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Granulocyte colony-stimulating factor ameliorates coronary artery elastin breakdown in a mouse model of Kawasaki
Junfeng Liu1, Zhi Chen2, Zhongdong Du3
1Key Laboratory of Major Diseases in Children, Ministry of Health, Beijing 100045, China.
Insights
Granulocyte colony-stimulating factor (G-CSF) enhances endothelial progenitor cell (EPC) function and number, improving coronary artery elastin breakdown in a Kawasaki disease (KD) mouse model via the nitric oxide (NO) system.
Area of Science:
- Cardiovascular Research
- Immunology
- Regenerative Medicine
Background:
- Kawasaki disease (KD) causes coronary artery damage linked to endothelial progenitor cell (EPC) dysfunction.
- Understanding modulatory effects on EPCs is crucial for treating KD-induced vascular damage.
Purpose of the Study:
- To evaluate the effect of granulocyte colony-stimulating factor (G-CSF) on EPCs and coronary artery elastin breakdown in a KD mouse model.
- To investigate the role of the nitric oxide (NO) system in G-CSF's protective effects.
Main Methods:
- Established a Lactobacillus casei cell wall extract (LCWE)-induced KD mouse model.
- Administered recombinant human G-CSF (rhG-CSF) and Nω-nitro-L-arginine methyl ester (L-NAME).
- Assessed coronary artery lesions, EPC number and function, and plasma NO concentration.
Main Results:
- KD model mice showed elastin breakdown, reduced circulating EPCs, and impaired EPC function.
- rhG-CSF administration increased EPCs, NO levels, and EPC function, improving elastin breakdown.
- L-NAME attenuated the protective effects of rhG-CSF, indicating NO system involvement.
Conclusions:
- G-CSF administration prevents coronary artery elastin breakdown in KD by enhancing EPCs via the NO system.
- G-CSF promotes the repair of coronary artery lesions in Kawasaki disease.
- The NO system is a key mediator of G-CSF's therapeutic effects in 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.
