Prestle, Jürgen

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Janssen, PML"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Smith, Godfrey L."],["dc.date.accessioned","2018-11-07T10:35:28Z"],["dc.date.available","2018-11-07T10:35:28Z"],["dc.date.issued","2000"],["dc.format.extent","61"],["dc.identifier.isi","000089136600237"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45104"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.issn","0195-668X"],["dc.title","Reduced ryanodine receptor-mediated SR Ca2+-leak in isolated adult cardiomyocytes upon adenovirus-mediated overexpression of FKBP12.6"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Rankin, A."],["dc.contributor.author","Reynolds, D. F."],["dc.contributor.author","Maceachern, K. E."],["dc.contributor.author","Hasenfuss, G."],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Smith, Godfrey L."],["dc.date.accessioned","2018-11-07T08:31:46Z"],["dc.date.available","2018-11-07T08:31:46Z"],["dc.date.issued","2001"],["dc.format.extent","132"],["dc.identifier.isi","000171895000631"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17194"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0009-7322"],["dc.title","FK506-binding protein FKBP12.6 overexpression alters the characteristics of the Ca2+ transient and caffeine-induced Ca2+ release in adult rabbit cardiac myocytes."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Gomez, A. M."],["dc.contributor.author","Schuster, I."],["dc.contributor.author","Fauconnier, J."],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Richard, S."],["dc.date.accessioned","2018-11-07T10:41:06Z"],["dc.date.available","2018-11-07T10:41:06Z"],["dc.date.issued","2003"],["dc.format.extent","202A"],["dc.identifier.isi","000183123800986"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46460"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Society"],["dc.publisher.place","Bethesda"],["dc.relation.conference","47th Annual Meeting of the Biophysical-Society"],["dc.relation.eventlocation","SAN ANTONIO, TEXAS"],["dc.relation.issn","0006-3495"],["dc.title","Functional effects of FKBP12.6 overexpression on SR [Ca2+]i transients and spontaneous Ca2+ sparks in rat ventricular myocytes."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","486"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Baudet, S."],["dc.contributor.author","Weisser, J"],["dc.contributor.author","Janssen, A. P."],["dc.contributor.author","Beulich, K ."],["dc.contributor.author","Bieligk, U."],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Noireaud, J"],["dc.contributor.author","Janssen, P. M. L."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Prestle, J."],["dc.date.accessioned","2017-09-07T11:46:07Z"],["dc.date.available","2017-09-07T11:46:07Z"],["dc.date.issued","2001"],["dc.description.abstract","Objective: Protein kinase C (PKC) is thought to be involved in the regulation of the mammalian cardiac excitation-contraction coupling process by vasoactive peptides Like endothelin-1 (ET-1). However, the demonstration of a causal link between activation of specific PKC isoforms and the increase in contractility mediated by ET-1 is still inferential. Methods: By means of adenovirus-mediated gene transfer, we specifically overexpressed PKC epsilon in cultured adult rabbit Ventricular myocytes (Ad-PKC epsilon). Myocyte shortening and [Ca2+](i) transients under basal and ET-1-stimulated conditions were measured in Ad-PKC epsilon and Ad-LacZ control transfected cells. Results: Infection with Ad-PKC epsilon resulted in a strong, virus dose-dependent increase in PKC epsilon protein Levels, whereas protein expression of other PKC isoforms remained unchanged. Using a multiplicity of infection of 100 plaque-forming units/myocyte, basal and cofactor-dependent PKC epsilon kinase activity was increased 28- and 90-fold, respectively, when compared to control. Myocyte basal fractional shortening and [Ca2+](i), transient amplitude were both increased by 21% (P<0.05 each) in Ad-PKC transfected myocytes when compared to Ad-LacZ transfected control myocytes. The positive Inotropic effect of ET-1 in control myocytes was markedly blunted in PKC epsilon -overexpressing myocytes. Conclusion: Specific overexpression of PKC epsilon in rabbit ventricular myocytes increases basal myocyte contractility and [Ca2+](i) transients, and modifies their responsiveness to ET-1. (C) 2001 Elsevier Science B.V. AII rights reserved."],["dc.identifier.doi","10.1016/S0008-6363(01)00225-5"],["dc.identifier.gro","3144281"],["dc.identifier.isi","000168918600010"],["dc.identifier.pmid","11376624"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1887"],["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","0008-6363"],["dc.title","Increased basal contractility of cardiomyocytes overexpressing protein kinase C epsilon and blunted positive inotropic response to endothelin-1"],["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","22"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Kussebi, N."],["dc.contributor.author","Kania, A."