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42 results on '"Hasenfuss, Gerd"'

1. Dysferlin Enables Tubular Membrane Proliferation in Cardiac Hypertrophy.

Author

Paulke, Nora Josefine, Fleischhacker, Carolin, Wegener, Justus B., Riedemann, Gabriel C., Cretu, Constantin, Mushtaq, Mufassra, Zaremba, Nina, Möbius, Wiebke, Zühlke, Yannik, Wedemeyer, Jasper, Liebmann, Lorenz, Gorshkova, Anastasiia A., Kownatzki-Danger, Daniel, Wagner, Eva, Kohl, Tobias, Wichmann, Carolin, Jahn, Olaf, Urlaub, Henning, Toischer, Karl, and Hasenfuß, Gerd

Published
2024
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2. Caveolin3 Stabilizes McT1-Mediated Lactate/Proton Transport in Cardiomyocytes

Author

Peper, Jonas, Kownatzki-Danger, Daniel, Weninger, Gunnar, Seibertz, Fitzwilliam, Pronto, Julius Ryan D., Sutanto, Henry, Pacheu-Grau, David, Hindmarsh, Robin, Brandenburg, Sören, Kohl, Tobias, Hasenfuss, Gerd, Gotthardt, Michael, Rog-Zielinska, Eva A., Wollnik, Bernd, Rehling, Peter, Urlaub, Henning, Wegener, Jörg, Heijman, Jordi, Voigt, Niels, Cyganek, Lukas, Lenz, Christof, and Lehnart, Stephan E.

Published
2021
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3. An Alternative Mechanism of Subcellular Iron Uptake Deficiency in Cardiomyocytes

Author

Dai, Yuanyuan, primary, Ignatyeva, Nadezda, additional, Xu, Hang, additional, Wali, Ruheen, additional, Toischer, Karl, additional, Brandenburg, Sören, additional, Lenz, Christof, additional, Pronto, Julius, additional, Fakuade, Funsho E., additional, Sossalla, Samuel, additional, Zeisberg, Elisabeth M., additional, Janshoff, Andreas, additional, Kutschka, Ingo, additional, Voigt, Niels, additional, Urlaub, Henning, additional, Rasmussen, Torsten Bloch, additional, Mogensen, Jens, additional, Lehnart, Stephan E., additional, Hasenfuss, Gerd, additional, and Ebert, Antje, additional

Published
2023
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5. Effects of Atrial Fibrillation on the Human Ventricle

Author

Pabel, Steffen, primary, Knierim, Maria, additional, Stehle, Thea, additional, Alebrand, Felix, additional, Paulus, Michael, additional, Sieme, Marcel, additional, Herwig, Melissa, additional, Barsch, Friedrich, additional, Körtl, Thomas, additional, Pöppl, Arnold, additional, Wenner, Brisca, additional, Ljubojevic-Holzer, Senka, additional, Molina, Cristina E., additional, Dybkova, Nataliya, additional, Camboni, Daniele, additional, Fischer, Thomas H., additional, Sedej, Simon, additional, Scherr, Daniel, additional, Schmid, Christof, additional, Brochhausen, Christoph, additional, Hasenfuß, Gerd, additional, Maier, Lars S., additional, Hamdani, Nazha, additional, Streckfuss-Bömeke, Katrin, additional, and Sossalla, Samuel, additional

Published
2022
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6. cAMP Imaging at Ryanodine Receptors Reveals β 2 -Adrenoceptor Driven Arrhythmias

Author

Berisha, Filip, primary, Götz, Konrad R., additional, Wegener, Jörg W., additional, Brandenburg, Sören, additional, Subramanian, Hariharan, additional, Molina, Cristina E., additional, Rüffer, André, additional, Petersen, Johannes, additional, Bernhardt, Alexander, additional, Girdauskas, Evaldas, additional, Jungen, Christiane, additional, Pape, Ulrike, additional, Kraft, Axel E., additional, Warnke, Svenja, additional, Lindner, Diana, additional, Westermann, Dirk, additional, Blankenberg, Stefan, additional, Meyer, Christian, additional, Hasenfuß, Gerd, additional, Lehnart, Stephan E., additional, and Nikolaev, Viacheslav O., additional

Published
2021
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7. cAMP Imaging at Ryanodine Receptors Reveals β2-Adrenoceptor Driven Arrhythmias.

