format.extent","E421"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.110.017566"],["dc.identifier.isi","000289833500003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23266"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0009-7322"],["dc.title","Response to Letter Regarding Article, \"Differential Cardiac Remodeling in Preload Versus Afterload\""],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["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","993"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","1003"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Rokita, Adam G."],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Zhu, Wuqiang"],["dc.contributor.author","Kararigas, Georgios"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Reuter, Sean P."],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Preuss, Lena"],["dc.contributor.author","Gupta, Shamindra N."],["dc.contributor.author","Schmidt, Kathie"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Krueger, Martina"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Backs, Johannes"],["dc.contributor.author","Regitz-Zagrosek, Vera"],["dc.contributor.author","Schaefer, Katrin"],["dc.contributor.author","Field, Loren J."],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:45:19Z"],["dc.date.available","2017-09-07T11:45:19Z"],["dc.date.issued","2010"],["dc.description.abstract","Background-Hemodynamic load regulates myocardial function and gene expression. We tested the hypothesis that afterload and preload, despite similar average load, result in different phenotypes. Methods and Results-Afterload and preload were compared in mice with transverse aortic constriction (TAC) and aortocaval shunt (shunt). Compared with sham mice, 6 hours after surgery, systolic wall stress (afterload) was increased in TAC mice (+40%; P<0.05), diastolic wall stress (preload) was increased in shunt (+277%; P < 0.05) and TAC mice (+74%; P<0.05), and mean total wall stress was similarly increased in TAC (69%) and shunt mice (67%) (P=NS, TAC versus shunt; each P<0.05 versus sham). At 1 week, left ventricular weight/tibia length was significantly increased by 22% in TAC and 29% in shunt mice (P=NS, TAC versus shunt). After 24 hours and 1 week, calcium/calmodulin-dependent protein kinase II signaling was increased in TAC. This resulted in altered calcium cycling, including increased L-type calcium current, calcium transients, fractional sarcoplasmic reticulum calcium release, and calcium spark frequency. In shunt mice, Akt phosphorylation was increased. TAC was associated with inflammation, fibrosis, and cardiomyocyte apoptosis. The latter was significantly reduced in calcium/calmodulin-dependent protein kinase II delta-knockout TAC mice. A total of 157 mRNAs and 13 microRNAs were differentially regulated in TAC versus shunt mice. After 8 weeks, fractional shortening was lower and mortality was higher in TAC versus shunt mice. Conclusions-Afterload results in maladaptive fibrotic hypertrophy with calcium/calmodulin-dependent protein kinase II-dependent altered calcium cycling and apoptosis. Preload is associated with Akt activation without fibrosis, little apoptosis, better function, and lower mortality. This indicates that different loads result in distinct phenotype differences that may require specific pharmacological interventions. (Circulation. 2010;122:993-1003.)"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.110.943431"],["dc.identifier.gro","3142865"],["dc.identifier.isi","000282020600008"],["dc.identifier.pmid","20733099"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/316"],["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","Lippincott Williams & Wilkins"],["dc.relation.issn","0009-7322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Differential Cardiac Remodeling in Preload Versus Afterload"],["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"]]