Effect of granulocyte colony-stimulating factor on endothelial progenitor cell for coronary artery lesion in Kawasaki disease mice model.
- Author:
Zhi CHEN
1
;
Jun-feng LIU
;
Zhong-dong DU
;
Sui-gui WAN
;
Yun-qian GUAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Coronary Vessels; drug effects; pathology; Disease Models, Animal; Endothelial Cells; cytology; drug effects; Flow Cytometry; Granulocyte Colony-Stimulating Factor; administration & dosage; therapeutic use; Male; Mice; Mice, Inbred C57BL; Mucocutaneous Lymph Node Syndrome; blood; drug therapy; pathology; Random Allocation; Stem Cells; cytology; drug effects; Up-Regulation
- From: Chinese Journal of Pediatrics 2012;50(10):788-792
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVENumber 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).
METHODC57BL/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.
RESULTIn 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).
CONCLUSIONG-CSF can up-regulate EPC number and function to prevent coronary artery lesion in mice model of KD.