Author

Berisha, Filip, Götz, Konrad R., Wegener, Jörg W., Brandenburg, Sören, Subramanian, Hariharan, Molina, Cristina E., Rüffer, André, Petersen, Johannes, Bernhardt, Alexander, Girdauskas, Evaldas, Jungen, Christiane, Pape, Ulrike, Kraft, Axel E., Warnke, Svenja, Lindner, Diana, Westermann, Dirk, Blankenberg, Stefan, Meyer, Christian, Hasenfuß, Gerd, and Lehnart, Stephan E.

Published
2021
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9. Transcription Factor Runx2 Promotes Aortic Fibrosis and Stiffness in Type 2 Diabetes Mellitus

Author

Raaz, Uwe, primary, Schellinger, Isabel N., additional, Chernogubova, Ekaterina, additional, Warnecke, Christina, additional, Kayama, Yosuke, additional, Penov, Kiril, additional, Hennigs, Jan K., additional, Salomons, Florian, additional, Eken, Suzanne, additional, Emrich, Fabian C., additional, Zheng, Wei H., additional, Adam, Matti, additional, Jagger, Ann, additional, Nakagami, Futoshi, additional, Toh, Ryuji, additional, Toyama, Kensuke, additional, Deng, Alicia, additional, Buerke, Michael, additional, Maegdefessel, Lars, additional, Hasenfuß, Gerd, additional, Spin, Joshua M., additional, and Tsao, Philip S., additional

Published
2015
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11. Abstract 055: β-Catenin Mediates an Interplay between Genetic Background and Growth-Regulating Effects of Estrogen in the Healthy Heart

Author

Kararigas, Georgios, primary, Nguyen, Ba Tiep, additional, Zelarayan, Laura C, additional, Hassenpflug, Maike, additional, Toischer, Karl, additional, Sanchez-Ruderisch, Hugo, additional, Hasenfuss, Gerd, additional, Bergmann, Martin W, additional, Jarry, Hubertus, additional, and Regitz-Zagrosek, Vera, additional

Published
2013
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12. Stimulated Emission Depletion Live-Cell Super-Resolution Imaging Shows Proliferative Remodeling of T-Tubule Membrane Structures After Myocardial Infarction

Author

Wagner, Eva, primary, Lauterbach, Marcel A., additional, Kohl, Tobias, additional, Westphal, Volker, additional, Williams, George S.B., additional, Steinbrecher, Julia H., additional, Streich, Jan-Hendrik, additional, Korff, Brigitte, additional, Tuan, Hoang-Trong M., additional, Hagen, Brian, additional, Luther, Stefan, additional, Hasenfuss, Gerd, additional, Parlitz, Ulrich, additional, Jafri, M. Saleet, additional, Hell, Stefan W., additional, Lederer, W. Jonathan, additional, and Lehnart, Stephan E., additional

Published
2012
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13. Inhibition of Elevated Ca 2+ /Calmodulin-Dependent Protein Kinase II Improves Contractility in Human Failing Myocardium

Author

Sossalla, Samuel, primary, Fluschnik, Nina, additional, Schotola, Hanna, additional, Ort, Katharina R., additional, Neef, Stefan, additional, Schulte, Timo, additional, Wittköpper, Katrin, additional, Renner, André, additional, Schmitto, Jan D., additional, Gummert, Jan, additional, El-Armouche, Ali, additional, Hasenfuss, Gerd, additional, and Maier, Lars S., additional

Published
2010
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15. Leptin Enhances the Recruitment of Endothelial Progenitor Cells Into Neointimal Lesions After Vascular Injury by Promoting Integrin-Mediated Adhesion

