alpha-Tocopherol enrichment of monocytes decreases agonist-induced adhesion to human endothelial cells

Article

关键词: NF-KAPPA-B;    LOW-DENSITY-LIPOPROTEIN;    DNA-BINDING ACTIVITY;    TRANSCRIPTION FACTOR;    VITAMIN-E;    ATHEROSCLEROTIC LESION;    GEL-ELECTROPHORESIS;    65-KD SUBUNIT;    IN-VITRO;    ACTIVATION;   

DOI  :  10.1161/01.CIR.98.21.2255

来源: SCIE

【 摘 要 】

Background-Monocyte-endothelium adhesion is a crucial early event in atherogenesis. Several reports indicate that cr-tocopherol (AT) is a patent antioxidant in plasma and LDL and also has intracellular effects that are antiatheronenic. Recently, it has been shown that AT supplementation results in decreased monocyte-endothelial cell adhesion. However, there is a paucity of data on the mechanisms by which AT inhibits adhesion of monocytes. We studied the effect of AT enrichment of a human monocytic cell line, U937, on adhesion to human umbilical vein endothelial cells (HUVECs). Methods and Results-Both lipopolysaccharide (LPS)- and N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated U937 adhesion to HUVECs were studied. AT (50 and 100 mu mol/L) significantly decreased adhesion of both LPS- and FMLP-stimulated U937 cells to HUVECs (LPS-treated cells, P<0.0125; FMLP-treated cells, P<0.05). Expression of the adhesion molecules CD11a, CD11b, CD11c, very late antigen-il (VLA-4), and L-selectin, as assessed by flow cytometry, was increased in the stimulated U937 cells, and AT resulted in significant reduction in the expression of CD11b and VLA-4. In addition, activation of the transcription factor nuclear factor-kappa B (NF-kappa B), as assessed by gel shift assays, was inhibited by pretreatment with AT in LPS-treated U937 cells. Conclusions-AT significantly decreases adhesion of activated monocytes to endothelial cells by decreasing expression of CD11b and VLA-4 on monocytes, possibly by inhibiting the activation of NF-kappa B.

【 授权许可】

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