22 results on '"Dendorfer A"'
Search Results
2. FgF23 and soluble klotho effects on the myocardium: an ex vivo study
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Sen, P, primary, D Alessio, C, additional, Hamers, J, additional, Sun, Z, additional, Dendorfer, A, additional, and Merkus, D, additional
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- 2024
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3. Contractility measurements for cardiotoxicity screening with ventricular myocardial slices of pigs
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Shi, Runzhu, primary, Reichardt, Marius, additional, Fiegle, Dominik J, additional, Küpfer, Linda K, additional, Czajka, Titus, additional, Sun, Zhengwu, additional, Salditt, Tim, additional, Dendorfer, Andreas, additional, Seidel, Thomas, additional, and Bruegmann, Tobias, additional
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- 2023
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4. Animal models and animal-free innovations for cardiovascular research
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van der Velden, Jolanda, Asselbergs, Folkert W, Bakkers, Jeroen, Batkai, Sandor, Bertrand, Luc, Bezzina, Connie R, Bot, Ilze, Brundel, Bianca, Carrier, Lucie, Chamuleau, Steven, Ciccarelli, Michele, Dawson, Dana, Davidson, Sean M, Dendorfer, Andreas, Duncker, Dirk J, Eschenhagen, Thomas, Fabritz, Larissa, Falcão-Pires, Ines, Ferdinandy, Péter, Giacca, Mauro, Girao, Henrique, Gollmann-Tepeköylü, Can, Gyongyosi, Mariann, Guzik, Tomasz J, Hamdani, Nazha, Heymans, Stephane, Hilfiker, Andres, Hilfiker-Kleiner, Denise, Hoekstra, Alfons G, Hulot, Jean-Sébastien, Kuster, Diederik W D, van Laake, Linda W, Lecour, Sandrine, Leiner, Tim, Linke, Wolfgang A, Lumens, Joost, Lutgens, Esther, Madonna, Rosalinda, Maegdefessel, Lars, Mayr, Manuel, van der Meer, Peter, Passier, Robert, Perbellini, Filippo, Perrino, Cinzia, Pesce, Maurizio, Priori, Silvia, Remme, Carol Ann, Rosenhahn, Bodo, Schotten, Ulrich, Sipido, Karin, Schulz, Rainer, Sluijter, Joost P G, van Steenbeek, Frank, Steffens, Sabine, Terracciano, Cesare M, Tocchetti, Carlo Gabriele, Vlasman, Patricia, Yeung, Kak Khee, Zacchigna, Serena, Zwaagman, Dayenne, Thum, Thomas, Interne geneeskunde GD, dCSCA AVR, CS_Genetics, Hubrecht Institute for Developmental Biology and Stem Cell Research, van der Velden, Jolanda, Asselbergs, Folkert W, Bakkers, Jeroen, Batkai, Sandor, Bertrand, Luc, Bezzina, Connie R, Bot, Ilze, Brundel, Bianca, Carrier, Lucie, Chamuleau, Steven, Ciccarelli, Michele, Dawson, Dana, Davidson, Sean M, Dendorfer, Andrea, Duncker, Dirk J, Eschenhagen, Thoma, Fabritz, Larissa, Falcão-Pires, Ine, Ferdinandy, Péter, Giacca, Mauro, Girao, Henrique, Gollmann-Tepeköylü, Can, Gyongyosi, Mariann, Guzik, Tomasz J, Hamdani, Nazha, Heymans, Stephane, Hilfiker, Andre, Hilfiker-Kleiner, Denise, Hoekstra, Alfons G, Hulot, Jean-Sébastien, Kuster, Diederik W D, van Laake, Linda W, Lecour, Sandrine, Leiner, Tim, Linke, Wolfgang A, Lumens, Joost, Lutgens, Esther, Madonna, Rosalinda, Maegdefessel, Lar, Mayr, Manuel, van der Meer, Peter, Passier, Robert, Perbellini, Filippo, Perrino, Cinzia, Pesce, Maurizio, Priori, Silvia, Remme, Carol Ann, Rosenhahn, Bodo, Schotten, Ulrich, Schulz, Rainer, Sipido, Karin, Sluijter, Joost P G, van Steenbeek, Frank, Steffens, Sabine, Terracciano, Cesare M, Tocchetti, Carlo Gabriele, Vlasman, Patricia, Yeung, Kak Khee, Zacchigna, Serena, Zwaagman, Dayenne, Thum, Thomas, Publica, Interne geneeskunde GD, dCSCA AVR, and CS_Genetics
- Subjects
big data ,bioinformatics ,cardiovascular disease ,co-morbidities ,iPSC ,multiomics ,network medicine ,tissue engineering ,Physiology ,Bioinformatics ,multiomic ,Review ,Comorbidities ,co-morbiditie ,Big data ,SDG 3 - Good Health and Well-being ,Models ,Physiology (medical) ,Humans ,Animals ,Tissue engineering ,Cardiovascular Diseases/diagnosis ,bioinformatic ,Animal ,Cardiovascular disease ,Multiomics ,Cardiovascular Diseases ,Research Design ,2023 OA procedure ,Models, Animal ,Network medicine ,Cardiology and Cardiovascular Medicine - Abstract
Cardiovascular diseases represent a major cause of morbidity and mortality, necessitating research to improve diagnostics, and to discover and test novel preventive and curative therapies. All of which warrant experimental models that recapitulate human disease. The translation of basic science results to clinical practice is a challenging task. In particular for complex conditions such as cardiovascular diseases, which often result from multiple risk factors and co-morbidities. This difficulty might lead some individuals to question the value of animal research, citing the translational 'valley of death', which largely reflects the fact that studies in rodents are difficult to translate to humans. This is also influenced by the fact that new, human-derived in vitro models can recapitulate aspects of disease processes. However, it would be a mistake to think that animal models cannot provide a vital step in the translational pathway as they do provide important pathophysiological insights into disease mechanisms particularly on a organ and systemic level. While stem cell-derived human models have the potential to become key in testing toxicity and effectiveness of new drugs, we need to be realistic, and carefully validate all new human-like disease models. In this position paper, we highlight recent advances in trying to reduce the number of animals for cardiovascular research ranging from stem cell-derived models to in situ modelling of heart properties, bioinformatic models based on large datasets, and improved current animal models, which show clinically relevant characteristics observed in patients with a cardiovascular disease. We aim to provide a guide to help researchers in their experimental design to translate bench findings to clinical routine taking the replacement, reduction and refinement (3R) as a guiding concept. [Abstract copyright: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2022. For permissions please email: journals.permissions@oup.com.]
