1. G-CSF/SCF reduces inducible arrhythmias in the infarcted heart potentially via increased connexin43 expression and arteriogenesis
- Author
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Wen Tian, Larissa Fabritz, Joachim Kienast, Rainer Klocke, Jörg Stypmann, Sigrid Nikol, Paulus Kirchhof, Melanie Zwiener, Günter Breithardt, Matthias Stelljes, Marcus Mueller, Lekbira Hasib, and Michael Kuhlmann
- Subjects
Male ,Cardiac function curve ,medicine.medical_specialty ,medicine.medical_treatment ,Immunology ,Myocardial Infarction ,Neovascularization, Physiologic ,Infarction ,Mice, Transgenic ,Stem cell factor ,Article ,Mice ,Ventricular Dysfunction, Left ,Internal medicine ,Granulocyte Colony-Stimulating Factor ,Animals ,Immunology and Allergy ,Medicine ,Myocytes, Cardiac ,cardiovascular diseases ,Myocardial infarction ,Cardiac Output ,Bone Marrow Transplantation ,Stem Cell Factor ,business.industry ,Myocardium ,Arrhythmias, Cardiac ,Heart ,Articles ,medicine.disease ,Granulocyte colony-stimulating factor ,Mice, Inbred C57BL ,Disease Models, Animal ,Cytokine ,Connexin 43 ,Receptors, Granulocyte Colony-Stimulating Factor ,cardiovascular system ,Cardiology ,Female ,Arteriogenesis ,business ,Homing (hematopoietic) - Abstract
Granulocyte colony-stimulating factor (G-CSF), alone or in combination with stem cell factor (SCF), can improve hemodynamic cardiac function after myocardial infarction. Apart from impairing the pump function, myocardial infarction causes an enhanced vulnerability to ventricular arrhythmias. Therefore, we investigated the electrophysiological effects of G-CSF/SCF and the underlying cellular events in a murine infarction model. G-CSF/SCF improved cardiac output after myocardial infarction. Although G-CSF/SCF led to a twofold increased, potentially proarrhythmic homing of bone marrow (BM)-derived cells to the area of infarction
- Published
- 2006
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