Monocyte-endothelial adhesion is a hallmark feature of atherosclerosis at early stage and emerging evidence suggests that the glycosylation of vascular adhesive molecules and its ligands is involved in this process. Nevertheless, the mechanism underlying this process remains incompletely elucidated. In this study, we reported that treatment with inflammatory factors interleukin-1β (IL-1β) pronouncedly upregulated α1,3-fucosyltransferase VII gene (FUT7) mRNA and protein expression level in EA.hy926 endothelial cells. Moreover, FUT7 overexpression significantly promoted monocyte-endothelial adhesion, while FUT7 knockdown obviously inhibited IL-1β-induced monocyte-endothelial adhesion. Further analysis demonstrated that fucosylation of selectin ligand endomucin was directly involved in IL-1β-induced monocyte-endothelial adhesion. Finally, we demonstrated that p38 and extracellular signal-regulated kinase (ERK) MAPK signaling pathway was activated by IL-1β, while inhibition of p38/ERK signaling pathway decreased FUT7 expression level and IL-1β-induced monocyte-endothelial adhesion. In summary, these results provide a novel insight that FUT7-mediated fucosylation contribute to the initiation and progression of atherosclerosis.
Keywords: Endomucin; IL-1β; Monocyte-endothelial adhesion; α1,3-Fucosyltransferase FUT7.
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