Forkhead Box C2 Attenuates Lipopolysaccharide-Induced Cell Adhesion via Suppression of Intercellular Adhesion Molecule-1 Expression in Human Umbilical Vein Endothelial Cells
Forkhead Box C2 Attenuates Lipopolysaccharide-Induced Cell Adhesion via Suppression of Intercellular Adhesion Molecule-1 Expression in Human Umbilical Vein Endothelial Cells
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Forkhead Box C2 通过抑制人脐静脉内皮细胞中细胞间粘附分子 1 的表达来减弱脂多糖诱导的细胞粘附
DOI：
10.1089/dna.2019.4663
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发表时间：
2019-04-17
影响因子：
3.1
通讯作者：
Wang, Qian
中科院分区：
文献类型：
--
作者：
Xu, Yuan-Jun;Li, Pan;Wang, Qian
动脉粥样硬化是一种慢性血管炎性疾病，涉及多种细胞类型和循环调节因子，包括细胞间粘附分子（ICAM）-1，一种促炎细胞因子。脂多糖（LPS）可增加ICAM-1表达，促进细胞粘附，但其机制尚不清楚。我们发现LPS诱导人脐静脉内皮细胞（HUVECs）ICAM-1表达上调和叉头盒蛋白C2（Foxc 2）表达下调的时间和剂量调节。Foxc 2过表达可显著抑制LPS诱导的HUVECs ICAM-1表达和LPS诱导的THP-1细胞与HUVECs的粘附。Foxc 2 siRNA显著增加LPS诱导的ICAM-1表达和LPS诱导的THP-1人单核细胞与HUVECs的粘附。我们的结论是，Foxc 2抑制LPS诱导的粘附THP-1细胞HUVECs抑制ICAM-1的表达。
Atherosclerosis is a chronic vascular inflammatory disease that involves diverse cell types and circulating regulatory factors, including intercellular adhesion molecule (ICAM)-1, a proinflammatory cytokine. Lipopolysaccharides (LPS) increase ICAM-1 expression and promote cell adhesion, but the mechanism is not clear. We found that LPS induced time- and dose-regulated upregulation of ICAM-1 expression and downregulation of forkhead box protein C2 (Foxc2) expression in human umbilical vein endothelial cells (HUVECs). Overexpression of Foxc2 significantly inhibited both LPS-induced ICAM-1 expression in HUVECs and LPS-induced adhesion of THP-1 cells to HUVECs. Foxc2 siRNA dramatically increased both LPS-induced ICAM-1 expression and LPS-induced adhesion of THP-1 human monocytes cells to HUVECs. We conclude that Foxc2 inhibited LPS-induced adhesion of THP-1 cells to HUVECs by suppressing ICAM-1 expression in HUVECs.