α-tocopherol enrichment of monocytes decreases agonist-induced adhesion to human endothelial cells

Kazi Nazrul Islam, Sridevi Devaraj, Ishwarlal Jialal

Research output: Contribution to journalArticlepeer-review

109 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)2255-2261
Number of pages7
JournalCirculation
Volume98
Issue number21
StatePublished - Nov 24 1998
Externally publishedYes

Keywords

  • Antioxidants
  • Cell adhesion molecules
  • Endothelium
  • NF-kappa B

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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