Immunosuppressive Siglec-E ligands on mouse aorta are up-regulated by LPS via NF-κB pathway

作者：Hongmei Liu, Yu Zheng, Yingxian Zhang, Jin Li, Steve M. Fernandes, Dongfeng Zeng, Xiaohui Li, Ronald L. Schnaar, Yi Jia · 发表于：Biomedicine & Pharmacotherapy · 年份：2019 · DOI：10.1016/j.biopha.2019.109760 · 被引用次数：15 · 研究领域：Glycosylation and Glycoproteins Research、Proteoglycans and glycosaminoglycans research、Cell Adhesion Molecules Research

AIMS: Siglec-E, the mouse ortholog of human Siglec-9, is an immunosuppressive cell surface receptor. Both Siglec-E and Siglec-9 are primarily found on neutrophils, macrophages, and monocytes. When Siglec-E binds to sialoglycan ligands in its extracellular environment, it halts the immune cells' inflammatory responses. In the present study, we aimed to investigate expression, mechanisms of action and regulation of Siglec-E ligands during vascular inflammation induced by E. coli lipopolysaccharides (LPS) in mouse aorta. METHODS: The distribution, molecular size and glycoprotein class of Siglec-E ligands on mouse aorta were determined, and the protein carrier of the ligands was identified. In vivo, the expression of Siglec-E ligands was detected after LPS treatment, with or without NF-κB inhibitor administration. In vitro, cultured primary mouse aortic endothelial cells (MAECs) were used to study changes in expression of Siglec-E ligands induced by LPS with or without NF-κB inhibitors. MAECs induced by LPS were co-cultured with macrophages and the effect of increased expression of Siglec-E ligands analyzed. RESULTS: Siglec-E ligands are O-linked sialoglycoproteins with molecular weights of 70-300 kDa and are distributed broadly on mouse aorta as well as on MAECs in vitro. In vivo, the expression of Siglec-E ligands was increased in mice aortas in response to LPS treatment in an NF-κB signaling pathway dependent manner. In MAECs, the expression of Siglec-E ligands was also increa...