Author

Schroeter, Marco R., primary, Leifheit, Maren, additional, Sudholt, Philipp, additional, Heida, Nana-Maria, additional, Dellas, Claudia, additional, Rohm, Ilonka, additional, Alves, Frauke, additional, Zientkowska, Marta, additional, Rafail, Stavros, additional, Puls, Miriam, additional, Hasenfuss, Gerd, additional, Konstantinides, Stavros, additional, and Schäfer, Katrin, additional

Published
2008
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20. Effects of Adenovirus-Mediated Sorcin Overexpression on Excitation-Contraction Coupling in Isolated Rabbit Cardiomyocytes

Author

Seidler, Tim, primary, Miller, Stewart L.W., additional, Loughrey, Christopher M., additional, Kania, Astrid, additional, Burow, Annika, additional, Kettlewell, Sarah, additional, Teucher, Nils, additional, Wagner, Stefan, additional, Kögler, Harald, additional, Meyers, Marian B., additional, Hasenfuss, Gerd, additional, and Smith, Godfrey L., additional

Published
2003
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26. Inhibition of Elevated Ca2+/Calmodulin-Dependent Protein Kinase II Improves Contractility in Human Failing Myocardium.

Author

Sossalla, Samuel, Fluschnik, Nina, Schotola, Hanna, Ort, Katharina R., Neef, Stefan, Wittköpper, Katrin, Renner, André, Schmitto, Jan D., Gummert, Jan, El-Armouche, Ali, Hasenfuss, Gerd, Maier, Lars S., and Schulte, Timo

Subjects
CALMODULIN, PROTEIN kinases, HEART failure, CARDIAC contraction, RESEARCH
Abstract

The article discusses research that investigated the detailed calcium/calmodulin-dependent protein kinase (CaMKII) expression in end-stage failing human hearts and its functional effects on contractility. Heart failure (HF) is associated with increased CaMKII expression and activity, though it has never been studied in human myocardium. Isometrically twitching trabeculae experiments revealed improved force frequency relationships in the presence of CaMKII inhibitors. CaMKII inhibition could be a possible therapeutic option for patient with HF.

Published
2010
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27. CaMKII-Dependent Diastolic SR Ca2+ Leak and Elevated Diastolic Ca2+ Levels in Right A trial Myocardium of Patients With A trial Fibrillation.

Author

Neef, Stefan, Dybkova, Nataliya, Sossafla, Samuel, Ort, Katharina R., Fluschnik, Nina, Neumann, Kay, Seipelt, Raif, Schöndube, Friedrich A., Hasenfuss, Gerd, and Maier, Lars S.

Subjects
CALMODULIN, ATRIAL fibrillation, RYANODINE receptors, PROTEIN kinases, SINOATRIAL node, PHOSPHORYLATION
Abstract

The article presents a study which evaluates the occurrence of CaMKII-dependent diastolic SR calmodulin-dependent protein kinase II (Ca2+) leak and high diastolic Ca2+ levels in atrial myocardium patients with atrial fibrillation (AF). The researchers used the isolated human right atrial myocytes of AF patients and compared them to the sinus rhythm found in CaMKII expression. It concludes that high RyR2 CaMKII-dependent phosphorylation can increase SR Ca2+ leak.

Published
2010
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40. Inhibition of elevated Ca2+/calmodulin-dependent protein kinase II improves contractility in human failing myocardium.

Author

Sossalla S, Fluschnik N, Schotola H, Ort KR, Neef S, Schulte T, Wittköpper K, Renner A, Schmitto JD, Gummert J, El-Armouche A, Hasenfuss G, and Maier LS

Subjects
Animals, Cells, Cultured, Heart Failure drug therapy, Heart Failure physiopathology, Humans, Myocardial Contraction drug effects, Myocardium pathology, Protein Kinase Inhibitors pharmacology, Protein Kinase Inhibitors therapeutic use, Sheep, Calcium-Calmodulin-Dependent Protein Kinase Type 2 antagonists & inhibitors, Calcium-Calmodulin-Dependent Protein Kinase Type 2 biosynthesis, Heart Failure enzymology, Myocardial Contraction physiology, Myocardium enzymology
Abstract

