Teucher, Nils

[["dc.bibliographiccitation.firstpage","553"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","563"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Viel, Tanja"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Hanekop, Gunnar"],["dc.contributor.author","Schoendube, Friedrich"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seipelt, Ralf G."],["dc.contributor.author","Schillinger, Wolfgang"],["dc.date.accessioned","2017-09-07T11:48:50Z"],["dc.date.available","2017-09-07T11:48:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Transcatheter aortic valve implantation (TAVI) has recently developed into an acceptable alternative to conventional surgery in high-risk patients. However, information on the identification of patients gaining most benefit from this procedure is still limited. The aim of this study was to evaluate safety and efficacy of TAVI in different patient cohorts. Between August 2008 and December 2010, 180 high-risk patients underwent TAVI at our institution (97 transapical and 83 transfemoral approaches). Periprocedural complications as well as mortality and incidence of MACCE during follow-up were recorded. Mean age was 82 +/- A 5 years, and mean logistic EuroScore 27 +/- A 14%. In the total cohort, 30-day mortality was 8.9% and 12-month survival (according to Kaplan-Meier-analysis) 72%, with no significant differences between the two approaches. However, a significant difference in survival was obvious after stratification of patients according to logistic EuroScore mortality estimates. Survival proportions at 1 year were 62% in patients with logistic EuroScore > 40%, 71% in patients with EuroScore 20-40% and 80% in octogenarians with EuroScore < 20% (P = 0.009). Furthermore, the observed median event-free survival as an indicator for morbidity ranged between 315 days in the first, 442 days in the second and 710 days in the third group (P = 0.1). TAVI proved to be feasible with reproducible results. However, mortality and rehospitalization rates were considerably high in specific patient cohorts, suggesting that the risk-to-benefit ratio of TAVI should be validated individually. In the present study, octogenarians with logistic EuroScore < 20% could be identified as candidates apparently gaining high benefit from the procedure."],["dc.identifier.doi","10.1007/s00392-012-0426-4"],["dc.identifier.gro","3142507"],["dc.identifier.isi","000305397200006"],["dc.identifier.pmid","22350751"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8866"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Edwards Lifesciences"],["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","1861-0684"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The risk-to-benefit ratio of transcatheter aortic valve implantation in specific patient cohorts: a single-centre experience"],["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","4743"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Proteome Research"],["dc.bibliographiccitation.lastpage","4752"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Koecher, Thomas"],["dc.contributor.author","Pichler, Peter"],["dc.contributor.author","Schutzbier, Michael"],["dc.contributor.author","Stingl, Christoph"],["dc.contributor.author","Kaul, Axel"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Penninger, Josef M."],["dc.contributor.author","Mechtler, Karl"],["dc.date.accessioned","2017-09-07T11:46:50Z"],["dc.date.available","2017-09-07T11:46:50Z"],["dc.date.issued","2009"],["dc.description.abstract","The development of quantitative techniques in mass spectrometry has generated the ability to systematically monitor protein expression. Isobaric tags for relative and absolute quantification (iTRAQ) have become a widely used tool for the quantification of proteins. However, application of iTRAQ methodology using ion traps and hybrid mass spectrometers containing an ion trap such as the LTQ-Orbitrap was not possible until the development of pulsed Q dissociation (PQD) and higher energy C-trap dissociation (HCD). Both methods allow iTRAQ-based quantification on an LTQ-Orbitrap but are less suited for protein identification at a proteomic scale than the commonly used collisional induced dissociation (CID) fragmentation. We developed an analytical strategy combining the advantages of CID and HCD, allowing sensitive and accurate protein identification and quantitation at the same time. In a direct comparison, the novel method