Effect of granulocyte colony-stimulating factor on endothelial progenitor cell for coronary artery lesion in Kawasaki disease mice model / 中华儿科杂志

ABSTRACT

<p><b>OBJECTIVE</b>Number and function of endothelial progenitor cell (EPC) and coronary artery lesion in Kawasaki disease (KD) model were evaluated to investigate therapeutic efficacy of granulocyte colony-stimulating factor (G-CSF).</p><p><b>METHOD</b>C57BL/6 mice were injected with L. casei cell wall extract (LCWE); 48 mice were divided into 3 groups randomly KD model group; G-CSF treated model group and control group, 16 in each. G-CSF was subcutaneously injected from day 5 to day 9 after injection of LCWE. Coronary artery lesion, number of circulating EPC and the function of bone marrow EPC were evaluated.</p><p><b>RESULT</b>In model group, inflammatory infiltration was found around coronary artery at 14 days. The number of circulating EPC was significantly decreased in model group (0.017% ± 0.008%) compared to control (0.028% ± 0.007%) (t = 2.037, P < 0.05). Disruption of elastin was consistently observed at 56 days. Stimulated by G-CSF, inflammatory infiltration was found around the coronary artery at day 14, while the number of circulating EPC (0.042% ± 0.015%) was increased significantly compared to models (t = 4.629, P < 0.05). At the day 56, the number of circulating EPC was decreased slightly (0.029% ± 0.012%), but still higher than the model group (t = 2.789, P < 0.05), and have no significant difference compared to controls (P > 0.05). Furthermore, there was no elastin disruption in the G-CSF group. In model group, bone marrow EPC's proliferation ability of absorbance (A value) was 0.38 ± 0.09 in thiazolyl blue assay, less than controls (0.61 ± 0.14, P < 0.01). Adhesion and migration function were down-regulated compared to controls [(3.1 ± 0.6) cells/HPF and (3.3 ± 0.6) cells/HPF vs. (6.4 ± 1.2) cells/HPF and (6.2 ± 0.5) cells/HPF, both P < 0.01]. In the G-CSF treated group, proliferation ability (A 0.58 ± 0.10), adhesion [(6.17 ± 1.13) cells/HPF], migration [(6.29 ± 0.42) cells/HPF] function were increased significantly compared to the model group (P < 0.01).</p><p><b>CONCLUSION</b>G-CSF can up-regulate EPC number and function to prevent coronary artery lesion in mice model of KD.</p>