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- 2022
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5. Desmoglein-2 interaction is crucial for cardiomyocyte cohesion and function
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Schlipp, Angela, Schinner, Camilla, Spindler, Volker, Vielmuth, Franziska, Gehmlich, Katja, Syrris, Petros, Mckenna, William J., Dendorfer, Andreas, Hartlieb, Eva, and Waschke, Jens
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- 2014
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6. SARS-CoV-2 infects and induces cytotoxic effects in human cardiomyocytes
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Denisa Bojkova, Stefan Günther, Andreas Dendorfer, Carsten Tschöpe, Achilleas S. Frangakis, Utz H Ermel, Umber Saleem, Sandra Ciesek, Andreas M. Zeiher, Julian U. G. Wagner, Hendrik Milting, Arne Hansen, Jaya Krishnan, Jindrich Cinatl, Guillermo Luxán, Galip Servet Aslan, Thomas Eschenhagen, Mariana Shumliakivska, Stefanie Dimmeler, Minh Duc Pham, Karin Klingel, Patrick N. Harter, and Publica
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0301 basic medicine ,Heart Diseases ,medicine.drug_class ,Physiology ,viruses ,Inflammation ,Apoptosis ,030204 cardiovascular system & hematology ,Lung injury ,medicine.disease_cause ,Antiviral Agents ,03 medical and health sciences ,0302 clinical medicine ,Interferon ,Physiology (medical) ,Cytotoxic T cell ,Medicine ,Humans ,AcademicSubjects/MED00200 ,Myocytes, Cardiac ,Coronavirus ,Cardiotoxicity ,Alanine ,business.industry ,SARS-CoV-2 ,COVID-19 ,Virology ,Cathepsins ,Adenosine Monophosphate ,3. Good health ,COVID-19 Drug Treatment ,030104 developmental biology ,Cell culture ,Host-Pathogen Interactions ,Angiotensin-Converting Enzyme 2 ,Antiviral drug ,medicine.symptom ,Caco-2 Cells ,business ,Cardiology and Cardiovascular Medicine ,Reactive Oxygen Species ,medicine.drug ,Signal Transduction - Abstract
Aims Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has emerged as a global pandemic. SARS-CoV-2 infection can lead to elevated markers of cardiac injury associated with higher risk of mortality. It is unclear whether cardiac injury is caused by direct infection of cardiomyocytes or is mainly secondary to lung injury and inflammation. Here, we investigate whether cardiomyocytes are permissive for SARS-CoV-2 infection. Methods and results Two strains of SARS-CoV-2 infected human induced pluripotent stem cell-derived cardiomyocytes (iPS-CMs) as demonstrated by detection of intracellular double-stranded viral RNA and viral spike glycoprotein expression. Increasing concentrations of viral RNA are detected in supernatants of infected cardiomyocytes, which induced infections in Caco-2 cell lines, documenting productive infections. SARS-COV-2 infection and induced cytotoxic and proapoptotic effects associated with it abolished cardiomyocyte beating. RNA sequencing confirmed a transcriptional response to viral infection as demonstrated by the up-regulation of genes associated with pathways related to viral response and interferon signalling, apoptosis, and reactive oxygen stress. SARS-CoV-2 infection and cardiotoxicity was confirmed in a 3D cardiosphere tissue model. Importantly, viral spike protein and viral particles were detected in living human heart slices after infection with SARS-CoV-2. Coronavirus particles were further observed in cardiomyocytes of a patient with COVID-19. Infection of iPS-CMs was dependent on cathepsins and angiotensin-converting enzyme 2 (ACE2), and was blocked by remdesivir. Conclusions This study demonstrates that SARS-CoV-2 infects cardiomyocytes in vitro in an ACE2- and cathepsin-dependent manner. SARS-CoV-2 infection of cardiomyocytes is inhibited by the antiviral drug remdesivir. Translational Perspective Although this study cannot address whether cardiac injury and dysfunction in COVID-19 patients is caused by direct infection of cardiomyocytes, the demonstration of direct cardiotoxicity in cardiomyocytes, organ mimics, human heart slices and human hearts warrants the further monitoring of cardiotoxic effects in COVID-19 patients., Graphical Abstract Graphical Abstract
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- 2020
7. Organotypic slice culture from human adult ventricular myocardium
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Brandenburger, Matthias, Wenzel, Jan, Bogdan, Roman, Richardt, Doreen, Nguemo, Filomain, Reppel, Michael, Hescheler, Jürgen, Terlau, Heinrich, and Dendorfer, Andreas
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- 2012
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8. SARS-CoV-2 infects and induces cytotoxic effects in human cardiomyocytes
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Bojkova, Denisa, primary, Wagner, Julian U G, additional, Shumliakivska, Mariana, additional, Aslan, Galip S, additional, Saleem, Umber, additional, Hansen, Arne, additional, Luxán, Guillermo, additional, Günther, Stefan, additional, Pham, Minh Duc, additional, Krishnan, Jaya, additional, Harter, Patrick N, additional, Ermel, Utz H, additional, Frangakis, Achilleas S, additional, Milting, Hendrik, additional, Zeiher, Andreas M, additional, Klingel, Karin, additional, Cinatl, Jindrich, additional, Dendorfer, Andreas, additional, Eschenhagen, Thomas, additional, Tschöpe, Carsten, additional, Ciesek, Sandra, additional, and Dimmeler, Stefanie, additional
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- 2020
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9. Establishment of organotypic slice cultures from human myocardium
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Brandenburger, M, Wenzel, J, Bogdan, R, Richardt, D, Reppel, M, Hescheler, J, Terlau, H, and Dendorfer, A
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- 2010
10. Remote vs. ischaemic preconditioning: the differential role of mitogen-activated protein kinase pathways