Rationale: Heart failure (HF) is known to be associated with increased Ca(2+)/calmodulin-dependent protein kinase (CaMK)II expression and activity. There is still controversial discussion about the functional role of CaMKII in HF. Moreover, CaMKII inhibition has never been investigated in human myocardium., Objective: We sought to investigate detailed CaMKIIδ expression in end-stage failing human hearts (dilated and ischemic cardiomyopathy) and the functional effects of CaMKII inhibition on contractility., Methods and Results: Expression analysis revealed that CaMKIIδ, both cytosolic δ(C) and nuclear δ(B) splice variants, were significantly increased in both right and left ventricles from patients with dilated or ischemic cardiomyopathy versus nonfailing. Experiments with isometrically twitching trabeculae revealed significantly improved force frequency relationships in the presence of CaMKII inhibitors (KN-93 and AIP). Increased postrest twitches after CaMKII inhibition indicated an improved sarcoplasmic reticulum (SR) Ca(2+) loading. This was confirmed in isolated myocytes by a reduced SR Ca(2+) spark frequency and hence SR Ca(2+) leak, resulting in increased SR Ca(2+) load when inhibiting CaMKII. Ryanodine receptor type 2 phosphorylation at Ser2815, which is known to be phosphorylated by CaMKII thereby contributing to SR Ca(2+) leak, was found to be markedly reduced in KN-93-treated trabeculae. Interestingly, CaMKII inhibition did not influence contractility in nonfailing sheep trabeculae., Conclusions: The present study shows for the first time that CaMKII inhibition acutely improves contractility in human HF where CaMKIIδ expression is increased. The mechanism proposed consists of a reduced SR Ca(2+) leak and consequently increased SR Ca(2+) load. Thus, CaMKII inhibition appears to be a possible therapeutic option for patients with HF and merits further investigation.

Published
2010
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41. CaMKII-dependent diastolic SR Ca2+ leak and elevated diastolic Ca2+ levels in right atrial myocardium of patients with atrial fibrillation.

Author

Neef S, Dybkova N, Sossalla S, Ort KR, Fluschnik N, Neumann K, Seipelt R, Schöndube FA, Hasenfuss G, and Maier LS

Subjects
Action Potentials, Anesthetics, Local pharmacology, Atrial Fibrillation pathology, Atrial Fibrillation physiopathology, Benzylamines pharmacology, Calcium Channels, L-Type metabolism, Calcium-Binding Proteins metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2 antagonists & inhibitors, Case-Control Studies, Cell Size, Diastole, Heart Atria enzymology, Humans, Microscopy, Confocal, Myocardium pathology, Patch-Clamp Techniques, Phosphorylation, Protein Kinase Inhibitors pharmacology, Ryanodine Receptor Calcium Release Channel metabolism, Sarcoplasmic Reticulum drug effects, Sarcoplasmic Reticulum Calcium-Transporting ATPases metabolism, Sodium-Calcium Exchanger metabolism, Sulfonamides pharmacology, Systole, Tetracaine pharmacology, Time Factors, Up-Regulation, Atrial Fibrillation enzymology, Calcium Signaling drug effects, Calcium-Calmodulin-Dependent Protein Kinase Type 2 metabolism, Myocardium enzymology, Sarcoplasmic Reticulum enzymology
Abstract

