Didié, Michael

[["dc.bibliographiccitation.firstpage","521"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","528"],["dc.bibliographiccitation.volume","90"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2017-09-07T11:44:13Z"],["dc.date.available","2017-09-07T11:44:13Z"],["dc.date.issued","2011"],["dc.description.abstract","Aims The calcineurin and nuclear factor of activated T cells (NFAT) pathway can mediate pro-hypertrophic signalling in the heart. Recently, it has been shown that dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) phosphorylates NFAT, which limits calcineurin/NFAT signal transduction in T cells and hypertrophy in cultured cardiomyocytes. The hypothesis tested in this study was that DYRK1A prevents calcineurin/NFAT-mediated cardiac hypertrophy in vivo. Methods and results In cultured rat cardiomyocytes, adenovirus-mediated overexpression of DYRK1A antagonized calcineurin-mediated nuclear NFAT translocation and the phenylephrine-induced hypertrophic growth response. To test the ability of DYRK1A to reduce hypertrophic cardiac growth in vivo, we created tetracycline-repressible Dyrk1a transgenic mice to avoid the cardiac developmental defects associated with embryonic DYRK1A expression. However, in the mouse model, histological determination of myocyte diameter, heart weight/body weight ratio, and echocardiographic measurements revealed that myocardial expression of DYRK1A failed to reduce hypertrophy induced via aortic banding or co-expression of calcineurin. This discrepancy is explained, at least in part, by insufficient long-term inhibition of NFAT and the activation of DYRK1A-resistant maladaptive genes in vivo. Conclusion Isolated augmentation of DYRK1A can be compensated for in vivo, and this may significantly limit anti-hypertrophic interventions aimed at enhancing DYRK1A activity."],["dc.identifier.doi","10.1093/cvr/cvr023"],["dc.identifier.gro","3142722"],["dc.identifier.isi","000290820200018"],["dc.identifier.pmid","21273244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/157"],["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","Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","452"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Melnychenko, Ivan"],["dc.contributor.author","Wasmeier, Gerald H."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Naito, Hiroshi"],["dc.contributor.author","Nixdorff, U"],["dc.contributor.author","Hess, Andreas"],["dc.contributor.author","Budinsky, L."],["dc.contributor.author","Brune, K"],["dc.contributor.author","Michaelis, B."],["dc.contributor.author","Dhein, S."],["dc.contributor.author","Schwoerer, Alexander Peter"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:53:08Z"],["dc.date.available","2017-09-07T11:53:08Z"],["dc.date.issued","2006"],["dc.description.abstract","The concept of regenerating diseased myocardium by implantation of tissue-engineered heart muscle is intriguing, but convincing evidence is lacking that heart tissues can be generated at a size and with contractile properties that would lend considerable support to failing hearts. Here we created large (thickness/ diameter, 1-4 mm/15 mm), force-generating engineered heart tissue from neonatal rat heart cells. Engineered heart tissue formed thick cardiac muscle layers when implanted on myocardial infarcts in immune-suppressed rats. When evaluated 28 d later, engineered heart tissue showed undelayed electrical coupling to the native myocardium without evidence of arrhythmia induction. Moreover, engineered heart tissue prevented further dilation, induced systolic wall thickening of infarcted myocardial segments and improved fractional area shortening of infarcted hearts compared to controls (sham operation and noncontractile constructs). Thus, our study provides evidence that large contractile cardiac tissue grafts can be constructed in vitro, can survive after implantation and can support contractile function of infarcted hearts."],["dc.identifier.doi","10.1038/nm1394"],["dc.identifier.gro","3143714"],["dc.identifier.isi","000236581300035"],["dc.identifier.pmid","16582915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1259"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Engineered heart tissue grafts improve systolic and diastolic function in infarcted rat hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","743"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","744"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T08:52:46Z"],["dc.date.available","2018-11-07T08:52:46Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1093/cvr/cvr193"],["dc.identifier.isi","000294069300024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22252"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Letter concerning: 'Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo': reply"],["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.issue","6"],["dc.bibliographiccitation.journal","British Journal of Clinical Pharmacology"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Buyandelger, Byambajav"],["dc.contributor.author","Luther, P."],["dc.contributor.author","Carrier, Lucie"],["dc.contributor.author","Gunkel, Sylvia"],["dc.contributor.author","Al-Hassani, A."],["dc.contributor.author","Bourajjaj, Meriem"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Oetjen, Elke"],["dc.contributor.author","Yacoub, M."],["dc.contributor.author","de