Granulocyte colony-stimulating factor ameliorates coronary artery elastin breakdown in a mouse model of Kawasaki disease  

作　　者：Liu Junfeng Chen Zhi Du Zhongdong Lu Dunxiang 

机构地区：[1]Key Laboratory of Major Diseases in Children, Ministry of Health, Beijing 100045, China [2]Department of Pediatric Internal Medicine, Beijing Children's Hospital, Capital Medical University, Beijing 100045, China

出　　处：《Chinese Medical Journal》2014年第21期3712-3717,共6页中华医学杂志（英文版）

基　　金：This study was supported by grants from the National Natural Science Foundation of China （No. 81274109 and 30973238）, the Key Research Project of Beijing Natural Science Foundation （B）/Beijing Education Committee （No. KZ201010025024）, and the Science and Technology Innovation Platform （PXM2011_014226_07_000085）.

摘　　要：Background Coronary artery damage from Kawasaki disease （KD） is closely linked to the dysfunction of the endothelial progenitor cells （EPCs）.The aim of the present study was to evaluate the modulatory effect of granulocyte colony stimulating factor （G-CSF） on EPCs and elastin breakdown of coronary arteries in a KD mouse model.Methods A Lactobacillus casei cell wall extract （LCWE）-induced KD model was established in C57BL/6 mice that were subsequently administrated with recombinant human G-CSF （rhG-CSF）.Nω-nitro-L-arginine methyl ester （L-NAME） was administrated for the negative intervention.Evaluations included coronary artery lesions,EPC number and functions,and the plasma concentration of nitric oxide （NO）.Results Elastin breakdown was found in the coronary arteries of model mice 56 days after injection of LCWE.The number of circulating EPCs,plasma concentration of NO,and functions of bone marrow EPCs,including proliferation,adhesion,and migration abilities,were all lower in the KD model group compared with those in the control group.After administration of rhG-CSF,the number of circulating EPCs and plasma concentration of NO were increased significantly compared with those in the KD model group.There were also increases in the functional indexes of EPCs.Furthermore,rhG-CSF administration improved the elastin breakdown effectively.However,these protective effects of rhG-CSF on coronary arteries were attenuated by L-NAME.Conclusion The present study indicated that the administration of G-CSF prevents elastin breakdown of the coronary arteries by enhancing the number and functions of EPCs via the NO system,and then accelerates the repair of coronary artery lesions in the KD.Background Coronary artery damage from Kawasaki disease （KD） is closely linked to the dysfunction of the endothelial progenitor cells （EPCs）.The aim of the present study was to evaluate the modulatory effect of granulocyte colony stimulating factor （G-CSF） on EPCs and elastin breakdown of coronary arteries in a KD mouse model.Methods A Lactobacillus casei cell wall extract （LCWE）-induced KD model was established in C57BL/6 mice that were subsequently administrated with recombinant human G-CSF （rhG-CSF）.Nω-nitro-L-arginine methyl ester （L-NAME） was administrated for the negative intervention.Evaluations included coronary artery lesions,EPC number and functions,and the plasma concentration of nitric oxide （NO）.Results Elastin breakdown was found in the coronary arteries of model mice 56 days after injection of LCWE.The number of circulating EPCs,plasma concentration of NO,and functions of bone marrow EPCs,including proliferation,adhesion,and migration abilities,were all lower in the KD model group compared with those in the control group.After administration of rhG-CSF,the number of circulating EPCs and plasma concentration of NO were increased significantly compared with those in the KD model group.There were also increases in the functional indexes of EPCs.Furthermore,rhG-CSF administration improved the elastin breakdown effectively.However,these protective effects of rhG-CSF on coronary arteries were attenuated by L-NAME.Conclusion The present study indicated that the administration of G-CSF prevents elastin breakdown of the coronary arteries by enhancing the number and functions of EPCs via the NO system,and then accelerates the repair of coronary artery lesions in the KD.

关 键 词：Kawasaki disease endothelial progenitor cell granulocyte colony-stimulating factor mouse model 

分 类 号：R725.4[医药卫生—儿科] R-332[医药卫生—临床医学]