Key result
Anti-SDF-1α treatment combined with EPC transplantation significantly decreased left ventricular function and diminished attracted bone marrow cells compared to untreated groups in a murine MI model.
Why the study?
Does anti-SDF-1α treatment affect left ventricular function and stem cell mobilization in mice undergoing EPC transplantation after myocardial infarction?
Does anti-SDF-1α treatment affect left ventricular function and stem cell mobilization in mice undergoing EPC transplantation after myocardial infarction?
SDF-1α plays a crucial role in mobilizing endogenous bone marrow cells to infarcted myocardium, and its blockade worsens left ventricular function recovery after EPC transplantation.
Answers are grounded in this paper and cite their sources.
Anti-SDF-1α impairs LV recovery with EPCs in murine MI; hypothesis-generating for SDF-1α blockade in stem cell therapy.
Aim of the presented study was to investigate the role of stromal derived factor 1 (SDF-1α) in mobilizing stem cells in combination with endothelial progenitor cell (EPC) transplantation in a regenerative strategy for myocardial infarction therapy in a murine ischemia/reperfusion model. Initially bone marrow was eradicated and reconstituted with the use of green fluorescent protein (GFP) labelled allogenic cells. After reconstitution, myocardial ischemia was induced by temporary ligation of the left anterior descending coronary artery (LAD) in C57/B16 mice and maintained for 1h. After reperfusion, EPCs (1 x 10(6) cells) or medium were injected directly into the border zones of the infarcted areas. In addition, the animals were divided in groups treated or not with specific antibodies against SDF-1α. 4 weeks after transplantation, echocardiography revealed a significantly decreased left ventricular function after application of EPCs in anti-SDF-1α treated animals compared to untreated groups. Histology revealed that EPC transplantation and anti-SDF-1α treatment diminished the amount of intramyocardially attracted GFP positive bone marrow cells. Interestingly, no significant changes in the density of CD31+ vessel structures compared to EPC transplantation alone were detectable in anti-SDF-1α treated groups. Anti-SDF-1α treatment also increased numbers of inflammatory cells (monocytes and neutrophiles) in infarcted areas. Rate of apoptotic cells and proliferation after transplantation did not differ. In conclusion, transplanted endothelial progenitor cells as well as SDF-1α are key factors in mobilization of endogenous bone marrow cells towards infarcted myocardium. Anti-SDF-1α treatment leads to a significant decreased left ventricular function, alters the inflammatory processes, but does not lead to significant alterations in neovascularization or collagen content of infarcted areas.
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Schuh et al. (2014) studied Myocardial infarction (murine model). Endothelial progenitor cell (EPC) transplantation and anti-SDF-1α treatment vs. Untreated groups / EPC transplantation alone was evaluated on Left ventricular function and mobilization of endogenous bone marrow cells. Anti-SDF-1α treatment combined with EPC transplantation significantly decreased left ventricular function and diminished attracted bone marrow cells compared to untreated groups in a murine MI model.
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