Citreoviridin enhances tumor necrosis factor-α-induced adhesion of human umbilical vein endothelial cells

Endothelial adhesion plays an important role in the process of atherosclerosis, which is regulated by endothelial adhesion molecules and chemoattractant molecules. In some areas of China, citreoviridin (CIT) is considered a risk factor for the development of atherosclerosis. Here, we investigated the role of CIT in adhesion of human umbilical vein endothelial cells (HUVECs) together with the stimulation of tumor necrosis factor-alpha (TNF-alpha). Adhesion of HUVECs to monocytes was analyzed by coculture experiments using U937 cells labeled with 2,7-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethylester. The expression of intercellular adhesion molecule-1 (ICAM-I), vascular cell adhesion molecule-1 (VCAM-I), and E-selectin was determined by Western blot and enzyme-linked immunosorbent assay (ELISA). The expression of monocyte chemoattractant kprotein-1 (MCP-1) was measured by reverse transcription polymerase chain reaction and ELISA. The activation of nuclear factor-kappa B (NF-kappa B) was assessed by Western blot and immunofluorescence staining. CIT markedly increased TNF-alpha-induced HUVECs adhesion to monocytes and the expression levels of ICAM-I, VCAM-I, E-selectin, and MCP-1. TNF-alpha-induced nuclear translocation of NF-kappa B in HUVECs was significantly elevated by CIT. Our study demonstrates that CIT upregulates TNF-alpha-induced endothelial adhesion via increasing activation of NF-kappa B, which results in the expression of ICAM-1, VCAM-1, E-selectin, and MCP-1. CIT plays a pivotal role in the process of endothelial cell adhesion and may thereby play an important role in the improvement of atherosclerosis in areas of China that have a high prevalence of CIT contamination and atherosclerosis.