Now showing 1 - 7 of 7
  • 2018Journal Article
    [["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Wagenhäuser, Markus U."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Yoshino, Takuya"],["dc.contributor.author","Toyama, Kensuke"],["dc.contributor.author","Kayama, Yosuke"],["dc.contributor.author","Deng, Alicia"],["dc.contributor.author","Guenther, Sabina P."],["dc.contributor.author","Petzold, Anne"],["dc.contributor.author","Mulorz, Joscha"],["dc.contributor.author","Mulorz, Pireyatharsheny"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Ibing, Wiebke"],["dc.contributor.author","Elvers, Margitta"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Ramasubramanian, Anand K."],["dc.contributor.author","Adam, Matti"],["dc.contributor.author","Schelzig, Hubert"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2020-12-10T18:44:37Z"],["dc.date.available","2020-12-10T18:44:37Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3389/fphys.2018.01459"],["dc.identifier.eissn","1664-042X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78531"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Chronic Nicotine Exposure Induces Murine Aortic Remodeling and Stiffness Segmentation—Implications for Abdominal Aortic Aneurysm Susceptibility"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2017Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","975"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","991"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Borchert, Thomas"],["dc.contributor.author","HĂĽbscher, Daniela"],["dc.contributor.author","Guessoum, Celina I."],["dc.contributor.author","Lam, Tuan-Dinh D."],["dc.contributor.author","Ghadri, Jelena R."],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liaw, Norman Y."],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Huber, Mia A."],["dc.contributor.author","Cyganek, Lukas"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","LĂĽscher, Thomas F."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Templin, Christian"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2018-04-23T11:48:11Z"],["dc.date.available","2018-04-23T11:48:11Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Takotsubo syndrome (TTS) is characterized by an acute left ventricular dysfunction and is associated with life-threating complications in the acute phase. The underlying disease mechanism in TTS is still unknown. A genetic basis has been suggested to be involved in the pathogenesis. Objectives The aims of the study were to establish an in vitro induced pluripotent stem cell (iPSC) model of TTS, to test the hypothesis of altered β-adrenergic signaling in TTS iPSC-cardiomyocytes (CMs), and to explore whether genetic susceptibility underlies the pathophysiology of TTS. Methods Somatic cells of patients with TTS and control subjects were reprogrammed to iPSCs and differentiated into CMs. Three-month-old CMs were subjected to catecholamine stimulation to simulate neurohumoral overstimulation. We investigated β-adrenergic signaling and TTS cardiomyocyte function. Results Enhanced β-adrenergic signaling in TTS-iPSC-CMs under catecholamine-induced stress increased expression of the cardiac stress marker NR4A1; cyclic adenosine monophosphate levels; and cyclic adenosine monophosphate–dependent protein kinase A–mediated hyperphosphorylation of RYR2-S2808, PLN-S16, TNI-S23/24, and Cav1.2-S1928, and leads to a reduced calcium time to transient 50% decay. These cellular catecholamine-dependent responses were mainly mediated by β1-adrenoceptor signaling in TTS. Engineered heart muscles from TTS-iPSC-CMs showed an impaired force of contraction and a higher sensitivity to isoprenaline-stimulated inotropy compared with control subjects. In addition, altered electrical activity and increased lipid accumulation were detected in catecholamine-treated TTS-iPSC-CMs, and were confirmed by differentially expressed lipid transporters CD36 and CPT1C. Furthermore, we uncovered genetic variants in different key regulators of cardiac function. Conclusions Enhanced β-adrenergic signaling and higher sensitivity to catecholamine-induced toxicity were identified as mechanisms associated with the TTS phenotype."],["dc.identifier.doi","10.1016/j.jacc.2017.06.061"],["dc.identifier.gro","3142333"],["dc.identifier.pmid","28818208"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13468"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/204"],["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 | D01: Erholung aus der Herzinsuffizienz – Einfluss von Fibrose und Transkriptionssignatur"],["dc.relation","SFB 1002 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG Cyganek (Stem Cell Unit)"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Guan (Application of patient-specific induced pluripotent stem cells in disease modelling)"],["dc.relation.workinggroup","RG HasenfuĂź (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Wollnik"],["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","Catecholamine-Dependent β-Adrenergic Signaling in a Pluripotent Stem Cell Model of Takotsubo Cardiomyopathy"],["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"]]
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  • 2016Conference Abstract
