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.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"]]

[["dc.bibliographiccitation.firstpage","H349"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","American Journal of Physiology - Heart and Circulatory Physiology"],["dc.bibliographiccitation.lastpage","H356"],["dc.bibliographiccitation.volume","282"],["dc.contributor.author","Janssen, P. M. L."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zeitz, Oliver"],["dc.contributor.author","Lehnart, Stephan Elmar"],["dc.contributor.author","Prestle, J."],["dc.contributor.author","Darmer, D."],["dc.contributor.author","Holtz, J."],["dc.contributor.author","Schumann, H."],["dc.date.accessioned","2017-09-07T11:52:36Z"],["dc.date.available","2017-09-07T11:52:36Z"],["dc.date.issued","2002"],["dc.description.abstract","Increased mechanical load has been proposed as an inductor of apoptosis, but it is unknown whether this can occur in the range of pre- and afterloads that prevail in the beating heart. We investigated apoptosis in cultured rabbit multicellular myocardial preparations over several days. Muscles contracted in absence of pre- and afterload (unloaded isotonic), in absence of preload but in presence of afterload (unloaded isometric), or in presence of both (loaded isometric). After up to 48 h of continuous contractions, apoptosis was assessed by TdT-mediated nick-end labeling (TUNEL) assay and DNA ladder analysis. In muscles that contracted loaded isometric, apoptosis was detected after 6–24 h. After 48 h, apoptosis was most prominent in this group, reflected by a high level of DNA ladder intensity (DLI; 27.8 ± 11.5), whereas Bcl-xL (on RNA level) was significantly downregulated, and Fas remained unchanged. In unloaded isometric preparations, apoptosis was significantly less (6.9 ± 5.9 DLI) and very similar to those contracting unloaded isotonic (6.1 ± 5.1 DLI). We conclude that load-dependent apoptosis can occur at sarcomere lengths achievable in vivo and may mainly result from increased preload."],["dc.identifier.doi","10.1152/ajpheart.00024.2001"],["dc.identifier.gro","3144976"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2661"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0363-6135"],["dc.title","Load-dependent induction of apoptosis in multicellular myocardial preparations"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]