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Heidbreder, Marc, Naumann, Annegret, Tempel, Klaus, Dominiak, Peter, and Dendorfer, Andreas
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- 2008
11. Saturday, 17 July 2010
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I. Dimova, R. Hlushchuk, A. Makanya, V. Djonov, M. Theurl, W. Schgoer, K. Albrecht, A. Beer, J. R. Patsch, P. Schratzberger, S. Mahata, R. Kirchmair, M. Didie, P. Christalla, T. Rau, T. Eschenhagen, U. Schumacher, Q. Lin, M. Zenke, W. Zimmmermann, M. Hoch, P. Fischer, B. Stapel, E. Missol-Kolka, S. Erschow, M. Scherr, H. Drexler, D. Hilfiker-Kleiner, I. Diebold, A. Petry, P. Kennel, T. Djordjevic, J. Hess, A. Goerlach, J. Castellano, R. Aledo, J. Sendra, P. Costales, L. Badimon, V. Llorente-Cortes, E. Dworatzek, S. Mahmoodzadeh, V. Regitz-Zagrosek, A. Posa, C. Varga, A. Berko, M. Veszelka, P. Szablics, B. Vari, I. Pavo, F. Laszlo, M. Brandenburger, J. Wenzel, R. Bogdan, D. Richardt, M. Reppel, J. Hescheler, H. Terlau, A. Dendorfer, J. Heijman, Y. Rudy, R. Westra, P. Volders, R. Rasmusson, V. Bondarenko, M. D. Ertas Gokhan, M. D. Ural Ertan, P. H. D. Karaoz Erdal, P. H. D. Aksoy Ayca, M. D. Kilic Teoman, M. D. Kozdag Guliz, M. D. Vural Ahmet, M. D. Ural Dilek, C. Poulet, T. Christ, E. Wettwer, U. Ravens, C. Van Der Pouw Kraan, S. Schirmer, J. Fledderus, P. Moerland, T. Leyen, J. Piek, N. Van Royen, A. Horrevoets, F. Fleissner, V. Jazbutyte, J. Fiedler, P. Galuppo, M. Mayr, G. Ertl, J. Bauersachs, T. Thum, S. Protze, A. Bussek, F. Li, R. Hoo, K. Lam, A. Xu, P. Subramanian, E. Karshovska, R. Megens, S. Akhtar, K. Heyll, Y. Jansen, C. Weber, A. Schober, M. Zafeiriou, C. Noack, A. Renger, R. Dietz, L. Zelarayan, M. Bergmann, I. Meln, A. Malashicheva, S. Anisimov, N. Kalinina, V. Sysoeva, A. Zaritskey, A. Barbuti, A. Scavone, N. Mazzocchi, A. Crespi, D. Capilupo, D. Difrancesco, L. Qian, W. Shim, Y. Gu, S. Mohammed, P. Wong, M. Zafiriou, H. Schaeffer, P. Kovacs, J. Simon, A. Varro, P. Athias, J. Wolf, O. Bouchot, D. Vandroux, A. Mathe, A. De Carvalho, G. Laurent, P. Rainer, M. Huber, F. Edelmann, T. Stojakovic, A. Trantina-Yates, M. Trauner, B. Pieske, D. Von Lewinski, A. De Jong, A. Maass, S. Oberdorf-Maass, I. Van Gelder, Y. Lin, J. Li, F. Wang, Y. He, X. Li, H. Xu, X. Yang, R. Coppini, C. Ferrantini, C. Ferrara, A. Rossi, A. Mugelli, C. Poggesi, E. Cerbai, N. Rozmaritsa, N. Voigt, D. Dobrev, M.-C. Kienitz, G. Zoidl, K. Bender, L. Pott, Z. Kohajda, A. Kristof, L. Virag, N. Jost, A. Trafford, B. Prnjavorac, E. Mujaric, J. Jukic, K. Abduzaimovic, K. Brack, V. Patel, J. Coote, G. Ng, R. Wilders, A. Van Ginneken, A. Verkerk, P. Xaplanteris, C. Vlachopoulos, K. Baou, C. Vassiliadou, I. Dima, N. Ioakeimidis, C. Stefanadis, W. Ruifrok, C. Qian, H. Sillje, H. Van Goor, D. Van Veldhuisen, W. Van Gilst, R. De Boer, K. Schmidt, F. Kaiser, J. Erdmann, C. De Wit, O. Barnett, Y. Kyyak, F. Cesana, L. Boffi, T. Mauri, M. Alloni, M. Betelli, S. Nava, C. Giannattasio, G. Mancia, R. Vilskersts, J. Kuka, B. Svalbe, E. Liepinsh, M. Dambrova, A. Zakrzewicz, J. Maroski, B. Vorderwuelbecke, K. Fiedorowicz, L. Da Silva-Azevedo, A. Pries, B. Gryglewska, M. Necki, M. Zelawski, T. Grodzicki, E. Scoditti, M. Massaro, M. Carluccio, A. Distante, C. Storelli, R. De Caterina, O. Kocgirli, S. Valcaccia, V. Dao, T. Suvorava, S. Kumpf, M. Floeren, M. Oppermann, G. Kojda, C. Leo, J. Ziogas, J. Favaloro, O. Woodman, W. Goettsch, A. Marton, C. Goettsch, H. Morawietz, E. Khalifa, Z. Ashour, V. Rupprecht, F. Scalera, J. Martens-Lobenhoffer, S. Bode-Boeger, W. Li, Y. Kwan, G. Leung, F. Patella, A. Mercatanti, L. Pitto, G. Rainaldi, I. Tsimafeyeu, Y. Tishova, N. Wynn, S. Kalinchenko, M. Clemente Lorenzo, M. Grande, F. Barriocanal, M. Aparicio, A. Martin, J. Hernandez, J. Lopez Novoa, C. Martin Luengo, A. Kurlianskaya, T. Denisevich, N. Barth, A. Loot, I. Fleming, Y. Wang, A. Gabrielsen, R. Ripa, E. Jorgensen, J. Kastrup, G. Arderiu, E. Pena, K. Kobus, J. Czyszek, A. Kozlowska-Wiechowska, P. Milkiewicz, M. Milkiewicz, R. Madonna, E. Montebello, Y. Geng, J. Chin-Dusting, D. Michell, M. Skilton, J. Dixon, A. Dart, X. Moore, M. Ehrbar, P. Reichmuth, N. Heinimann, B. Hewing, V. Stangl, K. Stangl, M. Laule, G. Baumann, A. Ludwig, R. Widmer-Teske, A. Mueller, P. Stieger, H. Tillmanns, R. Braun-Dullaeus, D. Sedding, K. Troidl, L. Eller, I. Benli, H. Apfelbeck, W. Schierling, C. Troidl, W. Schaper, T. Schmitz-Rixen, R. Hinkel, T. Trenkwalder, A. Pfosser, F. Globisch, G. Stachel, C. Lebherz, I. Bock-Marquette, C. Kupatt, C. Seyler, E. Duthil-Straub, E. Zitron, E. Scholz, D. Thomas, J. Gierten, C. Karle, R. Fink, T. Padro, R. Lugano, M. Garcia-Arguinzonis, M. Schuchardt, J. Pruefer, M. Toelle, N. Pruefer, V. Jankowski, J. Jankowski, W. Zidek, M. Van Der Giet, P. Fransen, C. Van Hove, C. Michiels, J. Van Langen, H. Bult, R. Quarck, M. Wynants, E. Alfaro-Moreno, M. Rosario Sepulveda, F. Wuytack, D. Van Raemdonck, B. Meyns, M. Delcroix, F. Christofi, S. Wijetunge, P. Sever, A. Hughes, J. Ohanian, S. Forman, V. Ohanian, C. Gibbons, S. Vernia, A. Das, V. Shah, M. Casado, W. Bielenberg, J. Daniel, J.-M. Daniel, K. Hersemeyer, T. Schmidt-Woell, D. Kaetzel, H. Tillmans, S. Kanse, E. Tuncay, H. Kandilci, E. Zeydanli, N. Sozmen, D. Akman, S. Yildirim, B. Turan, N. Nagy, K. Acsai, A. Farkas, J. Papp, A. Toth, C. Viero, S. Mason, A. Williams, S. Marston, D. Stuckey, E. Dyer, W. Song, M. El Kadri, G. Hart, M. Hussain, A. Faltinova, J. Gaburjakova, L. Urbanikova, M. Hajduk, B. Tomaskova, M. Antalik, A. Zahradnikova, P. Steinwascher, K. Jaquet, A. Muegge, G. Wang, M. Zhang, C. Tesi, H. Ter Keurs, S. Kettlewell, G. Smith, A. Workman, I. Lenaerts, P. Holemans, S. Sokolow, S. Schurmans, A. Herchuelz, K. Sipido, G. Antoons, X. Wehrens, N. Li, J. R. Respress, A. De Almeida, R. Van Oort, H. Lohmann, M. Saes, A. Messer, O. Copeland, M. Leung, F. Matthes, J. Steinbrecher, G. Salinas-Riester, L. Opitz, G. Hasenfuss, S. Lehnart, G. Caracciolo, M. Eleid, S. Carerj, K. Chandrasekaran, B. Khandheria, P. Sengupta, I. Riaz, L. Tyng, Y. Dou, A. Seymour, C. Dyer, S. Griffin, S. Haswell, J. Greenman, S. Yasushige, P. Amorim, T. Nguyen, M. Schwarzer, F. Mohr, T. Doenst, S. Popin