Endothelial progenitor cell transplantation ameliorates elastin breakdown in a Kawasaki disease mouse model.
- Author:
Zhi CHEN
1
;
Zhong-Dong DU
;
Jun-Feng LIU
;
Dun-Xiang LU
;
Li LI
;
Yun-Qian GUAN
;
Sui-Gui WAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Adhesion; physiology; Cell Proliferation; Disease Models, Animal; Elastin; metabolism; Endothelial Cells; cytology; Male; Mice; Mucocutaneous Lymph Node Syndrome; metabolism; therapy; Stem Cell Transplantation; psychology; Stem Cells; cytology; physiology
- From: Chinese Medical Journal 2012;125(13):2295-2301
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDCoronary artery damage from Kawasaki disease (KD) is closely linked to the dysfunction of endothelial progenitor cells (EPCs). The aim of the present study was to evaluate the therapeutic effect of EPCs transplantation in KD model.
METHODSLactobacillus casei cell wall extract (LCWE)-induced KD model in C57BL/6 mice was established. The model mice were injected intravenously with bone marrow-derived in vitro expanded EPCs. Histological evaluation, number of circulating EPCs and the function of bone marrow EPCs were examined at day 56.
RESULTSInflammation was found around the coronary artery of the model mice after 14 days, Elastin breakdown was observed after 56 days. CM-Dil labeled EPCs incorporated into vessel repairing foci was found. At day 56, the number of peripheral EPCs in the KD model group was lower than in EPCs transplanted and control group. The functional index of bone marrow EPCs from the KD model group decreased in proliferation, adhesion and migration. Increased number of circulating EPCs and improved function were observed on the EPCs transplanted group compared with model group.
CONCLUSIONExogenously administered EPCs, which represent a novel strategy could prevent the dysfunction of EPCs, accelerate the repair of coronary artery endothelium lesion and decrease the occurrence of aneurysm.