    [["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Tsao, Philip S."],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Raaz, Uwe"],["dc.date.accessioned","2018-11-07T10:15:54Z"],["dc.date.available","2018-11-07T10:15:54Z"],["dc.date.issued","2016"],["dc.format.extent","S75"],["dc.identifier.isi","000375417500148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40915"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Transcription factor Runx2 is induced in vascular aging and may promote age-related arterial stiffness"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2015Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","513"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","524"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Chernogubova, Ekaterina"],["dc.contributor.author","Warnecke, Christina"],["dc.contributor.author","Kayama, Yosuke"],["dc.contributor.author","Penov, Kiril"],["dc.contributor.author","Hennigs, Jan K."],["dc.contributor.author","Salomons, Florian"],["dc.contributor.author","Eken, Suzanne"],["dc.contributor.author","Emrich, Fabian C."],["dc.contributor.author","Zheng, Wei H."],["dc.contributor.author","Adam, Matti"],["dc.contributor.author","Jagger, Ann"],["dc.contributor.author","Nakagami, Futoshi"],["dc.contributor.author","Toh, Ryuji"],["dc.contributor.author","Toyama, Kensuke"],["dc.contributor.author","Deng, Alicia"],["dc.contributor.author","Buerke, Michael"],["dc.contributor.author","Maegdefessel, Lars"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2017-09-07T11:43:37Z"],["dc.date.available","2017-09-07T11:43:37Z"],["dc.date.issued","2015"],["dc.description.abstract","Rationale: Accelerated arterial stiffening is a major complication of diabetes mellitus with no specific therapy available to date. Objective: The present study investigates the role of the osteogenic transcription factor runt-related transcription factor 2 (Runx2) as a potential mediator and therapeutic target of aortic fibrosis and aortic stiffening in diabetes mellitus. Methods and Results: Using a murine model of type 2 diabetes mellitus (db/db mice), we identify progressive structural aortic stiffening that precedes the onset of arterial hypertension. At the same time, Runx2 is aberrantly upregulated in the medial layer of db/db aortae, as well as in thoracic aortic samples from patients with type 2 diabetes mellitus. Vascular smooth muscle cell-specific overexpression of Runx2 in transgenic mice increases expression of its target genes, Col1a1 and Col1a2, leading to medial fibrosis and aortic stiffening. Interestingly, increased Runx2 expression per se is not sufficient to induce aortic calcification. Using in vivo and in vitro approaches, we further demonstrate that expression of Runx2 in diabetes mellitus is regulated via a redox-sensitive pathway that involves a direct interaction of NF-B with the Runx2 promoter. Conclusions: In conclusion, this study highlights Runx2 as a previously unrecognized inducer of vascular fibrosis in the setting of diabetes mellitus, promoting arterial stiffness irrespective of calcification."],["dc.identifier.doi","10.1161/CIRCRESAHA.115.306341"],["dc.identifier.gro","3141842"],["dc.identifier.isi","000360142000007"],["dc.identifier.pmid","26208651"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1679"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Transcription Factor Runx2 Promotes Aortic Fibrosis and Stiffness in Type 2 Diabetes Mellitus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2016Conference Abstract
    [["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Maegdefessel, Lars"],["dc.contributor.author","Spin, Joshua M."],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2018-11-07T10:15:54Z"],["dc.date.available","2018-11-07T10:15:54Z"],["dc.date.issued","2016"],["dc.format.extent","S58"],["dc.identifier.isi","000375417500113"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40914"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","MicroRNA miR-29b is a mediator of aortic stiffness and hypertension in a murine model of diabetes mellitus type 2"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2018Journal Article
    [["dc.bibliographiccitation.issue","Suppl_1"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Dannert, Angelika"],["dc.contributor.author","Schellinger, Isabel N"],["dc.contributor.author","Jakubiczka-Smorag, Joanna"],["dc.contributor.author","Mattern, Karin"],["dc.contributor.author","Petzold, Anne"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Raaz, Uwe"],["dc.date.accessioned","2020-12-10T18:37:54Z"],["dc.date.available","2020-12-10T18:37:54Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1161/atvb.38.suppl_1.678"],["dc.identifier.eissn","1524-4636"],["dc.identifier.issn","1079-5642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77134"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Abstract 678: microRNA 146a Reduces Activity of Matrix-Metalloproteinases in the Context of Arterial Stiffness"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2017Conference Abstract
    [["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Raaz, Uwe"],["dc.contributor.author","Schellinger, Isabel N."],["dc.contributor.author","Mattern, Karin"],["dc.contributor.author","Mattes, Lena"],["dc.contributor.author","Spin, Joshua"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Maegdefessel, Lars"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Tsao, Philip S."],["dc.date.accessioned","2018-11-07T10:26:06Z"],["dc.date.available","2018-11-07T10:26:06Z"],["dc.date.issued","2017"],["dc.format.extent","2023"],["dc.identifier.isi","000397342302745"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42971"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.conference","66th Annual Scientific Session and Expo of the American-College-of-Cardiology (ACC)"],["dc.relation.eventlocation","Washington, DC"],["dc.relation.issn","1558-3597"],["dc.relation.issn","0735-1097"],["dc.title","NON-CODING RNAS COMPREHENSIVELY COUNTERACT ADVERSE ARTERIAL REMODELING AND STIFFENING IN TYPE 2 DIABETES"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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