Seidler, Tim

[["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.issue","7"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T11:24:12Z"],["dc.date.available","2018-11-07T11:24:12Z"],["dc.date.issued","2009"],["dc.format.extent","E18"],["dc.identifier.isi","000270150800052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56350"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","Basic Cardiovascular Sciences Conference 2009"],["dc.relation.eventlocation","Lake Las Vegas, Henderson, NV"],["dc.relation.issn","0009-7330"],["dc.title","Dual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A (DYRK1A) Strongly Antagonizes Calcineurin/NFAT Signaling but Can Be Prohypertrophic on Overexpression"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, T. M."],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:11:19Z"],["dc.date.available","2018-11-07T11:11:19Z"],["dc.date.issued","2008"],["dc.format.extent","712"],["dc.identifier.isi","000208702503546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53407"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Dual-specificity tyrosine phosphorylation-regulated kinase 1A is a NFAT kinase mediating negative feedback on Calcineurin/NFAT signaling in cardiac myocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.journal","European Heart Journal"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Keller, M."],["dc.contributor.author","Kogler, Harald"],["dc.contributor.author","Nguyen, P."],["dc.contributor.author","Schmidt, A."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schott, Peter"],["dc.date.accessioned","2018-11-07T09:28:02Z"],["dc.date.available","2018-11-07T09:28:02Z"],["dc.date.issued","2006"],["dc.format.extent","474"],["dc.identifier.isi","000240668403226"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30680"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Identification of BRCA1 associated Protein 2 (BRAP) as a modulator of myocardial hypertrophy and heart failure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","265"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Circulation: Heart Failure"],["dc.bibliographiccitation.lastpage","271"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Tenderich, Gero"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Van, Phuc Nguyen"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Knoell, Ralph"],["dc.contributor.author","Koerfer, Reiner"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:48:09Z"],["dc.date.available","2017-09-07T11:48:09Z"],["dc.date.issued","2008"],["dc.description.abstract","Background-In heart failure, brain-type natriuretic peptide (BNP) is elevated and the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) downregulated. We previously showed that preload-induced SERCA-upregulation is suppressed by exogenous BNP. Methods and Results-Here we tested the hypothesis that afterload and neurohumoral activation would counterregulate preload-dependent SERCA upregulation through BNP, which finally results in decreased SERCA levels. We studied the effects of 6 hours preload, afterload, and isoproterenol stimulation on BNP and SERCA mRNA expression in rabbit and human failing muscles strips. Preload resulted in a pronounced upregulation of SERCA by 149% (isotonic versus slack, P<0.01). This upregulation was largely suppressed in afterloaded muscles (isometric versus slack: +32%; P<0.05). Similarly, presence of isoproterenol prevented SERCA upregulation in isotonic muscles. Afterload and isoproterenol resulted in a pronounced increase in BNP expression compared with slack by 225% (P<0.05) and 198% (P<0.01), respectively. Isoproterenol also increased expression of phospholamban by 84% (P<0.0 1). SERCA upregulation in preloaded muscles is associated with frequency-dependent potentiation of contractile force, which is absent in afterloaded muscles. In failing human myocardium, BNP expression was upregulated compared with nonfailing (+631%; P<0.05). Neither unloading nor preload or afterload induced a change in SERCA or BNP expression after 6 hours. Conclusions-Afterload and neuroendocrine stimulation increase BNP expression thereby causing inhibition of preload-dependent SERCA upregulation. In failing human myocardium, high BNP expression may underlie the loss of preload-dependent upregulation of SERCA. BNP may thus contribute to adverse myocardial remodelling in heart failure. (Circ Heart Fail. 2008;1:265-271.)"],["dc.identifier.doi","10.1161/CIRCHEARTFAILURE.108.785279"],["dc.identifier.gro","3143215"],["dc.identifier.isi","000266128000009"],["dc.identifier.pmid","19808301"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/705"],["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.issn","1941-3289"],["dc.title","Elevated