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Prestle, J."],["dc.date.accessioned","2018-11-07T08:41:05Z"],["dc.date.available","2018-11-07T08:41:05Z"],["dc.date.issued","2001"],["dc.format.extent","149"],["dc.identifier.isi","000170988300577"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19393"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.issn","0195-668X"],["dc.title","Gene expression of FK506-binding proteins (FKBPs) in the human heart. Identification of an alternatively spliced transcript of FKBP12.6"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Weisser, J."],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Dieterich, E."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Pieske, Burkert M."],["dc.date.accessioned","2018-11-07T11:01:39Z"],["dc.date.available","2018-11-07T11:01:39Z"],["dc.date.issued","2000"],["dc.format.extent","109A"],["dc.identifier.isi","000084779300638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51196"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Society"],["dc.publisher.place","Bethesda"],["dc.relation.issn","0006-3495"],["dc.title","Adenovirus-mediated gene transfer in isolated human myocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","281"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.lastpage","291"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Stypmann, J."],["dc.contributor.author","Janssen, PML"],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Engelen, M. A."],["dc.contributor.author","Kogler, Harald"],["dc.contributor.author","Lullmann-Rauch, R."],["dc.contributor.author","Eckardt, Lars"],["dc.contributor.author","von Figura, Kurt"],["dc.contributor.author","Landgrebe, J."],["dc.contributor.author","Mleczko, A."],["dc.contributor.author","Saftig, P."],["dc.date.accessioned","2018-11-07T09:33:52Z"],["dc.date.available","2018-11-07T09:33:52Z"],["dc.date.issued","2006"],["dc.description.abstract","Mutations in the highly glycosylated lysosome associated membrane protein-2 (LAMP-2) cause, as recently shown, familial Danon disease with mental retardation, mild myopathy and fatal cardiomyopathy. Extent and basis of the contractile dysfunction is not completely understood. In LAMP-2 deficient mice, we investigated cardiac function in vivo using Doppler-echocardiography and contractile function in vitro in isolated myocardial trabeculae. LAMP-2 deficient mice displayed reduced ejection fraction (EF) (58.9 +/- 3.4 vs. 80.7 +/- 5.1%, P < 0.05) and reduced cardiac output (8.3 +/- 3.1 vs. 14.7 +/- 3.6 ml/min, P < 0.05) as compared to wild-type controls. Isolated multicellular muscle preparations from LAMP-2 deficient mice confirmed depressed force development (3.2 +/- 0.6 vs. 8.4 +/- 0.9 mN/mm(2), P < 0.01). All groups showed similar force-frequency behaviour when normalised to baseline force. Post-rest potentiation was significantly depressed at intervals > 15 s in LAMP-2 deficient mice (P < 0.05). Although attenuated in absolute force development, the normalised inotropic response to increased calcium and beta-adrenoreceptor stimulation was unaltered. Electron microscopic analysis revealed autophagic vacuoles in LAMP-2 deficient cardiomyocytes. Protein analysis showed unaltered levels of SERCA2a, calsequestrin and phospholamban. Cardiac contractile function in LAMP-2 deficient mice as a model for Danon disease is significantly attenuated. The occurrence of autophagic vacuoles in LAMP-2 deficient myocytes is likely to be causal for the depressed contractile function resulting in an attenuated cardiac pump reserve."],["dc.identifier.doi","10.1007/s00395-006-0591-6"],["dc.identifier.isi","000238516400002"],["dc.identifier.pmid","16604439"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32058"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0300-8428"],["dc.title","LAMP-2 deficient mice show depressed cardiac contractile function without significant changes in calcium handling"],["dc.type","journal_article"],["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","21"],["dc.contributor.author","Janssen, PML"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Donahue, J. K."],["dc.contributor.author","Zeitz, O."],["dc.contributor.author","Emami, S."],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Prestle, J."],["dc.date.accessioned","2018-11-07T10:36:00Z"],["dc.date.available","2018-11-07T10:36:00Z"],["dc.date.issued","2000"],["dc.format.extent","530"],["dc.identifier.isi","000089136602060"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45222"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.issn","0195-668X"],["dc.title","Gialfa-2 overexpression depresses the beta-adrenergic response in multicellular preparations and single myocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","A13"],["dc.bibliographiccitation.journal","Heart"],["dc.bibliographiccitation.lastpage","A14"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Reynolds, D."],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Smith, Godfrey