outperformed PQD and HCD regarding its limit of detection, the number of identified peptides and the analytical precision of quantitation. The new method was applied to study changes in protein expression in mouse hearts upon transverse aortic constriction, a model for cardiac stress."],["dc.identifier.doi","10.1021/pr900451u"],["dc.identifier.gro","3143049"],["dc.identifier.isi","000270353900032"],["dc.identifier.pmid","19663507"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/520"],["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","Amer Chemical Soc"],["dc.relation.issn","1535-3893"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","High Precision Quantitative Proteomics Using iTRAQ on an LTQ Orbitrap: A New Mass Spectrometric Method Combining the Benefits of All"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","673"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","680"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Christians, Claus"],["dc.contributor.author","Kohlhaas, Michael"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Van Nguyen, Phuc"],["dc.contributor.author","Schmidt, Albrecht G."],["dc.contributor.author","Schunck, Ortwin"],["dc.contributor.author","Nebendahl, Klaus"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Zeitz, Oliver"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:52:27Z"],["dc.date.available","2017-09-07T11:52:27Z"],["dc.date.issued","2006"],["dc.description.abstract","We investigated the hypothesis that increased intracellular [Na+](i) in heart failure contributes to preservation of SR Ca2+ load which may become particularly evident at slow heart rates. [Na+]i in SBFI-loaded myocytes from rabbits with pacing-induced heart failure (PHF) was significantly higher at each frequency as compared to Sham-operated animals. Furthermore, PHF rabbits demonstrated reduced SR Ca2+-ATPase protein levels (-37%, p < 0.04) but unchanged Na+/Ca2+ exchanger protein levels. At 0.25 Hz, isometric force was similar in cardiac trabeculae from PHF rabbits as compared to control (PHF, 3.6 +/- 1.3; Sham, 4.4 +/- 0.6 mN/mm(2)). Rapid cooling contractures (RCCs) were unchanged indicating preserved SR Ca2+ load at this frequency. In Sham, isometric twitch force increased with rising frequencies to 29.0 +/- 2.8 mN/mm(2) at 3.0 Hz (p < 0.05) as compared to 0.25 Hz. RCCs showed a parallel increase by 186 +/- 47% (p < 0.01). In PHF, frequency-dependent increase in force (15.8 +/- 4.7 mN/mm(2) at 3.0 Hz) and RCCs (increase by 70 +/- 40%) were significantly blunted. Thus, in PHF in rabbits SR Ca2+ load is preserved at low frequencies despite decreased SR Ca2+-ATPase expression. This may result from [Na+](i)-dependent changes in Na+/Ca2+ exchanger activity. (c) 2006 European Society of Cardiology. Published by Elsevier B.V All rights reserved."],["dc.identifier.doi","10.1016/j.ejheart.2006.01.013"],["dc.identifier.gro","3143598"],["dc.identifier.isi","000242383300002"],["dc.identifier.pmid","16540370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1130"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1388-9842"],["dc.title","High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","996"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","1003"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Ohler, A."],["dc.contributor.author","Embry, S. L."],["dc.contributor.author","Muller, F"],["dc.contributor.author","Christians, Claus"],["dc.contributor.author","Janssen, P. M. L."],["dc.contributor.author","Kogler, H."],["dc.contributor.author","Teucher, Niels"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2021-06-01T10:50:03Z"],["dc.date.available","2021-06-01T10:50:03Z"],["dc.date.issued","2003"],["dc.description.abstract","Objectives: The functional consequences of Na+/Ca2+ exchanger (NCX) overexpression in heart failure have been controversially discussed. NCX function strongly depends on intracellular sodium which has been shown to be increased in heart failure. Methods and results: We investigated the Na+/K+-ATPase (NKA) inhibitor ouabain (0.5-16 mumol/l) in electrically stimulated, isotonically contracting adult rabbit cardiocytes overexpressing NCX after adenoviral gene transfer (Ad-NCX-GFP, 48 h culture time). Myocytes transfected with adenovirus encoding for green fluorescent protein (Ad-GFP) served as a control. Contractions were analyzed by video-edge detection. In the Ad-NCX-GFP group, the maximum inotropic response was significantly