Afterload, Neuroendocrine Stimulation, and Human Heart Failure Increase BNP Levels and Inhibit Preload-Dependent SERCA Upregulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schmidt, A."],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Guan-Schmidt, Kaomei"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T10:58:53Z"],["dc.date.available","2018-11-07T10:58:53Z"],["dc.date.issued","2007"],["dc.format.extent","8"],["dc.identifier.isi","000208702200022"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50568"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Disturbed MAPK signaling and heart failure in Impedes Mitogenic Signaling (IMP) transgenic mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.issue","7"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Schmidt, Albrecht"],["dc.contributor.author","Kurz, Kathrin"],["dc.contributor.author","Knoell, Ralph"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:24:12Z"],["dc.date.available","2018-11-07T11:24:12Z"],["dc.date.issued","2009"],["dc.format.extent","E15"],["dc.identifier.isi","000270150800039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56352"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","Basic Cardiovascular Sciences Conference 2009"],["dc.relation.eventlocation","Lake Las Vegas, Henderson, NV"],["dc.relation.issn","0009-7330"],["dc.title","Impedes Mitogenic Signal Propagation (IMP) Is Essential for Embryonic Heart and Brain Development and Controls Cardiac Performance via MAPK Signaling in Vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2724"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","2732"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Milting, Hendrik"],["dc.contributor.author","Van, Phuc Nguyen"],["dc.contributor.author","Kohlhaas, Michael"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Kassner, Astrid"],["dc.contributor.author","Domeier, Erik"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Knoell, Ralph"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","El-Banayosy, Aly"],["dc.contributor.author","Koerfer, Reiner"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:52:41Z"],["dc.date.available","2017-09-07T11:52:41Z"],["dc.date.issued","2006"],["dc.description.abstract","Background - In heart failure ( HF), ventricular myocardium expresses brain natriuretic peptide ( BNP). Despite the association of elevated serum levels with poor prognosis, BNP release is considered beneficial because of its antihypertrophic, vasodilating, and diuretic properties. However, there is evidence that BNP-mediated signaling may adversely influence cardiac remodeling, with further impairment of calcium homeostasis. Methods and Results - We studied the effects of BNP on preload-dependent myocardial sarcoplasmic reticulum Ca2+ ATPase ( SERCA2a) expression. In rabbit isolated muscle strips stretched to high preload and shortening isotonically over 6 hours, the SERCA/glyceraldehyde phosphate dehydrogenase mRNA ratio was enhanced by 168% ( n = 8) compared with unloaded preparations ( n = 8; P < 0.001). Recombinant human BNP at a concentration typically found in end-stage HF patients ( 350 pg/mL) abolished SERCA upregulation by stretch ( n = 9; P < 0.0001 versus BNP free). Inhibition of cyclic guanosine 3', 5' monophosphate ( cGMP)-phosphodiesterase-5 mimicked this effect, whereas inhibition of cGMP-dependent protein kinase restored preload-dependent SERCA upregulation in the presence of recombinant human BNP. Furthermore, in myocardium from human end-stage HF patients undergoing cardiac transplantation ( n = 15), BNP expression was inversely correlated with SERCA levels. Moreover, among 23 patients treated with left ventricular assist devices, significant SERCA2a recovery occurred in those downregulating BNP. Conclusions - Our data indicate that preload stimulates SERCA expression. BNP antagonizes this mechanism via guanylyl cyclase-A, cGMP, and cGMP-dependent protein kinase. This novel action of BNP to uncouple preload-dependent SERCA expression may adversely affect contractility in patients with HF."],["dc.identifier.doi","10.1161/CIRCULATIONAHA.105.608828"],["dc.identifier.gro","3143676"],["dc.identifier.isi","000238223400010"],["dc.identifier.pmid","16754798"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1216"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Relevance of brain natriuretic peptide in preload-dependent regulation of cardiac sarcoplasmic reticulum Ca2+ ATPase expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]