Sanja, D. Lalosevic, I. Capo, T. Momcilov Popin, A. Astvatsatryan, M. Senan, G. Shafieian, N. Goncalves, I. Falcao-Pires, T. Henriques-Coelho, D. Moreira-Goncalves, A. Leite-Moreira, L. Bronze Carvalho, J. Azevedo, M. Andrade, I. Arroja, M. Relvas, G. Morais, M. Seabra, A. Aleixo, J. Winter, M. Zabunova, I. Mintale, D. Lurina, I. Narbute, I. Zakke, A. Erglis, Z. Marcinkevics, S. Kusnere, A. Abolins, J. Aivars, U. Rubins, Y. Nassar, D. Monsef, G. Hamed, S. Abdelshafy, L. Chen, Y. Wu, J. Wang, C. Cheng, M. Sternak, T. Khomich, A. Jakubowski, M. Szafarz, W. Szczepanski, L. Mateuszuk, J. Szymura-Oleksiak, S. Chlopicki, J. Sulicka, M. Strach, I. Kierzkowska, A. Surdacki, T. Mikolajczyk, W. Balwierz, T. Guzik, V. Dmitriev, E. Oschepkova, O. Polovitkina, V. Titov, A. Rogoza, R. Shakur, S. Metcalfe, J. Bradley, S. Demyanets, C. Kaun, S. Kastl, S. Pfaffenberger, I. Huk, G. Maurer, K. Huber, J. Wojta, O. Eriksson, M. Aberg, A. Siegbahn, G. Niccoli, G. Sgueglia, M. Conte, S. Giubilato, N. Cosentino, G. Ferrante, F. Crea, D. Ilisei, M. Leon, F. Mitu, E. Kyriakakis, M. Philippova, M. Cavallari, V. Bochkov, B. Biedermann, G. De Libero, P. Erne, T. Resink, C. Bakogiannis, C. Antoniades, D. Tousoulis, M. Demosthenous, C. Psarros, N. Sfyras, K. Channon, S. Del Turco, T. Navarra, G. Basta, V. Carnicelli, S. Frascarelli, R. Zucchi, A. Kostareva, G. Sjoberg, A. Gudkova, E. Semernin, E. Shlyakhto, T. Sejersen, N. Cucu, M. Anton, D. Stambuli, A. Botezatu, C. Arsene, E. Lupeanu, G. Anton, J. Patsch, E. Huber, C. Lande, A. Cecchettini, L. Tedeschi, M. Trivella, L. Citti, B. Chen, Y. Ma, Y. Yang, X. Ma, F. Liu, M. Hasanzad, L. Rejali, M. Fathi, A. Minassian, R. Mohammad Hassani, A. Najafi, M. Sarzaeem, S. Sezavar, A. Akhmedov, R. Klingenberg, K. Yonekawa, C. Lohmann, S. Gay, W. Maier, M. Neithard, T. Luescher, X. Xie, Z. Fu, A. Kevorkov, L. Verduci, F. Cremisi, A. Wonnerth, K. Katsaros, G. Zorn, T. Weiss, R. De Rosa, G. Galasso, F. Piscione, G. Santulli, G. Iaccarino, R. Piccolo, R. Luciano, M. Chiariello, M. Szymanski, R. Schoemaker, H. Hillege, S. Rizzo, C. Basso, G. Thiene, M. Valente, S. Rickelt, W. Franke, G. Bartoloni, S. Bianca, E. Giurato, C. Barone, G. Ettore, I. Bianca, P. Eftekhari, G. Wallukat, A. Bekel, F. Heinrich, M. Fu, M. Briedert, J. Briand, J. Roegel, K. Pilichou, S. Korkmaz, T. Radovits, S. Pali, K. Hirschberg, S. Zoellner, S. Loganathan, M. Karck, G. Szabo, A. Pucci, J. Pantaleo, S. Martino, G. Pelosi, M. Matteucci, C. Kusmic, N. Vesentini, F. Piccolomini, F. Viglione, A. L'abbate, J. Slavikova, M. Chottova Dvorakova, W. Kummer, A. Campanile, L. Spinelli, M. Ciccarelli, S. De Gennaro, E. Assante Di Panzillo, B. Trimarco, R. Akbarzadeh Najar, S. Ghaderian, A. Tabatabaei Panah, H. Vakili, A. Rezaei Farimani, G. Rezaie, A. Beigi Harchegani, N. Hamdani, C. Gavina, J. Van Der Velden, H. Niessen, G. Stienen, W. Paulus, C. Moura, I. Lamego, C. Eloy, J. Areias, T. Bonda, M. Dziemidowicz, T. Hirnle, I. Dmitruk, K. Kaminski, W. Musial, M. Winnicka, A. Villar, D. Merino, M. Ares, F. Pilar, E. Valdizan, M. Hurle, J. Nistal, V. Vera, P. Karuppasamy, S. Chaubey, T. Dew, R. Sherwood, J. Desai, L. John, M. Marber, G. Kunst, E. Cipolletta, A. Attanasio, C. Del Giudice, P. Campiglia, M. Illario, A. Berezin, E. Koretskaya, E. Bishop, I. Fearon, J. Heger, B. Warga, Y. Abdallah, B. Meyering, K. Schlueter, H. Piper, G. Euler, A. Lavorgna, S. Cecchetti, T. Rio, G. Coluzzi, C. Carrozza, E. Conti, F. Andreotti, A. Glavatskiy, O. Uz, E. Kardesoglu, O. Yiginer, S. Bas, O. Ipcioglu, N. Ozmen, M. Aparci, B. Cingozbay, F. Ivanes, M. Hillaert, S. Susen, F. Mouquet, P. Doevendans, B. Jude, G. Montalescot, E. Van Belle, C. Castellani, A. Angelini, O. De Boer, C. Van Der Loos, G. Gerosa, A. Van Der Wal, I. Dumitriu, P. Baruah, J. Kaski, O. Maytham, J. D Smith, M. Rose, A. Cappelletti, A. Pessina, M. Mazzavillani, G. Calori, A. Margonato, S. Cassese, C. D'anna, A. Leo, A. Silenzi, M. Baca', L. Biasucci, D. Baller, U. Gleichmann, J. Holzinger, T. Bitter, D. Horstkotte, A. Antonopoulos, A. Miliou, C. Triantafyllou, W. Masson, D. Siniawski, P. Sorroche, L. Casanas, W. Scordo, J. Krauss, A. Cagide, T. Huang, A. Wiedon, S. Lee, K. Walker, K. O'dea, P. Perez Berbel, V. Arrarte Esteban, M. Garcia Valentin, M. Sola Villalpando, C. Lopez Vaquero, L. Caballero, M. Quintanilla Tello, F. Sogorb Garri, G. Duerr, N. Elhafi, T. Bostani, L. Swieny, E. Kolobara, A. Welz, W. Roell, O. Dewald, N. Kaludercic, E. Takimoto, T. Nagayama, K. Chen, J. Shih, D. Kass, F. Di Lisa, N. Paolocci, L. Vinet, M. Pezet, F. Briec, M. Previlon, P. Rouet-Benzineb, A. Hivonnait, F. Charpentier, J. Mercadier, M. Cobo, M. Llano, C. Montalvo, V. Exposito, L. Meems, B. Westenbrink, L. Biesmans, V. Bito, R. Driessen, C. Huysmans, I. Mourouzis, C. Pantos, G. Galanopoulos, M. Gavra, P. Perimenis, D. Spanou, D. Cokkinos, T. Panasenko, S. Partsch, C. Harjung, A. Bogdanova, D. Mihov, P. Mocharla, S. Yakushev, J. Vogel, M. Gassmann, R. Tavakoli, D. Johansen, E. Sanden, C. Xi, R. Sundset, K. Ytrehus, M. Bliksoen, A. Rutkovskiy, L. Mariero, I. Vaage, K. Stenslokken, O. Pisarenko, V. Shulzhenko, I. Studneva, L. Serebryakova, O. Tskitishvili, Y. Pelogeykina, A. Timoshin, A. Vanin, L. Ziberna, M. Lunder, G. Drevensek, S. Passamonti, L. Gorza, B. Ravara, C. Scapin, M. Vitadello, F. Zigrino, J. Gwathmey, F. Del Monte, G. Vilahur, O. Juan-Babot, B. Onate, L. Casani, S. Lemoine, G. Calmettes, B. Jaspard-Vinassa, C. Duplaa, T. Couffinhal, P. Diolez, P. Dos Santos, A. Fusco, D. Sorriento, P. Cervero, A. Feliciello, E. Barnucz, K. Kozichova, M. Hlavackova, J. Neckar, F. Kolar, O. Novakova, F. Novak, C. Barsanti, N. Abraham, D. Muntean, S. Mirica, O. Duicu, A. Raducan, M. Hancu, O. Fira-Mladinescu, V. Ordodi, J. Voelkl, B. Haubner, G. Neely, C. Moriell, S. Seidl, O. Pachinger, J. Penninger, and B. Metzler