reduced by 50.7% (P < 0.05). This was a result of an enhanced susceptibility to contracture after exposure to the drug (median concentration (25-75%): 4 (4-8) vs. 8 (6-16) mumol/l, P < 0.05). When analyzing relaxation before contracture, the maximum relaxation velocity was reduced (0.15 +/- 0.04 vs. 0.27 +/- 0.04 mum/s, P < 0.05) and the time from peak shortening to 90% of relaxation was increased (298 +/- 39 vs. 185 +/- 15 ms, P < 0.05). No differences in systolic and diastolic parameters were observed with the Na+ channel modulator BDF9198 (1 mumol/l). Conclusions: Inhibition of NKA by ouabain induces a combined diastolic and systolic dysfunction in NCX overexpressing rabbit myocytes. This may be the consequence of cytoplasmic Ca2+ overload due to inhibition of forward mode or induction of reverse mode Na+/Ca2+ exchange. In end-stage failing human myocardium and during digitalis treatment this mechanism may be of major importance. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0008-6363(02)00829-5"],["dc.identifier.gro","3144121"],["dc.identifier.isi","000181975100014"],["dc.identifier.pmid","12650877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86511"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0008-6363"],["dc.title","The functional effect of adenoviral Na+/Ca2+ exchanger overexpression in rabbit myocytes depends on the activity of the Na+/K+-ATPase"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["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","643"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Circulation: Cardiovascular Genetics"],["dc.bibliographiccitation.lastpage","652"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Buyandelger, Byambajav"],["dc.contributor.author","Mansfield, Catherine"],["dc.contributor.author","Kostin, Sawa"],["dc.contributor.author","Choi, Onjee"],["dc.contributor.author","Roberts, Angharad M."],["dc.contributor.author","Ware, James S."],["dc.contributor.author","Mazzarotto, Francesco"],["dc.contributor.author","Pesce, Francesco"],["dc.contributor.author","Buchan, Rachel"],["dc.contributor.author","Isaacson, Rivka L."],["dc.contributor.author","Vouffo, Josee"],["dc.contributor.author","Gunkel, Sylvia"],["dc.contributor.author","Knoll, Gudrun"],["dc.contributor.author","McSweeney, Sara J."],["dc.contributor.author","Wei, Heming"],["dc.contributor.author","Perrot, Andreas"],["dc.contributor.author","Pfeiffer, Conny"],["dc.contributor.author","Toliat, Mohammad Reza"],["dc.contributor.author","Ilieva, Kristina"],["dc.contributor.author","Krysztofinska, Ewelina"],["dc.contributor.author","Lopez-Olaneta, Marina M."],["dc.contributor.author","Gomez-Salinero, Jesus M."],["dc.contributor.author","Schmidt, Albrecht"],["dc.contributor.author","Ng, Keat-Eng"],["dc.contributor.author","Teucher, Niels"],["dc.contributor.author","Chen, Ju"],["dc.contributor.author","Teichmann, Martin"],["dc.contributor.author","Eilers, Martin"],["dc.contributor.author","Haverkamp, Wilhelm"],["dc.contributor.author","Regitz-Zagrosek, Vera"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Braun, Thomas"],["dc.contributor.author","Pennell, Dudley J."],["dc.contributor.author","Gould, Ian"],["dc.contributor.author","Barton, Paul J. R."],["dc.contributor.author","Lara-Pezzi, Enrique"],["dc.contributor.author","Schaefer, Sebastian"],["dc.contributor.author","Hübner, Norbert"],["dc.contributor.author","Felkin, Leanne E."],["dc.contributor.author","O'Regan, D. P."],["dc.contributor.author","Brand, Thomas"],["dc.contributor.author","Milting, Hendrik"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Schneider, Michael D."],["dc.contributor.author","Prasad, Sanjay"],["dc.contributor.author","Petretto, Enrico"],["dc.contributor.author","Knoll, Ralph"],["dc.date.accessioned","2017-09-07T11:43:30Z"],["dc.date.available","2017-09-07T11:43:30Z"],["dc.date.issued","2015"],["dc.description.abstract","Background Mutations in sarcomeric and cytoskeletal proteins are a major cause of hereditary cardiomyopathies, but our knowledge remains incomplete as to how the genetic defects execute their effects. Methods and Results We used cysteine and glycine-rich protein 3, a known cardiomyopathy gene, in a yeast 2-hybrid screen and identified zinc-finger and BTB domain-containing protein 17 (ZBTB17) as a novel interacting partner. ZBTB17 is a transcription factor that contains the peak association signal (rs10927875) at the replicated 1p36 cardiomyopathy locus. ZBTB17 expression