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Your search keyword '"Theilmeier, Gregor"' showing total 9 results
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9 results on '"Theilmeier, Gregor"'

1. Continuous Glycoprotein-130–Mediated Signal Transducer and Activator of Transcription-3 Activation Promotes Inflammation, Left Ventricular Rupture, and Adverse Outcome in Subacute Myocardial Infarction

Author

Hilfiker-Kleiner, Denise, primary, Shukla, Praphulla, additional, Klein, Gunnar, additional, Schaefer, Arnd, additional, Stapel, Britta, additional, Hoch, Melanie, additional, Müller, Werner, additional, Scherr, Michaela, additional, Theilmeier, Gregor, additional, Ernst, Matthias, additional, Hilfiker, Andres, additional, and Drexler, Helmut, additional

Published
2010
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4. Response to Letter Regarding Article, “High-Density Lipoproteins and Their Constituent, Sphingosine-1-Phosphate, Directly Protect the Heart Against Ischemia/Reperfusion Injury In Vivo via the S1P 3 Lysophospholipid Receptor”

Author

Theilmeier, Gregor, primary, Schmidt, Christoph, additional, Herrmann, Jörg, additional, Keul, Petra, additional, Schäfers, Michael, additional, Herrgott, Ilka, additional, Mersmann, Jan, additional, Larmann, Jan, additional, Hermann, Sven, additional, Stypmann, Jörg, additional, Schober, Otmar, additional, Hildebrand, Reinhard, additional, Schulz, Reiner, additional, Heusch, Gerd, additional, Haude, Michael, additional, von Wnuck Lipinski, Karin, additional, Herzog, Christine, additional, Schmitz, Martina, additional, Erbel, Raimund, additional, Chun, Jerold, additional, and Levkau, Bodo, additional

Published
2007
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5. High-Density Lipoproteins and Their Constituent, Sphingosine-1-Phosphate, Directly Protect the Heart Against Ischemia/Reperfusion Injury In Vivo via the S1P 3 Lysophospholipid Receptor

Author

Theilmeier, Gregor, primary, Schmidt, Christoph, additional, Herrmann, Jörg, additional, Keul, Petra, additional, Schäfers, Michael, additional, Herrgott, Ilka, additional, Mersmann, Jan, additional, Larmann, Jan, additional, Hermann, Sven, additional, Stypmann, Jörg, additional, Schober, Otmar, additional, Hildebrand, Reinhard, additional, Schulz, Rainer, additional, Heusch, Gerd, additional, Haude, Michael, additional, Lipinski, Karin von Wnuck, additional, Herzog, Christine, additional, Schmitz, Martina, additional, Erbel, Raimund, additional, Chun, Jerold, additional, and Levkau, Bodo, additional

Published
2006
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7. Hypercholesterolemia in Minipigs Impairs Left Ventricular Response to Stress

Author

Theilmeier, Gregor, primary, Verhamme, Peter, additional, Dymarkowski, Steven, additional, Beck, Heike, additional, Bernar, Hilde, additional, Lox, Marleen, additional, Janssens, Stefan, additional, Herregods, Marie-Christine, additional, Verbeken, Erik, additional, Collen, Désiré, additional, Plate, Karl, additional, Flameng, Willem, additional, and Holvoet, Paul, additional

Published
2002
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8. Adenovirus-Mediated Gene Transfer of Human Platelet-Activating Factor–Acetylhydrolase Prevents Injury-Induced Neointima Formation and Reduces Spontaneous Atherosclerosis in Apolipoprotein E–Deficient Mice

Author

Quarck, Rozenn, primary, De Geest, Bart, additional, Stengel, Dominique, additional, Mertens, Ann, additional, Lox, Marleen, additional, Theilmeier, Gregor, additional, Michiels, Carine, additional, Raes, Martine, additional, Bult, Hidde, additional, Collen, Désiré, additional, Van Veldhoven, Paul, additional, Ninio, Ewa, additional, and Holvoet, Paul, additional

Published
2001
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9. High-density lipoproteins and their constituent, sphingosine-1-phosphate, directly protect the heart against ischemia/reperfusion injury in vivo via the S1P3 lysophospholipid receptor.

Author

Theilmeier G, Schmidt C, Herrmann J, Keul P, Schäfers M, Herrgott I, Mersmann J, Larmann J, Hermann S, Stypmann J, Schober O, Hildebrand R, Schulz R, Heusch G, Haude M, von Wnuck Lipinski K, Herzog C, Schmitz M, Erbel R, Chun J, and Levkau B

Subjects
Animals, Apoptosis drug effects, Cardiotonic Agents pharmacology, Cell Adhesion drug effects, Cells, Cultured drug effects, Chemotaxis, Leukocyte drug effects, Endothelial Cells drug effects, Endothelial Cells physiology, Female, Humans, Lipoproteins, HDL pharmacology, Lipoproteins, HDL physiology, Lipoproteins, LDL pharmacology, Lysophospholipids pharmacology, Lysophospholipids physiology, Macrophages physiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Myocytes, Cardiac drug effects, Myocytes, Cardiac pathology, NG-Nitroarginine Methyl Ester pharmacology, Nitric Oxide Synthase antagonists & inhibitors, Receptors, Lysosphingolipid deficiency, Receptors, Lysosphingolipid drug effects, Receptors, Lysosphingolipid genetics, Sphingosine pharmacology, Sphingosine physiology, Sphingosine therapeutic use, Sphingosine-1-Phosphate Receptors, Tumor Necrosis Factor-alpha pharmacology, Cardiotonic Agents therapeutic use, Lipoproteins, HDL therapeutic use, Lysophospholipids therapeutic use, Myocardial Ischemia drug therapy, Myocardial Reperfusion Injury prevention & control, Nitric Oxide physiology, Receptors, Lysosphingolipid physiology, Sphingosine analogs & derivatives
Abstract

Background: All treatments of acute myocardial infarction are aimed at rapid revascularization of the occluded vessel; however, no clinical strategies are currently available to protect the heart from ischemia/reperfusion injury after restitution of blood flow. We hypothesized that some of the cholesterol transport-independent biological properties of high-density lipoprotein (HDL) implied in atheroprotection may also be beneficial in settings of acute myocardial reperfusion injury., Methods and Results: In an in vivo mouse model of myocardial ischemia/reperfusion, we observed that HDL and its sphingolipid component, sphingosine-1-phosphate (S1P), dramatically attenuated infarction size by approximately 20% and 40%, respectively. The underlying mechanism was an inhibition of inflammatory neutrophil recruitment and cardiomyocyte apoptosis in the infarcted area. In vitro, HDL and S1P potently suppressed leukocyte adhesion to activated endothelium under flow and protected rat neonatal cardiomyocytes against apoptosis. In vivo, HDL- and S1P-mediated cardioprotection was dependent on nitric oxide (NO) and the S1P3 lysophospholipid receptor, because it was abolished by pharmacological NO synthase inhibition and was completely absent in S1P3-deficient mice., Conclusions: Our data demonstrate that HDL and its constituent, S1P, acutely protect the heart against ischemia/reperfusion injury in vivo via an S1P3-mediated and NO-dependent pathway. A rapid therapeutic elevation of S1P-containing HDL plasma levels may be beneficial in patients at high risk of acute myocardial ischemia.

Published
2006
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