Soong, Poh Loong

[["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Trautsch, Irina"],["dc.contributor.author","Heta, Eriona"],["dc.contributor.author","Soong, Poh Loong"],["dc.contributor.author","Levent, Elif"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Mayr, Manuel"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2020-12-10T18:44:38Z"],["dc.date.available","2020-12-10T18:44:38Z"],["dc.date.issued","2019"],["dc.description.abstract","Redox signaling affects all aspects of cardiac function and homeostasis. With the development of genetically encoded fluorescent redox sensors, novel tools for the optogenetic investigation of redox signaling have emerged. Here, we sought to develop a human heart muscle model for in-tissue imaging of redox alterations. For this, we made use of (1) the genetically-encoded Grx1-roGFP2 sensor, which reports changes in cellular glutathione redox status (GSH/GSSG), (2) human embryonic stem cells (HES2), and (3) the engineered heart muscle (EHM) technology. We first generated HES2 lines expressing Grx1-roGFP2 in cytosol or mitochondria compartments by TALEN-guided genomic integration. Grx1-roGFP2 sensor localization and function was verified by fluorescence imaging. Grx1-roGFP2 HES2 were then subjected to directed differentiation to obtain high purity cardiomyocyte populations. Despite being able to report glutathione redox potential from cytosol and mitochondria, we observed dysfunctional sarcomerogenesis in Grx1-roGFP2 expressing cardiomyocytes. Conversely, lentiviral transduction of Grx1-roGFP2 in already differentiated HES2-cardiomyocytes and human foreskin fibroblast was possible, without compromising cell function as determined in EHM from defined Grx1-roGFP2-expressing cardiomyocyte and fibroblast populations. Finally, cell-type specific GSH/GSSG imaging was demonstrated in EHM. Collectively, our observations suggests a crucial role for redox signaling in cardiomyocyte differentiation and provide a solution as to how this apparent limitation can be overcome to enable cell-type specific GSH/GSSG imaging in a human heart muscle context."],["dc.identifier.doi","10.3389/fphys.2019.00272"],["dc.identifier.pmid","31024328"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78535"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/265"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/67"],["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 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.eissn","1664-042X"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Bogeski"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Optogenetic Monitoring of the Glutathione Redox State in Engineered Human Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1177"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","1199"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Gotz, M. E."],["dc.contributor.author","Malz, Cordula R."],["dc.contributor.author","Dirr, A."],["dc.contributor.author","Blum, D."],["dc.contributor.author","Gsell, W."],["dc.contributor.author","Schmidt, S."],["dc.contributor.author","Burger, R."],["dc.contributor.author","Pohli, S."],["dc.contributor.author","Riederer, Peter"],["dc.date.accessioned","2018-11-07T10:56:18Z"],["dc.date.available","2018-11-07T10:56:18Z"],["dc.date.issued","2005"],["dc.description.abstract","Aging, a process occuring in all vertebrates, is closely related to a loss in physical and functional abilities. There is widespread interest in clarifying the relevance of environmental, metabolic, and genetic factors for vertebrate aging. In the Pacific salmon a dramatic example of aging is known. Looking for changes in the salmon brain, perhaps even in the role of initiating the aging processes, we investigated several biochemical parameters that should reflect brain functional activity and stress response such as the neurotransmitters dopamine, and serotonin, and two of their respective metabolites 3,4-dihydroxyphenylacetic acid, and 5-hydroxyindole acetic acid, as well as glutathione, glutathione disulfide, and the extent of terminal deoxynucleotidyltransferase-mediated dUTP nick end-labelling. The aging of migrating sockeye salmon (Oncorhynchus nerka nerka) is accompanied by gradual increase in dopamine and serotonin turnover and a gradual decrease of brain total protein and glutathione levels. There appears to be an increased need for detoxification of reactive biological intermediates since activities of superoxide dismutase and catalase increase with age. However, our data do not support a major increase in apoptotic cell death during late aging but rather implicate an age related downward regulation of protein and glutathione synthesis and proteolysis increasing the need for autophagocytosis or heterophagocytosis in the course of cell death."],["dc.identifier.doi","10.1007/s00702-004-0257-1"],["dc.identifier.isi","000231502400004"],["dc.identifier.pmid","15682270"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49981"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","1435-1463"],["dc.relation.issn","0300-9564"],["dc.title","Brain aging phenomena in migrating sockeye salmon Oncorhynchus nerka nerka"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","209"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Dai, Yuanyuan"],["dc.contributor.author","Amenov, Asset"],["dc.contributor.author","Ignatyeva, Nadezda"],["dc.contributor.author","Koschinski, Andreas"],["dc.contributor.author","Xu, Hang"],["dc.contributor.author","Soong, Poh