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α-Tocopherol Enrichment Of Monocytes Decreases Agonist-Induced Adhesion To Human Endothelial Cells
K. Islam, S. Devaraj, I. Jialal
Published 1998 · Biology
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Background —Monocyte-endothelium adhesion is a crucial early event in atherogenesis. Several reports indicate that α-tocopherol (AT) is a potent antioxidant in plasma and LDL and also has intracellular effects that are antiatherogenic. 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 μmol/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-4 (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-κB (NF-κB), 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-κB.
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