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• W2000619105 abstract "ObjectiveBesides its classical function in the field of autologous and allogenic stem cell transplantation, granulocyte colony-stimulating factor (G-CSF) was shown to have protective effects after myocardial infarction (MI) by mobilization of bone marrow—derived progenitor cells (BMCs) and in addition by activation of multiple signaling pathways. In the present study, we focused on the impact of G-CSF on migration of BMCs and the impact on resident cardiac cells after MI.Materials and MethodsMice (C57BL/6J) were sublethally irradiated, and BM from green fluorescent protein (GFP)—transgenic mice was transplanted. Coronary artery ligation was performed 10 weeks later. G-CSF (100 μg/kg) was daily injected for 6 days. Subpopulations of enhanced GFP+ cells in peripheral blood, bone marrow, and heart were characterized by flow cytometry. Growth factor expression in the heart was analyzed by quantitative real-time polymerase chain reaction. Perfusion was investigated in vivo by gated single photon emission computed tomography (SPECT).ResultsG-CSF—treated animals revealed a reduced migration of c-kit+ and CXCR-4+ BMCs associated with decreased expression levels of the corresponding growth factors, namely stem cell factor and stromal-derived factor-1α in ischemic myocardium. In contrast, the number of resident cardiac Sca-1+ cells was significantly increased. However, SPECT-perfusion showed no differences in infarct size between G-CSF—treated and control animals 6 days after MI.ConclusionOur study shows that G-CSF treatment after MI reduces migration capacity of BMCs into ischemic tissue, but increases the number of resident cardiac cells. To optimize homing capacity a combination of G-CSF with other agents may optimize cytokine therapy after MI. Besides its classical function in the field of autologous and allogenic stem cell transplantation, granulocyte colony-stimulating factor (G-CSF) was shown to have protective effects after myocardial infarction (MI) by mobilization of bone marrow—derived progenitor cells (BMCs) and in addition by activation of multiple signaling pathways. In the present study, we focused on the impact of G-CSF on migration of BMCs and the impact on resident cardiac cells after MI. Mice (C57BL/6J) were sublethally irradiated, and BM from green fluorescent protein (GFP)—transgenic mice was transplanted. Coronary artery ligation was performed 10 weeks later. G-CSF (100 μg/kg) was daily injected for 6 days. Subpopulations of enhanced GFP+ cells in peripheral blood, bone marrow, and heart were characterized by flow cytometry. Growth factor expression in the heart was analyzed by quantitative real-time polymerase chain reaction. Perfusion was investigated in vivo by gated single photon emission computed tomography (SPECT). G-CSF—treated animals revealed a reduced migration of c-kit+ and CXCR-4+ BMCs associated with decreased expression levels of the corresponding growth factors, namely stem cell factor and stromal-derived factor-1α in ischemic myocardium. In contrast, the number of resident cardiac Sca-1+ cells was significantly increased. However, SPECT-perfusion showed no differences in infarct size between G-CSF—treated and control animals 6 days after MI. Our study shows that G-CSF treatment after MI reduces migration capacity of BMCs into ischemic tissue, but increases the number of resident cardiac cells. To optimize homing capacity a combination of G-CSF with other agents may optimize cytokine therapy after MI." @default.
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• W2000619105 date "2008-06-01" @default.
• W2000619105 modified "2023-10-04" @default.
• W2000619105 title "G-CSF treatment after myocardial infarction: Impact on bone marrow—derived vs cardiac progenitor cells" @default.
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• W2000619105 doi "https://doi.org/10.1016/j.exphem.2008.01.011" @default.
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