Loong"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Zaccolo, Manuela"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Ebert, Antje"],["dc.date.accessioned","2020-04-14T14:41:47Z"],["dc.date.available","2020-04-14T14:41:47Z"],["dc.date.issued","2020"],["dc.description.abstract","The sarcomeric troponin-tropomyosin complex is a critical mediator of excitation-contraction coupling, sarcomeric stability and force generation. We previously reported that induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) from patients with a dilated cardiomyopathy (DCM) mutation, troponin T (TnT)-R173W, display sarcomere protein misalignment and impaired contractility. Yet it is not known how TnT mutation causes dysfunction of sarcomere microdomains and how these events contribute to misalignment of sarcomeric proteins in presence of DCM TnT-R173W. Using a human iPSC-CM model combined with CRISPR/Cas9-engineered isogenic controls, we uncovered that TnT-R173W destabilizes molecular interactions of troponin with tropomyosin, and limits binding of PKA to local sarcomere microdomains. This attenuates troponin phosphorylation and dysregulates local sarcomeric microdomains in DCM iPSC-CMs. Disrupted microdomain signaling impairs MYH7-mediated, AMPK-dependent sarcomere-cytoskeleton filament interactions and plasma membrane attachment. Small molecule-based activation of AMPK can restore TnT microdomain interactions, and partially recovers sarcomere protein misalignment as well as impaired contractility in DCM TnT-R173W iPSC-CMs. Our findings suggest a novel therapeutic direction targeting sarcomere- cytoskeleton interactions to induce sarcomere re-organization and contractile recovery in DCM."],["dc.identifier.doi","10.1038/s41598-019-56597-3"],["dc.identifier.pmid","31937807"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64087"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/336"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A12: Alternative molekulare Signaltransduktionswege durch Kardiomyopathie-verursachende Troponin-Mutationen"],["dc.relation.issn","2045-2322"],["dc.relation.workinggroup","RG Ebert (Cardiovascular Cell Biology and Systems Medicine)"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Linke (Kardiovaskuläre Physiologie)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.title","Troponin destabilization impairs sarcomere-cytoskeleton interactions in iPSC-derived cardiomyocytes from dilated cardiomyopathy patients"],["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","167"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.seriesnr","1181"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Meyer, Tim"],["dc.contributor.author","Soong, Poh Loong"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:54:28Z"],["dc.date.available","2017-09-07T11:54:28Z"],["dc.date.issued","2014"],["dc.description.abstract","Cardiac muscle engineering has evolved over nearly 20 years from a scientific oddity to a mainstream technology with a wide range of applications. Of the many published methods it appears that hydrogels constitute the preferred scaffolds for myocardial tissue engineering and support of organotypic development. Here we describe a simple and highly robust protocol for the generation of engineered heart muscle using a collagen-based hydrogel method."],["dc.identifier.doi","10.1007/978-1-4939-1047-2_15"],["dc.identifier.gro","3145187"],["dc.identifier.pmid","25070336"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2895"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/63"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.publisher","Humana Press"],["dc.publisher.place","New York"],["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.crisseries","Methods in Molecular Biology"],["dc.relation.isbn","978-1-4939-1046-5"],["dc.relation.ispartof","Cardiac Tissue Engineering"],["dc.relation.ispartofseries","Methods in Molecular Biology;1181"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Collagen-Based Engineered Heart Muscle"],["dc.type","book_chapter"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Current Protocols in Cell Biology"],["dc.contributor.author","Soong, Poh Loong"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:54:28Z"],["dc.date.available","2017-09-07T11:54:28Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1002/0471143030.cb2308s55"],["dc.identifier.gro","3145185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2893"],["dc.notes.intern","Crossref Import"],["dc.notes.status","public"],["dc.publisher","Wiley-Blackwell"],["dc.title","Cardiac Differentiation of Human Embryonic Stem Cells and their Assembly into Engineered Heart Muscle"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","P2545"],["dc.bibliographiccitation.firstpage","533"],["dc.bibliographiccitation.issue","suppl_1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Soong, P. L."],["dc.contributor.author","Sur, S."],["dc.contributor.author","Fujita, B."],["dc.contributor.author","Grishina, E."],["dc.contributor.author","Kuzyakova, M."],["dc.contributor.author","Tiburcy, M."],["dc.contributor.author","Zimmermann, W. H."],["dc.date.accessioned","2019-02-27T09:52:25Z"],["dc.date.available","2019-02-27T09:52:25Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/eurheartj/ehx502.P2545"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57635"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/178"],["dc.language.iso","en"],["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.issn","0195-668X"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Inducible paracrine release of IGF-1 improves heart muscle thickness and function"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]