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Physiology ,Physiology (medical) ,Cardiology and Cardiovascular Medicine - Published
- 2010
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12. Remote vs. ischaemic preconditioning: the differential role of mitogen-activated protein kinase pathways
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Peter Dominiak, Marc Heidbreder, Klaus Tempel, Annegret Naumann, and Andreas Dendorfer
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Male ,MAPK/ERK pathway ,medicine.medical_specialty ,MAP Kinase Signaling System ,Physiology ,p38 mitogen-activated protein kinases ,Blotting, Western ,Myocardial Infarction ,Myocardial Reperfusion Injury ,p38 Mitogen-Activated Protein Kinases ,Physiology (medical) ,Internal medicine ,Intestine, Small ,medicine ,Animals ,Mitogen-Activated Protein Kinase 9 ,Mitogen-Activated Protein Kinase 8 ,cardiovascular diseases ,Phosphorylation ,Rats, Wistar ,Protein Kinase Inhibitors ,Mitogen-Activated Protein Kinase 1 ,Cardioprotection ,Mitogen-Activated Protein Kinase 3 ,biology ,Kinase ,business.industry ,Myocardium ,Hemodynamics ,Rats ,Blot ,Endocrinology ,Mitogen-activated protein kinase ,Ischemic Preconditioning, Myocardial ,biology.protein ,Ischemic preconditioning ,sense organs ,Mitogen-Activated Protein Kinases ,Cardiology and Cardiovascular Medicine ,business - Abstract
Aims Since mitogen-activated protein kinases (MAPKs) were found to be implicated in the signalling of ischaemic preconditioning (IPC), we tested the hypothesis of a contribution of these protein kinases to remote preconditioning (RPC). Methods and results To determine the role of p38, ERK1/2, and JNK1/2 MAPKs in mediating cardiac protection, an in vivo model of myocardial infarction was applied in male Wistar rats. RPC or IPC was induced by occlusion of the superior mesenteric artery or the left coronary artery, respectively. Infarct size (IS) was determined based on 2,3,5-triphenyltetrazolium chloride staining. Phosphorylation of the various MAPKs was analysed by immunoblotting in samples of the small intestine and myocardium obtained after IPC or RPC procedures. The MAPK inhibitors SB203580 (p38), PD98059 (ERK1/2), and SP600125 (JNK1/2) were administered to assess the potential significance of MAPK signalling in RPC. Both preconditioning stimuli decreased myocardial IS significantly after a lethal period of ischaemia. Each of the applied MAPK inhibitors was capable of abrogating the RPC-induced cardioprotection. Western blot analysis of myocardial samples revealed an increase in phosphorylated amounts of ERK1/2 and JNK1 after IPC, whereas phosphorylation of p38 protein was decreased significantly. Likewise, RPC resulted in a considerable increase in phosphorylation of ERK1/2 and JNK1/2 proteins in the small intestine, whereas it did not alter the MAPK phosphorylation state in the myocardium. Conclusion All investigated MAPK pathways appear to be involved in RPC-induced cardioprotection; however, they do not contribute to the alterations that define the preconditioned state of the myocardium prior to the infarction.
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- 2007
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13. Remote preconditioning protects the heart by activating myocardial PKCε-isoform
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Peter Dominiak, Sebastian Wolfrum, Marc Heidbreder, Kathrin Schneider, Julie Nienstedt, and Andreas Dendorfer
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Male ,Physiology ,Ganglionic Blockers ,Adrenergic beta-Antagonists ,Myocardial Infarction ,Ischemia ,Bradykinin ,Pharmacology ,Hexamethonium ,Random Allocation ,chemistry.chemical_compound ,Alkaloids ,Reperfusion therapy ,Physiology (medical) ,medicine ,Animals ,Enzyme Inhibitors ,Rats, Wistar ,Ischemic Preconditioning ,Protein Kinase C ,Benzophenanthridines ,Cardioprotection ,business.industry ,Myocardium ,medicine.disease ,Phenanthridines ,Rats ,Enzyme Activation ,Intestines ,Isoenzymes ,Chelerythrine ,chemistry ,Coronary occlusion ,Anesthesia ,Ischemic Preconditioning, Myocardial ,Ischemic preconditioning ,sense organs ,Cardiology and Cardiovascular Medicine ,business - Abstract
Myocardial protection can be achieved by brief ischemia-reperfusion of remote organs, a phenomenon described as remote preconditioning (RPC). Since the intracellular mechanisms of RPC are not known, we tested the hypothesis that RPC might activate myocardial PKCepsilon, an essential mediator of classical ischemic preconditioning. Furthermore, we tried to delineate the mechanisms by which RPC is transduced to the heart with respect to the possible contribution of kinins and neuronal reflexes.Anesthetized rats were randomised to undergo either 30 min of waiting (controls) or RPC (brief mesenteric artery occlusion followed by reperfusion) in the absence or presence of chelerythrine (5 mg kg(-1)), a specific PKC inhibitor. Myocardial infarct size was measured by TTC staining after 30 min of coronary artery occlusion followed by 150 min of reperfusion. In separate sets of experiments RPC was performed with or without pretreatment with HOE140, a selective B(2)-antagonist or hexamethonium was used to explore the influence of ganglion blockade on RPC. Translocation of PKCepsilon from cytosol to the particulate fraction was measured by quantitative immunoblotting.RPC significantly reduced infarct size which was completely blocked by the PKC inhibitor. RPC shifted the ratio between cytosolic and particulate PKCepsilon, an indicator for PKC-activation, from 0.95+/-0.06 in controls to 0.41+/-0.09 (P0.05), and this effect was abolished by HOE140. Activation of PKCepsilon could not be achieved after pretreatment with HEX (0.69+/-0.06 in HEX vs. 0.78+/-0.06 in HEX+RPC).RPC activates myocardial PKCepsilon through a neuronal and bradykinin-dependent pathway. We assume that activation of PKCepsilon is an important step in cardioprotection induced by remote preconditioning.
