Didié, Michael

[["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Therapeutics"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:44:39Z"],["dc.date.available","2017-09-07T11:44:39Z"],["dc.date.issued","2015"],["dc.description.abstract","BackgroundPantoprazole has been shown to exert a negative inotropic effect in isolated myocardium. The purpose of this study was to evaluate the hemodynamic effects of pantoprazole in vivo in healthy myocardium and in the setting of heart failure. Methods and ResultsHealthy mice and mice with heart failure 4weeks after myocardial infarction induced by permanent LAD ligation were instrumented with a Millar Mikrotip conductance catheter to record pressure-volume loops. Pantoprazole was infused at rates of 3 and 10mg/kg/min intravenously, and hemodynamic parameters were recorded. Infusion of pantoprazole at increasing rates lead to a significant decline of end systolic LV pressure by decreasing heart rate, myocardial contractility and arterial elastance. These effects were quick, beginning immediately with the infusion and usually reaching a plateau after 2 or 3min of infusion. The effects on blood pressure and heart rate were of comparable size in healthy mice and mice with MI. However, in sham-operated mice, there was a compensatory increase in stroke volume that sufficed to maintain cardiac output at a constant level, which was missing in mice with MI. In 4 of 13 mice with MI infusion of 10mg/kg/min pantoprazole lead to pump failure, which was lethal in 2 of these animals. ConclusionAt higher infusion rates, pantoprazole is able to induce negative hemodynamic responses. In particular, in the setting of heart failure, these effects can lead to significant impairment of cardiac function. Therefore, high infusion rates of pantoprazole should be avoided especially in heart failure patients."],["dc.identifier.doi","10.1111/1755-5922.12102"],["dc.identifier.gro","3141966"],["dc.identifier.isi","000348660500004"],["dc.identifier.pmid","25529757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3057"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.eissn","1755-5922"],["dc.relation.issn","1755-5914"],["dc.title","Negative Hemodynamic Effects of Pantoprazole at High Infusion Rates in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","758"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","U153"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Knöll, Ralph"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Zou, Peijian"],["dc.contributor.author","Miocic, Snjezana"],["dc.contributor.author","Kostin, Sawa"],["dc.contributor.author","Buyandelger, Byambajav"],["dc.contributor.author","Ku, Ching-Hsin"],["dc.contributor.author","Neef, Stefan"],["dc.contributor.author","Bug, Monika"],["dc.contributor.author","Schaefer, Katrin"],["dc.contributor.author","Knöll, Gudrun"],["dc.contributor.author","Felkin, Leanne E."],["dc.contributor.author","Wessels, Johannes T."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hagn, Franz"],["dc.contributor.author","Kessler, Horst"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Quentin, Thomas"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schmidt, Albrecht"],["dc.contributor.author","Birks, Emma J."],["dc.contributor.author","Gunkel, Sylvia"],["dc.contributor.author","Lang, Patrick"],["dc.contributor.author","Granzier, Henk"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Field, Loren J."],["dc.contributor.author","Faulkner, Georgine"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Barton, Paul J. R."],["dc.contributor.author","Sattler, Michael"],["dc.contributor.author","Wilmanns, Matthias"],["dc.contributor.author","Chien, Kenneth R."],["dc.date.accessioned","2017-09-07T11:43:24Z"],["dc.date.available","2017-09-07T11:43:24Z"],["dc.date.issued","2011"],["dc.description.abstract","Rationale: Telethonin (also known as titin-cap or t-cap) is a 19-kDa Z-disk protein with a unique beta-sheet structure, hypothesized to assemble in a palindromic way with the N-terminal portion of titin and to constitute a signalosome participating in the process of cardiomechanosensing. In addition, a variety of telethonin mutations are associated with the development of several different diseases; however, little is known about the underlying molecular mechanisms and telethonin's in vivo function. Objective: Here we aim to investigate the role of telethonin in vivo and to identify molecular mechanisms underlying disease as a result of its mutation. Methods and Results: By using a variety of different genetically altered animal models and biophysical experiments we show that contrary to previous views, telethonin is not an indispensable component of the titin-anchoring system, nor is deletion of the gene or cardiac specific overexpression associated with a spontaneous cardiac phenotype. Rather, additional titin-anchorage sites, such as actin-titin cross-links via alpha-actinin, are sufficient to maintain Z-disk stability despite the loss of telethonin. We demonstrate that a main novel function of telethonin is to modulate the turnover of the proapoptotic tumor suppressor p53 after biomechanical stress in the nuclear compartment, thus linking telethonin, a protein well known to be present at the Z-disk, directly to apoptosis (\"mechanoptosis\"). In addition, loss of telethonin mRNA and nuclear accumulation of this protein is associated with human heart failure, an effect that may contribute to enhanced rates of apoptosis found in these hearts. Conclusions: Telethonin knockout mice do not reveal defective heart development or heart function under basal conditions, but develop heart failure following biomechanical stress, owing at least in part to apoptosis of cardiomyocytes, an effect that may also play a role in human heart failure. (Circ Res. 2011; 109: 758-769.)"],["dc.identifier.doi","10.1161/CIRCRESAHA.111.245787"],["dc.identifier.gro","3142667"],["dc.identifier.isi","000294950000008"],["dc.identifier.pmid","21799151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/96"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0009-7330"],["dc.title","Telethonin Deficiency Is Associated With Maladaptation to Biomechanical Stress in the Mammalian Heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Kurz, Katrin"],["dc.contributor.author","Koenll, Ralph"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T09:03:19Z"],["dc.date.available","2018-11-07T09:03:19Z"],["dc.date.issued","2012"],["dc.identifier.isi","000208885002013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24881"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Brca1-associated