Dewenter, Matthias

[["dc.bibliographiccitation.firstpage","599a"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Lindner, Marta"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Riedel, Merle"],["dc.contributor.author","Lämmle, Simon"],["dc.contributor.author","Mason, Fleur"],["dc.contributor.author","Meinecke, Simon"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Karam, Sarah"],["dc.contributor.author","Lechene, Patrick"],["dc.contributor.author","Leroy, Jerome"],["dc.contributor.author","Vandecasteele, Gregoire"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.date.accessioned","2020-12-10T14:22:42Z"],["dc.date.available","2020-12-10T14:22:42Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/j.bpj.2015.11.3199"],["dc.identifier.issn","0006-3495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71701"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cardiac-Specific Overexpression of Phosphodiesterase 2 (PDE2) in Mouse is Cardioprotective"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1596"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","1606"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Emons, Julius"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Wittköpper, Katrin"],["dc.contributor.author","Seppelt, Danilo"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Lechêne, Patrick"],["dc.contributor.author","Leroy, Jérôme"],["dc.contributor.author","Lefebvre, Florence"],["dc.contributor.author","Varin, Audrey"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Nattel, Stanley"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Vandecasteele, Grégoire"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2019-01-14T16:02:22Z"],["dc.date.available","2019-01-14T16:02:22Z"],["dc.date.issued","2013"],["dc.description.abstract","Objectives This study investigated whether myocardial phosphodiesterase-2 (PDE2) is altered in heart failure (HF) and determined PDE2-mediated effects on beta-adrenergic receptor (β-AR) signaling in healthy and diseased cardiomyocytes. Background Diminished cyclic adenosine monophosphate (cAMP) and augmented cyclic guanosine monophosphate (cGMP) signaling is characteristic for failing hearts. Among the PDE superfamily, PDE2 has the unique property of being able to be stimulated by cGMP, thus leading to a remarkable increase in cAMP hydrolysis mediating a negative cross talk between cGMP and cAMP signaling. However, the role of PDE2 in HF is poorly understood. Methods Immunoblotting, radioenzymatic- and fluorescence resonance energy transfer–based assays, video edge detection, epifluorescence microscopy, and L-type Ca2+ current measurements were performed in myocardial tissues and/or isolated cardiomyocytes from human and/or experimental HF, respectively. Results Myocardial PDE2 expression and activity were ∼2-fold higher in advanced human HF. Chronic β-AR stimulation via catecholamine infusions in rats enhanced PDE2 expression ∼2-fold and cAMP hydrolytic activity ∼4-fold, which correlated with blunted cardiac β-AR responsiveness. In diseased cardiomyocytes, higher PDE2 activity could be further enhanced by stimulation of cGMP synthesis via nitric oxide donors, whereas specific PDE2 inhibition partially restored β-AR responsiveness. Accordingly, PDE2 overexpression in healthy cardiomyocytes reduced the rise in cAMP levels and L-type Ca2+ current amplitude, and abolished the inotropic effect following acute β-AR stimulation, without affecting basal contractility. Importantly, PDE2-overexpressing cardiomyocytes showed marked protection from norepinephrine-induced hypertrophic responses. Conclusions PDE2 is markedly up-regulated in failing hearts and desensitizes against acute β-AR stimulation. This may constitute an important defense mechanism during cardiac stress, for example, by antagonizing excessive β-AR drive. Thus, activating myocardial PDE2 may represent a novel intracellular antiadrenergic therapeutic strategy in HF."],["dc.identifier.doi","10.1016/j.jacc.2013.05.057"],["dc.identifier.gro","3142269"],["dc.identifier.isi","000325937400010"],["dc.identifier.pmid","23810893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57317"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/37"],["dc.language.iso","en"],["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 | A01: cAMP- und cGMP- Mikrodomänen bei Herzhypertrophie und Insuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | C02: RhoGTPasen und ihre Bedeutung für die Last-abhängige Myokardfibrose"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1558-3597"],["dc.relation.issn","1558-3597"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Phosphodiesterase-2 Is Up-Regulated in Human Failing Hearts and Blunts β-Adrenergic Responses in Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","120"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","132"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Lindner, Marta"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Lorenz, Kristina"],["dc.contributor.author","Schanbacher, Constanze"],["dc.contributor.author","Riedel, Merle"],["dc.contributor.author","Lämmle, Simon"],["dc.contributor.author","Meinecke, Simone"],["dc.contributor.author","Mason, Fleur E."],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Geerts, Andreas"],["dc.contributor.author","Hoffmann, Michael"],["dc.contributor.author","Wunder, Frank"],["dc.contributor.author","Brunner, Fabian J."],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Karam, Sarah"],["dc.contributor.author","Lechêne, Patrick"],["dc.contributor.author","Leroy, Jérôme"],["dc.contributor.author","Vandecasteele, Grégoire"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2020-12-10T18:37:59Z"],["dc.date.available","2020-12-10T18:37:59Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1161/CIRCRESAHA.116.310069"],["dc.identifier.pmid","27799254"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77159"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/309"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["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.