(Circulation. 1998;98:2255-2261.)
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports |
-Tocopherol Enrichment of Monocytes Decreases Agonist-Induced Adhesion to Human Endothelial Cells
From the Departments of Pathology (K.N.I., S.D., I.J.) and Internal Medicine (I.J.), University of Texas Southwestern Medical Center at Dallas.
Correspondence to Ishwarlal Jialal, MD, PhD, Department of Pathology and Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, Dallas, TX 75235-9073. E-mail jialal.i{at}pathology.swmed.edu
Background—Monocyte-endothelium
adhesion is a crucial early event in atherogenesis. Several reports
indicate that -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-
B (NF-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-B.
Key Words: cell adhesion molecules • antioxidants • endothelium • NF-kappa B
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