Windt, L."],["dc.contributor.author","Knoell, Ralph"],["dc.date.accessioned","2018-11-07T09:10:05Z"],["dc.date.available","2018-11-07T09:10:05Z"],["dc.date.issued","2012"],["dc.format.extent","1003"],["dc.identifier.isi","000303918900065"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26414"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","London, ENGLAND"],["dc.relation.issn","0306-5251"],["dc.title","Pharmacological calcineurin modification improves the phenotype of cardiac myosin binding protein C knockout mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","263"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","272"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Maurer, Ulrike"],["dc.contributor.author","Schotola, Hanna"],["dc.contributor.author","Hartmann, Nico H."],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:44:20Z"],["dc.date.available","2017-09-07T11:44:20Z"],["dc.date.issued","2011"],["dc.description.abstract","Transgenic (TG) Ca2+/calmodulin-dependent protein kinase II (CaMKII) delta(C) mice develop systolic heart failure (HF). CaMKII regulates intracellular Ca2+ handling proteins as well as sarcolemmal Na+ channels. We hypothesized that CaMKII also contributes to diastolic dysfunction and arrhythmias via augmentation of the late Na+ current (late I (Na)) in early HF (8-week-old TG mice). Echocardiography revealed severe diastolic dysfunction in addition to decreased systolic ejection fraction. Premature arrhythmogenic contractions (PACs) in isolated isometrically twitching papillary muscles only occurred in TG preparations (5 vs. 0, P < 0.05) which could be completely terminated when treated with the late I (Na) inhibitor ranolazine (Ran, 5 mu mol/L). Force-frequency relationships revealed significantly reduced twitch force amplitudes in TG papillary muscles. Most importantly, diastolic tension increased with raising frequencies to a greater extent in TG papillary muscles compared to WT specimen (at 10 Hz: 3.7 +/- A 0.4 vs. 2.5 +/- A 0.3 mN/mm(2); P < 0.05). Addition of Ran improved diastolic dysfunction to 2.1 +/- A 0.2 mN/mm(2) (at 10 Hz; P < 0.05) without negative inotropic effects. Mechanistically, the late I (Na) was markedly elevated in myocytes isolated from TG mice and could be completely reversed by Ran. In conclusion, our results show for the first time that TG CaMKII delta(C) overexpression induces diastolic dysfunction and arrhythmogenic triggers possibly via an enhanced late I (Na). Inhibition of elevated late I (Na) had beneficial effects on arrhythmias as well as diastolic function in papillary muscles from CaMKII delta(C) TG mice. Thus, late I (Na) inhibition appears to be a promising option for diastolic dysfunction and arrhythmias in HF where CaMKII is found to be increased."],["dc.identifier.doi","10.1007/s00395-010-0136-x"],["dc.identifier.gro","3142765"],["dc.identifier.isi","000286934300008"],["dc.identifier.pmid","21174213"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7315"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/205"],["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","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0300-8428"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Diastolic dysfunction and arrhythmias caused by overexpression of CaMKII delta(C) can be reversed by inhibition of late Na+ current"],["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","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.firstpage","223"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","230"],["dc.bibliographiccitation.volume","90"],["dc.contributor.author","Zimmermann, W.-H."],["dc.contributor.author","Schneiderbanger, K."],["dc.contributor.author","Schubert, P."],["dc.contributor.author","Didié, M."],["dc.contributor.author","Münzel, F."],["dc.contributor.author","Heubach, J."],["dc.contributor.author","Kostin, S."],["dc.contributor.author","Neuhuber, W. L."],["dc.contributor.author","Eschenhagen, T."],["dc.date.accessioned","2017-09-07T11:45:56Z"],["dc.date.available","2017-09-07T11:45:56Z"],["dc.date.issued","2002"],["dc.description.abstract","Cardiac tissue engineering is an emerging field. The suitability of engineered heart tissue (EHT) for both in vitro and in vivo applications will depend on the degree of syncytoid tissue formation and cardiac myocyte differentiation in vitro, contractile function, and electrophysiological properties. Here, we demonstrate that cardiac myocytes from neonatal rats, when mixed with collagen I and matrix factors, cast in circular molds, and subjected to phasic mechanical stretch, reconstitute ring-shaped EHTs that display important hallmarks of differentiated myocardium. Comparative histological analysis of EHTs with native heart tissue from newborn, 6-day-old, and adult rats revealed that cardiac cells in EHTs reconstitute intensively interconnected, longitudinally oriented, cardiac muscle bundles with morphological features resembling adult rather than immature native tissue. Confocal and electron microscopy demonstrated characteristic features of native differentiated myocardium; some of these features are absent in myocytes from newborn rats: (1) highly organized sarcomeres in registry; (2) adherens junctions, gap junctions, and desmosomes; (3) a well-developed T-tubular system and dyad formation with the sarcoplasmic reticulum; and (4) a basement membrane surrounding cardiac myocytes. Accordingly, EHTs displayed contractile characteristics of native myocardium with a high ratio of twitch (0.4 to 0.8 