The role of oxLDL in coronary artery lesion in Kawasaki disease through CXCL16 and ERK1/2 signaling pathways
Objective To investigate the relationship between oxidized low density lipoprotein(oxLDL)and coronary artery lesion(CAL)in Kawasaki disease(KD)through CXCL16/ERK1/2 signaling pathway.Methods Cell models of KD were established and divided into three groups:normal control group(Con group),normal coronary artery group(NCAL group,10%serum from NCAL patients),and coronary artery lesion group(CAL group,10%serum from CAL patients).After 24 hours of cell culture,the expression level of oxLDL in the cell supernatant was detected by Elisa.In addition,the potential targets of oxLDL in KD were screened according to the public database,and the expression level of CXCL16 was detected by RT-qPCR.The expression level of cell protein CXCL16 and p-ERK were detected by Western Blot.CCK8 assay and Edu assay were used to evaluate the viability and proliferation of endothelial cells,and scratch assay was used to detect the migration ability of endothelial cells.The expression of ERK1/2 was interfered by ERK1/2 inhibitor(SCH772984),and four different treatment groups were established:NCAL group,NCAL+SCH group,CAL group and CAL+SCH group.The expression levels of CXCL16 and p-ERK were detected by Western Blot.Results Compared with Con group,the oxLDL and the expression of CXCL16 levels were higher in the NCAL group,but the trend was more significant in the CAL group(P＜0.05).Compared with the Con group,the expression of CXCL16 and p-ERK in the NCAL group showed an upward trend,and this trend was further enhanced in the CAL group(P＜0.05).CCK-8 test showed that the cell activity was lower after stimulation with the serum of CAL patients(P＜0.05).Edu test results showed that the number of Edu positive cells in the CAL group was significantly reduced(P＜0.05),and the cell scratch healing speed was slowed down(P＜0.05).The results showed that the expression of CXCL16 in the inhibition of ERK1/2 group was significantly decreased after the inhibition of ERK1/2 expression(P＜0.05).Conclusion oxLDL may aggravate the dysfunction of endothelial cells through CXCL16/ERK1/2 signaling pathway,thereby triggering the occurrence of CAL in KD patients.
Kawasaki diseaseOxidized low density lipoproteinCoronary artery lesionEndothelial dysfunction
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