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- 2002
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14. Desmoglein-2 interaction is crucial for cardiomyocyte cohesion and function
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Petros Syrris, Andreas Dendorfer, Katja Gehmlich, Franziska Vielmuth, Jens Waschke, Volker Spindler, Angela Schlipp, Eva Hartlieb, Camilla Schinner, and William J. McKenna
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medicine.medical_specialty ,Physiology ,Plakoglobin ,Connexin ,Desmoglein-2 ,Biology ,Cell Line ,stomatognathic system ,Desmosome ,Physiology (medical) ,Internal medicine ,medicine ,Cell Adhesion ,Myocyte ,Animals ,Myocytes, Cardiac ,Cell adhesion ,Mice, Inbred BALB C ,Desmoglein 2 ,Dose-Response Relationship, Drug ,integumentary system ,Cadherin ,Tryptophan ,Gap Junctions ,Isolated Heart Preparation ,Cadherins ,Cell biology ,medicine.anatomical_structure ,Endocrinology ,Connexin 43 ,Mutation ,Calcium ,Receptors, Adrenergic, beta-1 ,Cardiology and Cardiovascular Medicine ,Intercalated disc ,Peptides ,Signal Transduction - Abstract
AIMS: We determined the contribution of the desmosomal cadherin desmoglein-2 to cell-cell cohesion in cardiomyocytes. In the intercalated disc, providing mechanical strength and electrical communication between adjacent cardiomyocytes, desmoglein-2 is closely associated with N-cadherin and gap junctions. METHODS AND RESULTS: We studied intercalated discs of HL-1 cardiomyocytes by immunostaining of desmoglein-2 and N-cadherin. Cohesion was measured using a liberase-based dissociation-assay and compared with cell-free single-molecule atomic force microscopy measurements. L-tryptophan caused irregular desmoglein-2 condensation, weakened cell-cell cohesion and impaired both homophilic desmoglein-2 and N-cadherin trans-interaction, whereas l-phenylalanine had no effect. L-tryptophan did not affect N-cadherin localization and its inhibitory effect on cell-cohesion and desmoglein-2 binding, but not on N-cadherin interaction, was blocked by a desmoglein-specific tandem peptide. Moreover, Ca(2+)-depletion, desmoglein-2 knockdown, a desmoglein-specific single peptide and certain desmoglein-2 mutations associated with arrhythmogenic cardiomyopathy reduced cell-cell cohesion, whereas cell adhesion was strengthened by desmoglein-2 overexpression. Since single peptide did not interfere with N-cadherin trans-interaction, these data indicate that (i) desmoglein-2 binding is crucial for cardiomyocyte cohesion and (ii) L-tryptophan reduced both desmoglein-2 and N-cadherin binding, whereas single and tandem peptide can be used to specifically target desmoglein-2-mediated adhesion. L-tryptophan and single peptide also induced ultrastructural alterations of areae compositae. Functional analyses at the organ level revealed reduced cardiomyocyte function and inefficient response to adrenergic stimulation in both L-tryptophan- and single peptide-challenged murine Langendorff hearts paralleled by redistribution of connexin 43 in L-tryptophan-treated heart slices. CONCLUSION: Our data demonstrate that desmoglein-2 plays a critical role in cardiomyocyte cohesion and function.
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- 2014
15. Organotypic slice culture from human adult ventricular myocardium
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Matthias Brandenburger, Michael Reppel, Jürgen Hescheler, Andreas Dendorfer, Filomain Nguemo, Jan Wenzel, Roman Bogdan, Heinrich Terlau, and Doreen Richardt
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Adult ,Myosin light-chain kinase ,Physiology ,Heart Ventricles ,Myocardium ,Cardiac myocyte ,Models, Cardiovascular ,Stimulation ,Anatomy ,Biology ,Myocardial Contraction ,Potassium channel ,Cell biology ,Electrophysiological Phenomena ,Contractility ,Cardiovascular Physiological Phenomena ,Preload ,Real-time polymerase chain reaction ,Organ Culture Techniques ,Tissue engineering ,Physiology (medical) ,Humans ,Cardiology and Cardiovascular Medicine - Abstract
Aims Cardiovascular research requires complex and functionally intact experimental models. Due to major differences in the cellular and subcellular composition of the myocardium between species, the use of human heart tissue is highly desirable. To enhance the experimental use of the human myocardium, we established methods for the preparation of vital tissue slices from the adult ventricular myocardium as well as conditions for their long-term preservation in organotypic culture. Methods and results Human ventricular heart samples were derived from surgical specimens excised during a therapeutic Morrow myectomy and cut into 300 μm thick slices. Slices were either characterized in acute experiments or cultured at a liquid–air interface. Viability and functionality were proven by viability staining, enzyme activity tests, intracellular potential recordings, and force measurements. Precision-cut slices showed high viability throughout 28 days in culture and displayed typical cardiomyocyte action potential characteristics, which enabled pharmacological safety testing on the rapid component of the delayed rectifier potassium current ( I Kr) and ATP-dependent potassium channels throughout the whole culture period. Constant expression of major ion channels was confirmed by quantitative PCR. Acute slices developed excitation-dependent contractions with a clear preload dependency and a β-adrenergic response. Contractility and myosin light chain expression decreased during the first days in culture but reached a steady state with reactivity upon β-adrenergic stimulation being preserved. Conclusion Organotypic heart slices represent a multicellular model of the human myocardium and a novel platform for studies ranging from the investigation of molecular interactions to tissue engineering.
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- 2011
16. Cardiovascular and renal function of angiotensin II type-2 receptors
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Andreas Dendorfer, Olaf Jöhren, and Peter Dominiak
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endocrine system ,medicine.medical_specialty ,Physiology ,Bradykinin ,Apoptosis ,Mice, Inbred Strains ,Biology ,Kidney ,Nitric Oxide ,Receptor, Angiotensin, Type 2 ,Nitric oxide ,chemistry.chemical_compound ,Mice ,Physiology (medical) ,Internal medicine ,Renin–angiotensin system ,medicine ,Animals ,Humans ,Receptor ,Cyclic GMP ,Aorta ,Mice, Knockout ,Angiotensin II receptor type 1 ,Angiotensin II ,Myocardium ,Rats ,Mice, Inbred C57BL ,Endocrinology ,medicine.anatomical_structure ,chemistry ,cardiovascular system ,Cardiology and Cardiovascular Medicine ,hormones, hormone substitutes, and hormone antagonists ,circulatory and respiratory physiology ,Signal Transduction - Abstract
While all of the well-known cardiovascular and renal effects of angiotensin II (ANG) are attributed to the ANG type-1 (AT(1)) receptor, much less is known about the function of ANG type-2 (AT(2)) receptors. This review focuses on progress made in AT(2) receptor research over the past 10 years mainly enabled by the availability of AT(2) receptor-deficient mice. Two general mechanisms regarding AT(2) receptor-mediated actions emerge from recent experiments. Firstly, AT(2) receptor stimulation inhibits growth and promotes apoptosis, an important mechanism during development and tissue remodeling. Secondly, ANG stimulates the release of nitric oxide (NO)/cGMP via AT(2) receptor activation, as described in the aorta, heart, and kidney. This effect appears to be indirectly mediated by the modulation of bradykinin release. Thus, activation of AT(2) receptors may be potentially protective and appears to oppose the effects mediated by AT(1) receptors. The question whether AT(2) receptors are activated in patients with elevated ANG levels when treated with AT(1) receptor antagonists and whether these effects are relevant awaits further clarification.