protected cardiac myocytes from apoptosis in vitro and in a mouse model with cardiac myocyte-specific deletion of Zbtb17, which develops cardiomyopathy and fibrosis after biomechanical stress. ZBTB17 also regulated cardiac myocyte hypertrophy in vitro and in vivo in a calcineurin-dependent manner. Conclusions We revealed new functions for ZBTB17 in the heart, a transcription factor that may play a role as a novel cardiomyopathy gene."],["dc.identifier.doi","10.1161/CIRCGENETICS.113.000690"],["dc.identifier.gro","3141815"],["dc.identifier.isi","000363373800003"],["dc.identifier.pmid","26175529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1379"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1942-3268"],["dc.relation.issn","1942-325X"],["dc.title","ZBTB17 (MIZ1) Is Important for the Cardiac Stress Response and a Novel Candidate Gene for Cardiomyopathy and Heart Failure"],["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","24"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Miller, SLW"],["dc.contributor.author","Loughrey, C."],["dc.contributor.author","Kania, A."],["dc.contributor.author","Burow, A."],["dc.contributor.author","Teucher, N."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Smith, Godfrey L."],["dc.date.accessioned","2018-11-07T10:37:13Z"],["dc.date.available","2018-11-07T10:37:13Z"],["dc.date.issued","2003"],["dc.format.extent","667"],["dc.identifier.doi","10.1016/S0195-668X(03)96074-X"],["dc.identifier.isi","000185638802427"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45512"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.conference","Congress of the European-Society-of-Cardiology"],["dc.relation.eventlocation","VIENNA, AUSTRIA"],["dc.relation.issn","0195-668X"],["dc.title","Sorcin over-expression reduces contractility by affecting intracellular and trans-sarcolemmal Ca2+ cycling in cardiomyocytes"],["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.firstpage","795"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","804"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Kuhn, Michaela"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:45:12Z"],["dc.date.available","2017-09-07T11:45:12Z"],["dc.date.issued","2010"],["dc.description.abstract","Heart failure is characterised by reduced expression of sarcoplasmic reticulum calcium-ATPase (SERCA) and increased expression of B-type natriuretic peptide (BNP). The present study was performed to investigate causality of this inverse relationship under in vivo conditions in the transversal aortic constriction mouse model (TAC). Left ventricular SERCA-mRNA expression was significantly upregulated in TAC by 32% after 6 h, but not different from sham after 24 h. Serum proANP and BNP levels were increased in TAC after 24 h (BNP +274%, p < 0.01; proANP +60%, p < 0.05), but only proANP levels were increased after 6 h (+182%, p < 0.01). cGMP levels were only increased 24 h after TAC (+307%, p < 0.01), but not 6 h after TAC. BNP infusion inhibited the increase in SERCA expression 6 h after TAC. In BNP-receptor-knockout animals (GC-A), the expression of SERCA was still significantly increased 24 h after TAC at the mRNA level by 35% (p < 0.05), as well as at the protein level by 25% (p < 0.05). MCIP expression as an indicator of calcineurin activity was regulated in parallel to SERCA after 6 and 24 h. MCIP-mRNA was increased by 333% 6 h after TAC, but not significantly different from sham after 24 h. In the GC-A-KO mice, MCIP-mRNA was significantly increased in TAC compared to WT after 24 h. In mice with BNP infusion, MCIP was significantly lower 6 h after TAC compared to control animals. In conclusion, mechanical load leads to an upregulation of SERCA expression. This is followed by upregulation of natriuretic peptides with subsequent suppression of SERCA upregulation. Elevated natriuretic peptides may suppress SERCA expression by inhibition of calcineurin activity via activation of GC-A."],["dc.identifier.doi","10.1007/s00395-010-0115-2"],["dc.identifier.gro","3142835"],["dc.identifier.isi","000283589000011"],["dc.identifier.pmid","20711735"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5974"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/283"],["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","BNP controls early load-dependent regulation of SERCA through calcineurin"],["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","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"]]