L."],["dc.date.accessioned","2018-11-07T10:39:12Z"],["dc.date.available","2018-11-07T10:39:12Z"],["dc.date.issued","2003"],["dc.identifier.isi","000182474700037"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45987"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","B M J Publishing Group"],["dc.publisher.place","London"],["dc.relation.conference","Annual Scientific Conference of the British-Cardiac-Society"],["dc.relation.eventlocation","GLASGOW, SCOTLAND"],["dc.relation.issn","1355-6037"],["dc.title","Measurement of intra-SR calcium concentration in isolated cardiac myocytes using a targeted aequorin probe"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","641"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","648"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Preuss, Michael"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Prestle, Jürgen"],["dc.contributor.author","Minami, Kazutomo"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2022-03-01T11:43:48Z"],["dc.date.available","2022-03-01T11:43:48Z"],["dc.date.issued","1999"],["dc.description.abstract","Background —In the failing human heart, sarcoplasmic reticulum (SR) calcium handling is impaired, and therefore, calcium elimination and diastolic function may depend on the expression of sarcolemmal Na + -Ca 2+ exchanger. Methods and Results —Force-frequency relations were studied in ventricular muscle strip preparations from failing human hearts (n=29). Protein levels of Na + -Ca 2+ exchanger and SR Ca 2+ -ATPase were measured in the same hearts. Hearts were divided into 3 groups by discriminant analysis according to the behavior of diastolic function when stimulation rate of muscle strips was increased from 30 to 180 min −1 . At 180 compared with 30 min −1 , diastolic force was increased by 160%, maximum rate of force decline was decreased by 46%, and relaxation time was unchanged in group III. In contrast, in group I, diastolic force and maximum rate of force decline did not change, and relaxation time decreased by 20%. Na + -Ca 2+ exchanger was 66% higher in group I than in group III. Na + -Ca 2+ exchanger was inversely correlated with the frequency-dependent rise of diastolic force when stimulation rate was increased ( r =−0.74; P <0.001). Compared with nonfailing human hearts (n=6), SR Ca 2+ -ATPase was decreased and Na + -Ca 2+ exchanger unchanged in group III, whereas Na + -Ca 2+ exchanger was increased and SR Ca 2+ -ATPase unchanged in group I. Results with group II hearts were between those of group I and group III hearts. Conclusions —By discriminating failing human hearts according to their diastolic function, we identified different phenotypes. Disturbed diastolic function occurs in hearts with decreased SR Ca 2+ -ATPase and unchanged Na + -Ca 2+ exchanger, whereas increased expression of the Na + -Ca 2+ exchanger is associated with preserved diastolic function."],["dc.description.abstract","Background —In the failing human heart, sarcoplasmic reticulum (SR) calcium handling is impaired, and therefore, calcium elimination and diastolic function may depend on the expression of sarcolemmal Na + -Ca 2+ exchanger. Methods and Results —Force-frequency relations were studied in ventricular muscle strip preparations from failing human hearts (n=29). Protein levels of Na + -Ca 2+ exchanger and SR Ca 2+ -ATPase were measured in the same hearts. Hearts were divided into 3 groups by discriminant analysis according to the behavior of diastolic function when stimulation rate of muscle strips was increased from 30 to 180 min −1 . At 180 compared with 30 min −1 , diastolic force was increased by 160%, maximum rate of force decline was decreased by 46%, and relaxation time was unchanged in group III. In contrast, in group I, diastolic force and maximum rate of force decline did not change, and relaxation time decreased by 20%. Na + -Ca 2+ exchanger was 66% higher in group I than in group III. Na + -Ca 2+ exchanger was inversely correlated with the frequency-dependent rise of diastolic force when stimulation rate was increased ( r =−0.74; P <0.001). Compared with nonfailing human hearts (n=6), SR Ca 2+ -ATPase was decreased and Na + -Ca 2+ exchanger unchanged in group III, whereas Na + -Ca 2+ exchanger was increased and SR Ca 2+ -ATPase unchanged in group I. Results with group II hearts were between those of group I and group III hearts. Conclusions —By discriminating failing human hearts according to their diastolic function, we identified different phenotypes. Disturbed diastolic function occurs in hearts with decreased SR Ca 2+ -ATPase and unchanged Na + -Ca 2+ exchanger, whereas increased expression of the Na + -Ca 2+ exchanger is associated with preserved diastolic function."],["dc.identifier.doi","10.1161/01.CIR.99.5.641"],["dc.identifier.gro","3144987"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102848"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.notes.status","final"],["dc.relation.eissn","1524-4539"],["dc.relation.issn","0009-7322"],["dc.title","Relationship Between Na + -Ca 2+ –Exchanger Protein Levels and Diastolic Function of Failing Human Myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]