mN) to resting tension (0.1 to 0.3 mN) and a strong beta-adrenergic inotropic response. Action potential recordings demonstrated stable resting membrane potentials of -66 to -78 mV, fast upstroke kinetics, and a prominent plateau phase. The data indicate that EHTs represent highly differentiated cardiac tissue constructs, making EHTs a promising material for in vitro studies of cardiac function and tissue replacement therapy."],["dc.identifier.doi","10.1161/hh0202.103644"],["dc.identifier.gro","3144219"],["dc.identifier.isi","000173821800018"],["dc.identifier.pmid","11834716"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1819"],["dc.language.iso","en"],["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","Tissue engineering of a differentiated cardiac muscle construct"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.contributor.author","Volland, Cornelia"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Männer, Jörg"],["dc.contributor.author","Unsöld, Bernhard"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Schmidt, Carla"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Nickels, Katrin"],["dc.contributor.author","Knoll, Ralph"],["dc.contributor.author","Schmidt, Albrecht"],["dc.contributor.author","Guan-Schmidt, Kaomei"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2019-08-06T12:26:12Z"],["dc.date.available","2019-08-06T12:26:12Z"],["dc.date.issued","2019"],["dc.description.abstract","Identifying the key components in cardiomyocyte cell cycle regulation is of relevance for the understanding of cardiac development and adaptive and maladaptive processes in the adult myocardium. BRCA1-associated protein (BRAP) has been suggested as a cytoplasmic retention factor for several proteins including Cyclin-dependent-kinase inhibitor p21Cip. We observed profound expressional changes of BRAP in early postnatal myocardium and investigated the impact of BRAP on cardiomyocyte cell cycle regulation."],["dc.identifier.doi","10.1093/cvr/cvz177"],["dc.identifier.pmid","31286143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62317"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.relation.issn","1755-3245"],["dc.title","Control of p21Cip by BRAP is Critical for Cardiomyocyte Cell Cycle Progression and Survival"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2665"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Gröschel, Carina"],["dc.contributor.author","Sasse, André"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Röhrborn, Charlotte"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Reupke, Verena"],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Lichtman, Andrew H."],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2019-07-09T11:49:35Z"],["dc.date.available","2019-07-09T11:49:35Z"],["dc.date.issued","2018"],["dc.description.abstract","Heart failure due to pressure overload is frequently associated with inflammation. In addition to inflammatory responses of the innate immune system, autoimmune reactions of the adaptive immune system appear to be triggered in subgroups of patients with heart failure as demonstrated by the presence of autoantibodies against myocardial antigens. Moreover, T cell-deficient and T cell-depleted mice have been reported to be protected from heart failure induced by transverse aortic constriction (TAC) and we have shown recently that CD4+-helper T cells with specificity for an antigen in cardiomyocytes accelerate TAC-induced heart failure. In this study, we set out to investigate the potential contribution of CD8+-cytotoxic T cells with specificity to a model antigen (ovalbumin, OVA) in cardiomyocytes to pressure overload-induced heart failure. In 78% of cMy-mOVA mice with cardiomyocyte-specific OVA expression, a low-grade OVA-specific cellular cytotoxicity was detected after TAC. Adoptive transfer of OVA-specific CD8+-T cells from T cell receptor transgenic OT-I mice before TAC did not increase the risk of OVA-specific autoimmunity in cMy-mOVA mice. After TAC, again 78% of the mice displayed an OVA-specific cytotoxicity with on average only a three-fold higher killing of OVA-expressing target cells. More CD8+ cells were present after TAC in the myocardium of cMy-mOVA mice with OT-I T cells (on average 17.5/mm2) than in mice that did not receive OVA-specific CD8+-T cells (3.6/mm2). However, the extent of fibrosis was similar in both groups. Functionally, as determined by echocardiography, the adoptive transfer of OVA-specific CD8+-T cells did not significantly accelerate the progression from hypertrophy to heart failure in cMy-mOVA mice. These findings argue therefore against a major impact of cytotoxic T cells with specificity for autoantigens of cardiomyocytes in pressure overload-induced heart failure."],["dc.identifier.doi","10.3389/fimmu.2018.02665"],["dc.identifier.pmid","30498501"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15720"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59587"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/298"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["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 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.workinggroup","RG Dressel"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","CD8+-T Cells With Specificity for a Model Antigen in Cardiomyocytes Can Become Activated After Transverse Aortic Constriction but Do Not Accelerate Progression to Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]