Monocyte-endothelial cell interaction induces expression of adhesion molecules on human umbilical cord endothelial cells.

Abstract:

OBJECTIVE:The adhesive interaction of monocytes and endothelial cells has been implicated as a regulatory signal in the cell activation that is involved in the pathogenesis of atherosclerosis. We investigated the effect of monocyte-endothelial cell interaction on the expression of adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), in human umbilical cord vein endothelial cells (HUVECs). METHODS:ICAM-1 and VCAM-1 protein and mRNA expression were determined by cellular ELISA and Northern blot analysis, respectively. RESULTS:The addition of unstimulated human monocytes, as well as interleukin-1 beta (IL-1 beta: 25 U/ml) and tumor necrosis factor-alpha (TNF: 100 U/ml), to HUVECs rapidly induced the expression of ICAM-1 and VCAM-1 protein and mRNA in HUVECs, whereas the addition of polymorphonuclear leukocytes (PMNs) had no significant effect on their expression. The induction of ICAM-1 and VCAM-1 by the co-culture of HUVECs and monocytes was significantly, but partially, inhibited by the combination of anti-IL-1 alpha, anti-IL-1 beta and anti-TNF Abs. Actinomycin D and genistein, but not calphostin C, also significantly inhibited the co-culture-induced adhesion molecule expression. CONCLUSIONS:These results suggest that the monocyte-endothelial cell interaction induces the expression of ICAM-1 and VCAM-1 in endothelial cells partially through the production of IL-1 and TNF. These findings also suggest that the monocyte-endothelial interaction further augments their interaction through the up-regulation of endothelial adhesion molecules, as a positive feedback mechanism.

journal_name

Cardiovasc Res

journal_title

Cardiovascular research

authors

Takahashi M,Ikeda U,Masuyama J,Kitagawa S,Kasahara T,Shimpo M,Kano S,Shimada K

doi

10.1016/0008-6363(96)00085-5

subject

Has Abstract

pub_date

1996-08-01 00:00:00

pages

422-9

issue

2

eissn

0008-6363

issn

1755-3245

pii

0008636396000855

journal_volume

32

pub_type

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