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- 2003
17. Organotypic slice culture from human adult ventricular myocardium
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Brandenburger, Matthias, primary, Wenzel, Jan, additional, Bogdan, Roman, additional, Richardt, Doreen, additional, Nguemo, Filomain, additional, Reppel, Michael, additional, Hescheler, Jürgen, additional, Terlau, Heinrich, additional, and Dendorfer, Andreas, additional
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- 2011
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18. Saturday, 17 July 2010
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Dimova, I., primary, Hlushchuk, R., additional, Makanya, A., additional, Djonov, V., additional, Theurl, M., additional, Schgoer, W., additional, Albrecht, K., additional, Beer, A., additional, Patsch, J. R., additional, Schratzberger, P., additional, Mahata, S., additional, Kirchmair, R., additional, Didie, M., additional, Christalla, P., additional, Rau, T., additional, Eschenhagen, T., additional, Schumacher, U., additional, Lin, Q., additional, Zenke, M., additional, Zimmmermann, W., additional, Hoch, M., additional, Fischer, P., additional, Stapel, B., additional, Missol-Kolka, E., additional, Erschow, S., additional, Scherr, M., additional, Drexler, H., additional, Hilfiker-Kleiner, D., additional, Diebold, I., additional, Petry, A., additional, Kennel, P., additional, Djordjevic, T., additional, Hess, J., additional, Goerlach, A., additional, Castellano, J., additional, Aledo, R., additional, Sendra, J., additional, Costales, P., additional, Badimon, L., additional, Llorente-Cortes, V., additional, Dworatzek, E., additional, Mahmoodzadeh, S., additional, Regitz-Zagrosek, V., additional, Posa, A., additional, Varga, C., additional, Berko, A., additional, Veszelka, M., additional, Szablics, P., additional, Vari, B., additional, Pavo, I., additional, Laszlo, F., additional, Brandenburger, M., additional, Wenzel, J., additional, Bogdan, R., additional, Richardt, D., additional, Reppel, M., additional, Hescheler, J., additional, Terlau, H., additional, Dendorfer, A., additional, Heijman, J., additional, Rudy, Y., additional, Westra, R., additional, Volders, P., additional, Rasmusson, R., additional, Bondarenko, V., additional, Ertas Gokhan, M. D., additional, Ural Ertan, M. D., additional, Karaoz Erdal, P. H. D., additional, Aksoy Ayca, P. H. D., additional, Kilic Teoman, M. D., additional, Kozdag Guliz, M. D., additional, Vural Ahmet, M. D., additional, Ural Dilek, M. D., additional, Poulet, C., additional, Christ, T., additional, Wettwer, E., additional, Ravens, U., additional, Van Der Pouw Kraan, C., additional, Schirmer, S., additional, Fledderus, J., additional, Moerland, P., additional, Leyen, T., additional, Piek, J., additional, Van Royen, N., additional, Horrevoets, A., additional, Fleissner, F., additional, Jazbutyte, V., additional, Fiedler, J., additional, Galuppo, P., additional, Mayr, M., additional, Ertl, G., additional, Bauersachs, J., additional, Thum, T., additional, Protze, S., additional, Bussek, A., additional, Li, F., additional, Hoo, R., additional, Lam, K., additional, Xu, A., additional, Subramanian, P., additional, Karshovska, E., additional, Megens, R., additional, Akhtar, S., additional, Heyll, K., additional, Jansen, Y., additional, Weber, C., additional, Schober, A., additional, Zafeiriou, M., additional, Noack, C., additional, Renger, A., additional, Dietz, R., additional, Zelarayan, L., additional, Bergmann, M., additional, Meln, I., additional, Malashicheva, A., additional, Anisimov, S., additional, Kalinina, N., additional, Sysoeva, V., additional, Zaritskey, A., additional, Barbuti, A., additional, Scavone, A., additional, Mazzocchi, N., additional, Crespi, A., additional, Capilupo, D., additional, Difrancesco, D., additional, Qian, L., additional, Shim, W., additional, Gu, Y., additional, Mohammed, S., additional, Wong, P., additional, Zafiriou, M., additional, Schaeffer, H., additional, Kovacs, P., additional, Simon, J., additional, Varro, A., additional, Athias, P., additional, Wolf, J., additional, Bouchot, O., additional, Vandroux, D., additional, Mathe, A., additional, De Carvalho, A., additional, Laurent, G., additional, Rainer, P., additional, Huber, M., additional, Edelmann, F., additional, Stojakovic, T., additional, Trantina-Yates, A., additional, Trauner, M., additional, Pieske, B., additional, Von Lewinski, D., additional, De Jong, A., additional, Maass, A., additional, Oberdorf-Maass, S., additional, Van Gelder, I., additional, Lin, Y., additional, Li, J., additional, Wang, F., additional, He, Y., additional, Li, X., additional, Xu, H., additional, Yang, X., additional, Coppini, R., additional, Ferrantini, C., additional, Ferrara, C., additional, Rossi, A., additional, Mugelli, A., additional, Poggesi, C., additional, Cerbai, E., additional, Rozmaritsa, N., additional, Voigt, N., additional, Dobrev, D., additional, Kienitz, M.-C., additional, Zoidl, G., additional, Bender, K., additional, Pott, L., additional, Kohajda, Z., additional, Kristof, A., additional, Virag, L., additional, Jost, N., additional, Trafford, A., additional, Prnjavorac, B., additional, Mujaric, E., additional, Jukic, J., additional, Abduzaimovic, K., additional, Brack, K., additional, Patel, V., additional, Coote, J., additional, Ng, G., additional, Wilders, R., additional, Van Ginneken, A., additional, Verkerk, A., additional, Xaplanteris, P., additional, Vlachopoulos, C., additional, Baou, K., additional, Vassiliadou, C., additional, Dima, I., additional, Ioakeimidis, N., additional, Stefanadis, C., additional, Ruifrok, W., additional, Qian, C., additional, Sillje, H., additional, Van Goor, H., additional, Van Veldhuisen, D., additional, Van Gilst, W., additional, De Boer, R., additional, Schmidt, K., additional, Kaiser, F., additional, Erdmann, J., additional, De Wit, C., additional, Barnett, O., additional, Kyyak, Y., additional, Cesana, F., additional, Boffi, L., additional, Mauri, T., additional, Alloni, M., additional, Betelli, M., additional, Nava, S., additional, Giannattasio, C., additional, Mancia, G., additional, Vilskersts, R., additional, Kuka, J., additional, Svalbe, B., additional, Liepinsh, E., additional, Dambrova, M., additional, Zakrzewicz, A., additional, Maroski, J., additional, Vorderwuelbecke, B., additional, Fiedorowicz, K., additional, Da Silva-Azevedo, L., additional, Pries, A., additional, Gryglewska, B., additional, Necki, M., additional, Zelawski, M., additional, Grodzicki, T., additional, Scoditti, E., additional, Massaro, M., additional, Carluccio, M., additional, Distante, A., additional, Storelli, C., additional, De Caterina, R., additional, Kocgirli, O., additional, Valcaccia, S., additional, Dao, V., additional, Suvorava, T., additional, Kumpf, S., additional, Floeren, M., additional, Oppermann, M., additional, Kojda, G., additional, Leo, C., additional, Ziogas, J., additional, Favaloro, J., additional, Woodman, O., additional, Goettsch, W., additional, Marton, A., additional, Goettsch, C., additional, Morawietz, H., additional, Khalifa, E., additional, Ashour, Z., additional, Rupprecht, V., additional, Scalera, F., additional, Martens-Lobenhoffer, J., additional, Bode-Boeger, S., additional, Li, W., additional, Kwan, Y., additional, Leung, G., additional, Patella, F., additional, Mercatanti, A., additional, Pitto, L., additional, Rainaldi, G., additional, Tsimafeyeu, I., additional, Tishova, Y., additional, Wynn, N., additional, Kalinchenko, S., additional, Clemente Lorenzo, M., additional, Grande, M., additional, Barriocanal, F., additional, Aparicio, M., additional, Martin, A., additional, Hernandez, J., additional, Lopez Novoa, J., additional, Martin