Notch4 signaling pathway in a Kawasaki disease mouse model induced by Lactobacillus casei cell wall extract.

Abstract

The present study aimed to explore the role of the Notch4 signaling pathway in a mouse model of Kawasaki disease (KD) induced by Lactobacillus casei cell wall extract (LCWE). BALB/c male mice (4–6 weeks old) were intraperitoneally injected with 500 µg LCWE in phosphate-buffered saline (PBS) or PBS alone (control group). At days 3, 7, 14 and 28, the numbers of circulating endothelial progenitor cells (EPCs) in the peripheral blood and the expression of Notch4 on the surface of EPCs were detected. In addition, the levels of vascular cell adhesion molecule 1 (VCAM-1) and P-selectin in the roots of coronary arteries were evaluated. The results demonstrated that the level of circulating EPCs increased significantly at day 3, decreased progressively from day 3 onwards, and recovered to the normal level at day 28. Furthermore, the expression of Notch4 on the surface of EPCs was evidently higher in the KD model compared with that in the control group at day 7. In the endothelial cells of the coronary artery root, the protein levels of VCAM-1 and P-selectin protein increased in the KD model. In conclusion, the Notch4 signaling pathway participated in the coronary artery lesions in the KD animal model induced by LCWE.