Protein 2 (BRAP) is Essential for Embryonic Heart Development and for Neonatal Cardiomyocyte Proliferation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","396"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","406"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Weinberger, Florian"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Grimm, Michael"],["dc.contributor.author","Peeck, Micha"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:48:07Z"],["dc.date.available","2017-09-07T11:48:07Z"],["dc.date.issued","2008"],["dc.description.abstract","Phosphatase inhibitor-1 (I-1) is a conditional amplifier of beta-adrenergic signalling downstream of protein kinase A by inhibiting type-1 phosphatases only in its PKA-phosphorylated form. I-1 is downregulated in failing hearts and thus contributes to beta-adrenergic desensitization. It is unclear whether this should be viewed as a predominantly adverse or protective response. We generated transgenic mice with cardiac-specific I-1 overexpression (I-1-TG) and evaluated cardiac function and responses to catecholamines in mice with targeted disruption of the I-1 gene (I-1-KO). Both groups were compared with their wild-type (WT) littermates. I-1-TG developed cardiac hypertrophy and mild dysfunction which was accompanied by a substantial compensatory increase in PP1 abundance and activity, confounding cause-effect relationships. I-1-KO had normal heart structure with mildly reduced sensitivity, but unchanged maximal contractile responses to beta-adrenergic stimulation, both in vitro and in vivo. Notably, I-1-KO were partially protected from lethal catecholamine-induced arrhythmias and from hypertrophy and dilation induced by a 7 day infusion with the beta-adrenergic agonist isoprenaline. Moreover, I-1-KO exhibited a partially preserved acute beta-adrenergic response after chronic isoprenaline, which was completely absent in similarly treated WT. At the molecular level, I-1-KO showed lower steady-state phosphorylation of the cardiac ryanodine receptor/Ca(2+) release channel and the sarcoplasmic reticulum (SR) Ca(2+)-ATPase-regulating protein phospholamban. These alterations may lower the propensity for diastolic Ca(2+) release and Ca(2+) uptake and thus stabilize the SR and account for the protection. Taken together, loss of I-1 attenuates detrimental effects of catecholamines on the heart, suggesting I-1 downregulation in heart failure as a beneficial desensitization mechanism and I-1 inhibition as a potential novel strategy for heart failure treatment."],["dc.identifier.doi","10.1093/cvr/cvn208"],["dc.identifier.gro","3143199"],["dc.identifier.isi","000260973500012"],["dc.identifier.pmid","18689792"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/687"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Phosphatase inhibitor-1-deficient mice are protected from catecholamine-induced arrhythmias and myocardial hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","90"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Obesity"],["dc.bibliographiccitation.lastpage","99"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Bremen, Eva"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schaefer, Katrin"],["dc.date.accessioned","2017-09-07T11:45:21Z"],["dc.date.available","2017-09-07T11:45:21Z"],["dc.date.issued","2015"],["dc.description.abstract","ObjectiveElevated insulin and inflammatory cytokine levels in obesity may chronically activate signaling pathways regulating cardiac growth and contractility. Our aim was to examine the effect of obesity on cardiac PI3K isoform and Akt activation during left ventricular (LV) hypertrophy and heart failure. MethodsWild-type mice were fed normal chow or high-fat diet (HFD) for 2, 4, or 6 months. A subset of mice was subjected to chronic myocardial ischemia (MI). ResultsEchocardiography revealed a progressive increase in LV mass, wall thickness, and diameters in obese mice. Systolic pump function was not impaired. Increased cardiac levels of PI3K, phosphorylated Akt, GSK3, and Epac were observed after HFD for 2 months but gradually declined and were normal or reduced after 6 months, paralleled by elevated PP2A and SOCS3 levels. MI resulted in heart failure, independent of obesity, but compensatory LV hypertrophy was absent in obese mice. Histochemical analyses revealed similar increases in cardiac fibrosis, inflammation, apoptosis, and angiogenesis in lean and obese mice. ConclusionsOur findings suggest that activation of Akt initially contributes to cardiac hypertrophy and that chronic metabolic and inflammatory stimulation and overexpression of inhibitory mediators decrease PI3K-mediated Akt signaling and blunt compensatory hypertrophy after MI."],["dc.identifier.doi","10.1002/oby.20888"],["dc.identifier.gro","3141992"],["dc.identifier.isi","000346770100018"],["dc.identifier.pmid","25175008"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3346"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: EU [LSHM-CT-2005-018833]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.eissn","1930-739X"],["dc.relation.issn","1930-7381"],["dc.title","Differential PI3K Signal Transduction in Obesity-Associated Cardiac Hypertrophy and Response to Ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Zafeiriou, Maria Patapia"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Bergmann, Martin W."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2018-11-07T09:07:19Z"],["dc.date.available","2018-11-07T09:07:19Z"],["dc.date.issued","2012"],["dc.identifier.isi","000312506400227"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25767"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7330"],["dc.title","Role of Erythropoietin Signaling in the Biology of Mouse Cardiac Progenitor Cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Zafeiriou, Maria Patapia"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Bergmann, Martin W."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayan, Laura"],["dc.date.accessioned","2018-11-07T09:21:25Z"],["dc.date.available","2018-11-07T09:21:25Z"],["dc.date.issued","2013"],["dc.identifier.isi","000332063200120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29101"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.eventlocation","Las Vegas, NV"],["dc.relation.issn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Erythropoietin Enhances Abundance of Cardiomyogenic Precursors in vitro and in vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]