Luengo, C., additional, Kurlianskaya, A., additional, Denisevich, T., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Wang, Y., additional, Gabrielsen, A., additional, Ripa, R., additional, Jorgensen, E., additional, Kastrup, J., additional, Arderiu, G., additional, Pena, E., additional, Kobus, K., additional, Czyszek, J., additional, Kozlowska-Wiechowska, A., additional, Milkiewicz, P., additional, Milkiewicz, M., additional, Madonna, R., additional, Montebello, E., additional, Geng, Y., additional, Chin-Dusting, J., additional, Michell, D., additional, Skilton, M., additional, Dixon, J., additional, Dart, A., additional, Moore, X., additional, Ehrbar, M., additional, Reichmuth, P., additional, Heinimann, N., additional, Hewing, B., additional, Stangl, V., additional, Stangl, K., additional, Laule, M., additional, Baumann, G., additional, Ludwig, A., additional, Widmer-Teske, R., additional, Mueller, A., additional, Stieger, P., additional, Tillmanns, H., additional, Braun-Dullaeus, R., additional, Sedding, D., additional, Troidl, K., additional, Eller, L., additional, Benli, I., additional, Apfelbeck, H., additional, Schierling, W., additional, Troidl, C., additional, Schaper, W., additional, Schmitz-Rixen, T., additional, Hinkel, R., additional, Trenkwalder, T., additional, Pfosser, A., additional, Globisch, F., additional, Stachel, G., additional, Lebherz, C., additional, Bock-Marquette, I., additional, Kupatt, C., additional, Seyler, C., additional, Duthil-Straub, E., additional, Zitron, E., additional, Scholz, E., additional, Thomas, D., additional, Gierten, J., additional, Karle, C., additional, Fink, R., additional, Padro, T., additional, Lugano, R., additional, Garcia-Arguinzonis, M., additional, Schuchardt, M., additional, Pruefer, J., additional, Toelle, M., additional, Pruefer, N., additional, Jankowski, V., additional, Jankowski, J., additional, Zidek, W., additional, Van Der Giet, M., additional, Fransen, P., additional, Van Hove, C., additional, Michiels, C., additional, Van Langen, J., additional, Bult, H., additional, Quarck, R., additional, Wynants, M., additional, Alfaro-Moreno, E., additional, Rosario Sepulveda, M., additional, Wuytack, F., additional, Van Raemdonck, D., additional, Meyns, B., additional, Delcroix, M., additional, Christofi, F., additional, Wijetunge, S., additional, Sever, P., additional, Hughes, A., additional, Ohanian, J., additional, Forman, S., additional, Ohanian, V., additional, Gibbons, C., additional, Vernia, S., additional, Das, A., additional, Shah, V., additional, Casado, M., additional, Bielenberg, W., additional, Daniel, J., additional, Daniel, J.-M., additional, Hersemeyer, K., 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Schuchardt, M., primary, Toelle, M., additional, Huang, T., additional, Wiedon, A., additional, Van Der Giet, M., additional, Mill, C., additional, George, S., additional, Jeremy, J., additional, Santulli, G., additional, Illario, M., additional, Cipolletta, E., additional, Sorriento, D., additional, Del Giudice, C., additional, Anastasio, A., additional, Trimarco, B., additional, Iaccarino, G., additional, Jobs, A., additional, Wagner, C., additional, Kurtz, A., additional, De Wit, C., additional, Koller, A., additional, Suvorava, T., additional, Weber, M., additional, Dao, V., additional, Kojda, G., additional, Tsaousi, A., additional, Lyon, C., additional, Williams, H., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Keul, P., additional, Lucke, S., additional, Graeler, M., additional, Heusch, G., additional, Levkau, B., additional, Biessen, E., additional, De Jager, S., additional, Bermudez-Pulgarin, B., additional, Bot, I., additional, Abia, R., additional, Van Berkel, T., additional, Renger, A., additional, Noack, C., additional, Zafiriou, M., additional, Dietz, R., additional, Bergmann, M., additional, Zelarayan, L., additional, Hammond, J., additional, Hamelet, J., additional, Van Assche, T., additional, Belge, C., additional, Vanderper, A., additional, Langin, D., additional, Herijgers, P., additional, Balligand, J., additional, Perrot, A., additional, Neubert, M., additional, Posch, M., additional, Oezcelik, C., additional, Waldmuller, S., additional, Berger, F., additional, Scheffold, T., additional, Bouvagnet, P., additional, Ozcelik, C., additional, Lebreiro, A., additional, Martins, E., additional, Lourenco, P., additional, Cruz, C., additional, Martins, M., additional, Bettencourt, P., additional, Maciel, M., additional, Abreu-Lima, C., additional, Pilichou, K., additional, Bauce, B., additional, Rampazzo, A., additional, Carturan, E., additional, Corrado, D., additional, Thiene, G., additional, Basso, C., 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- Published
- 2010
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20. Remote vs. ischaemic preconditioning: the differential role of mitogen-activated protein kinase pathways
- Author
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Heidbreder, M., primary, Naumann, A., additional, Tempel, K., additional, Dominiak, P., additional, and Dendorfer, A., additional
- Published
- 2007
- Full Text
- View/download PDF
21. Cardiovascular and renal function of angiotensin II type-2 receptors
- Author
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Jöhren, Olaf, Dendorfer, Andreas, and Dominiak, Peter
- Subjects
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BLOOD circulation , *ANGIOTENSINS , *APOPTOSIS , *CELL death - Abstract
While all of the well-known cardiovascular and renal effects of angiotensin II (ANG) are attributed to the ANG type-1 (AT1) receptor, much less is known about the function of ANG type-2 (AT2) receptors. This review focuses on progress made in AT2 receptor research over the past 10 years mainly enabled by the availability of AT2 receptor-deficient mice. Two general mechanisms regarding AT2 receptor-mediated actions emerge from recent experiments. Firstly, AT2 receptor stimulation inhibits growth and promotes apoptosis, an important mechanism during development and tissue remodeling. Secondly, ANG stimulates the release of nitric oxide (NO)/cGMP via AT2 receptor activation, as described in the aorta, heart, and kidney. This effect appears to be indirectly mediated by the modulation of bradykinin release. Thus, activation of AT2 receptors may be potentially protective and appears to oppose the effects mediated by AT1 receptors. The question whether AT2 receptors are activated in patients with elevated ANG levels when treated with AT1 receptor antagonists and whether these effects are relevant awaits further clarification. [Copyright &y& Elsevier]
- Published
- 2004
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22. Remote preconditioning protects the heart by activating myocardial PKC∊-isoform
- Author
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Wolfrum, Sebastian, Schneider, Kathrin, Heidbreder, Marc, Nienstedt, Julie, Dominiak, Peter, and Dendorfer, Andreas
- Subjects
ISCHEMIA ,NEUROTRANSMITTERS ,PROTEIN kinases - Abstract
Objective: Myocardial protection can be achieved by brief ischemia-reperfusion of remote organs, a phenomenon described as remote preconditioning (RPC). Since the intracellular mechanisms of RPC are not known, we tested the hypothesis that RPC might activate myocardial PKC∊, an essential mediator of classical ischemic preconditioning. Furthermore, we tried to delineate the mechanisms by which RPC is transduced to the heart with respect to the possible contribution of kinins and neuronal reflexes. Methods: Anesthetized rats were randomised to undergo either 30 min of waiting (controls) or RPC (brief mesenteric artery occlusion followed by reperfusion) in the absence or presence of chelerythrine (5 mg kg
−1 ), a specific PKC inhibitor. Myocardial infarct size was measured by TTC staining after 30 min of coronary artery occlusion followed by 150 min of reperfusion. In separate sets of experiments RPC was performed with or without pretreatment with HOE140, a selective B2 -antagonist or hexamethonium was used to explore the influence of ganglion blockade on RPC. Translocation of PKC∊ from cytosol to the particulate fraction was measured by quantitative immunoblotting. Results: RPC significantly reduced infarct size which was completely blocked by the PKC inhibitor. RPC shifted the ratio between cytosolic and particulate PKC∊, an indicator for PKC-activation, from 0.95±0.06 in controls to 0.41±0.09 (P<0.05), and this effect was abolished by HOE140. Activation of PKC∊ could not be achieved after pretreatment with HEX (0.69±0.06 in HEX vs. 0.78±0.06 in HEX+RPC). Conclusions: RPC activates myocardial PKC∊ through a neuronal and bradykinin-dependent pathway. We assume that activation of PKC∊ is an important step in cardioprotection induced by remote preconditioning. [Copyright &y& Elsevier]- Published
- 2002
- Full Text
- View/download PDF
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