Rationale: Although research suggests that diastolic Ca(2+) levels might be increased in atrial fibrillation (AF), this hypothesis has never been tested. Diastolic Ca(2+) leak from the sarcoplasmic reticulum (SR) might increase diastolic Ca(2+) levels and play a role in triggering or maintaining AF by transient inward currents through Na(+)/Ca(2+) exchange. In ventricular myocardium, ryanodine receptor type 2 (RyR2) phosphorylation by Ca(2+)/calmodulin-dependent protein kinase (CaMK)II is emerging as an important mechanism for SR Ca(2+) leak., Objective: We tested the hypothesis that CaMKII-dependent diastolic SR Ca(2+) leak and elevated diastolic Ca(2+) levels occurs in atrial myocardium of patients with AF., Methods and Results: We used isolated human right atrial myocytes from patients with AF versus sinus rhythm and found CaMKII expression to be increased by 40+/-14% (P<0.05), as well as CaMKII phosphorylation by 33+/-12% (P<0.05). This was accompanied by a significantly increased RyR2 phosphorylation at the CaMKII site (Ser2814) by 110+/-53%. Furthermore, cytosolic Ca(2+) levels were elevated during diastole (229+/-20 versus 164+/-8 nmol/L, P<0.05). Most likely, this resulted from an increased SR Ca(2+) leak in AF (P<0.05), which was not attributable to higher SR Ca(2+) load. Tetracaine experiments confirmed that SR Ca(2+) leak through RyR2 leads to the elevated diastolic Ca(2+) level. CaMKII inhibition normalized SR Ca(2+) leak and cytosolic Ca(2+) levels without changes in L-type Ca(2+) current., Conclusion: Increased CaMKII-dependent phosphorylation of RyR2 leads to increased SR Ca(2+) leak in human AF, causing elevated cytosolic Ca(2+) levels, thereby providing a potential arrhythmogenic substrate that could trigger or maintain AF.

Published
2010
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42. Hydroxyl radical-induced acute diastolic dysfunction is due to calcium overload via reverse-mode Na(+)-Ca(2+) exchange.

Author

Zeitz O, Maass AE, Van Nguyen P, Hensmann G, Kögler H, Möller K, Hasenfuss G, and Janssen PM

Subjects
Actin Cytoskeleton drug effects, Actin Cytoskeleton metabolism, Animals, Calcium pharmacology, Calcium Channels, L-Type physiology, Diastole physiology, Dose-Response Relationship, Drug, Female, Heart Ventricles metabolism, Heart Ventricles physiopathology, In Vitro Techniques, Male, Microscopy, Electron, Myocardial Contraction drug effects, Myocardium metabolism, Myocardium ultrastructure, Rabbits, Rats, Rats, Wistar, Sarcoplasmic Reticulum physiology, Calcium metabolism, Diastole drug effects, Heart Ventricles drug effects, Hydroxyl Radical pharmacology, Sodium-Calcium Exchanger physiology
Abstract

Hydroxyl radicals (OH) are involved in the development of reperfusion injury and myocardial failure. In the acute phase of the OH-mediated diastolic dysfunction, increased intracellular Ca(2+) levels and alterations of myofilaments may play a role, but the relative contribution of these systems to myocardial dysfunction is unknown. Intact contracting cardiac trabeculae from rabbits were exposed to OH, resulting in an increase in diastolic force (F(dia)) by 540%. Skinned fiber experiments revealed that OH-exposed preparations were sensitized for Ca(2+) (EC(50): 3.27+/-0.24 x 10(-6) versus 2.69+/-0.15 x 10(-6) mol/L; P<0.05), whereas maximal force development was unaltered. Western blots showed a proteolytic degradation of troponin T (TnT) with intact troponin I (TnI). Blocking of calpain I by MDL-28.170 inhibited both TnT-proteolysis and Ca(2+) sensitization, but failed to prevent the acute diastolic dysfunction in the intact preparation. The OH-induced diastolic dysfunction was similar in preparations with intact (540+/-93%) and pharmacologically blocked sarcoplasmic reticulum (539+/-77%), and was also similar in presence of the L-type Ca(2+)-channel antagonist verapamil. In sharp contrast, inhibition of the reverse-mode sodium-calcium exchange by KB-R7943 preserved diastolic function completely. Additional experiments were performed in rat myocardium; the rise in diastolic force was comparable to rabbit myocardium, but Ca(2+) sensitivity was unchanged and maximal force development was reduced. This was associated with a degradation of TnI, but not TnT. Electron microscopic analysis revealed that OH did not cause irreversible membrane damage. We conclude that OH-induced acute diastolic dysfunction is caused by Ca(2+) influx via reverse mode of the sodium-calcium exchanger. Degradation of troponins appears to be species-dependent but does not contribute to the acute diastolic dysfunction.

Published
2002
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