Abstract
Chemokines and their receptors induce the qualitative and quantitative changes of the pool of bone marrow-derived and resident cardiac stem/progenitor cells, which in turn can modulate myocardial recovery after myocardial infarction (MI). Primary role of the chemokines, such as stromal cell-derived factor-1 (SDF-1), stem cell factor (SCF), hepatocyte growth factor (HGF) and leukaemia inhibitory factor (LIF) is the mobilization and homing of the bone marrow-derived stem/progenitor cells to the infarcted myocardium. In the setting of the acute MI there is an increased expression of SDF-1, HGF, LIF in the peri-infarct zone. The most important chemokine–chemokine receptor axis is SDF-1/CXCR4 which is significantly upregulated during acute MI. It corresponds with the significant mobilization of cells expressing cardiac and endothelial markers, which also express the chemokine receptors CXCR4, c-met, CD117 and leukemia inhibitory factor receptor. Specific population of small non-haematopoietic cells expressing the CXCR4 receptor was identified, which have the capability of cardiogenic differentiation. The mobilization of stem/progenitor cells expressing the receptors for chemoattractant cytokines is significantly correlated with the improvement of left ventricular ejection fraction (LVEF) and remodelling in 1-year follow-up after the acute MI. Patients with reduced LVEF after MI have also impaired mobilization of the stem/progenitor cells. The number of circulating cells is inversely correlated with the infarct area and positively with myocardial perfusion. Also the migratory response of the endothelial progenitor cells (EPCs) to the SDF-1 gradient is positively correlated with their capability to improve the perfusion and is one of the factors that seem to determine the outcome of the progenitor cell-based therapy after acute MI.
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