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.title","Phosphodiesterase 2 Protects Against Catecholamine-Induced Arrhythmia and Preserves Contractile Function After Myocardial Infarction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","388"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Linder, M."],["dc.contributor.author","Riedel, Michael"],["dc.contributor.author","Laemmle, Simon"],["dc.contributor.author","Mason, F."],["dc.contributor.author","Meinecke, S."],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Vandecasteele, Gregoire"],["dc.contributor.author","Geerts, A."],["dc.contributor.author","Wunderlich, F. Thomas"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T10:01:10Z"],["dc.date.available","2018-11-07T10:01:10Z"],["dc.date.issued","2015"],["dc.format.extent","S42"],["dc.identifier.isi","000359539100167"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37959"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","81st Annual Meeting of the Deutsche-Gesellschaft-fur-Experimentelle-und-Klinische-Pharmakologie-und Toxikologie-e-V"],["dc.relation.eventlocation","Kiel, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","Phosphodiesterase 2 regulates resting heart rate and protects against arrhythmias and beta-adrenergic overstimulation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","386"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Emons, J."],["dc.contributor.author","Wittkoepper, Katrin"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Laemmle, Simon"],["dc.contributor.author","Seppelt, D."],["dc.contributor.author","Riedel, Michael"],["dc.contributor.author","Napiany, S."],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Sossalla, Samuel Tobias"],["dc.contributor.author","Lechene, Patrick"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Vandecasteele, Gregoire"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T09:28:54Z"],["dc.date.available","2018-11-07T09:28:54Z"],["dc.date.issued","2013"],["dc.identifier.isi","000209476400353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30898"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.title","Phosphodiesterase-2 is upregulated in failing hearts and blunts beta-AR mediated chronotropic and inotropic effects"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","97"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","106"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Slimane, Zeineb Haj"],["dc.contributor.author","Bedioune, Ibrahim"],["dc.contributor.author","Lechene, Patrick"],["dc.contributor.author","Varin, Audrey"],["dc.contributor.author","Lefebvre, Florence"],["dc.contributor.author","Mateo, Philippe"],["dc.contributor.author","Domergue-Dupont, Valerie"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Richter, Wito"],["dc.contributor.author","Conti, Marco"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","Vandecasteele, Gregoire"],["dc.date.accessioned","2018-11-07T09:41:56Z"],["dc.date.available","2018-11-07T09:41:56Z"],["dc.date.issued","2014"],["dc.description.abstract","Aims The cAMP-dependent protein kinase (PKA) mediates beta-adrenoceptor (beta-AR) regulation of cardiac contraction and gene expression. Whereas PKA activity is well characterized in various subcellular compartments of adult cardiomyocytes, its regulation in the nucleus remains largely unknown. The aim of the present study was to compare the modalities of PKA regulation in the cytoplasm and nucleus of cardiomyocytes. Methods and results Cytoplasmic and nuclear cAMP and PKA activity were measured with targeted fluorescence resonance energy transfer probes in adult rat ventricular myocytes. beta-AR stimulation with isoprenaline (Iso) led to fast cAMP elevation in both compartments, whereas PKA activity was fast in the cytoplasm but markedly slower in the nucleus. Iso was also more potent and efficient in activating cytoplasmic than nuclear PKA. Similar slow kinetics of nuclear PKA activation was observed upon adenylyl cyclase activation with L-858051 or phosphodiesterase (PDE) inhibition with 3-isobutyl-1-methylxantine. Consistently, pulse stimulation with Iso (15 s) maximally induced PKA and myosin-binding protein C phosphorylation in the cytoplasm, but marginally activated PKA and cAMP response element-binding protein phosphorylation in the nucleus. Inhibition of PDE4 or ablation of the Pde4d gene in mice prolonged cytoplasmic PKA activation and enhanced nuclear PKA responses. In the cytoplasm, phosphatase 1 (PP1) and 2A (PP2A) contributed to the termination of PKA responses, whereas only PP1 played a role in the nucleus. Conclusion Our study reveals a differential integration of cytoplasmic and nuclear PKA responses to beta-AR stimulation in cardiac myocytes. This may have important implications in the physiological and pathological hypertrophic response to beta-AR stimulation."],["dc.identifier.doi","10.1093/cvr/cvu029"],["dc.identifier.isi","000334105600013"],["dc.identifier.pmid","24550350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33843"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/56"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["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.issn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.relation.workinggroup","RG El-Armouche"],["dc.title","Control of cytoplasmic and nuclear protein kinase A by phosphodiesterases and phosphatases in cardiac myocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]