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Monocytes induce E-selectin gene expression in endothelial cells: role of CD11/CD18 and extracellular matrix proteins.

Abstract：

:E-selectin is an endothelium-specific inducible adhesion molecule which binds several inflammatory cell types, including neutrophils, monocytes, natural killer cells and a subset of memory T cells. E-selectin is important in the initial rolling interaction of these cells on inflamed endothelium. The transient kinetics of E-selectin induction in vitro contrast with in vivo observations of prolonged expression of this adhesion molecule in chronic inflammation. This raises the possibility that signals generated within inflammatory tissues are more complex than the agonists used to activate endothelial cells in vitro. We investigated whether adhesive interactions with extravasating monocytes are able to provide activating signals that can induce E-selectin expression on endothelium, and prolong the response to cytokine stimulation. We report that co-culture with monocytes led to transcriptional activation of the E-selectin gene in endothelial cells, and marked enhancement of the response to substimulatory concentrations of interleukin-1. In addition, the presence of monocytes resulted in prolonged up-regulation of E-selectin. Induction of E-selectin by monocytes was inhibited when cell contact between monocytes and endothelium was prevented (80 +/- 8% inhibition, p < 0.001, n = 4). Monoclonal antibody (mAb) against tumor necrosis factor (TNF) was able to abolish 57.2 +/- 9.7% of the response (p < 0.01, n = 4). The ability of adherent monocytes to induce sustained E-selectin expression in endothelial cells could not be reproduced either by supernatants harvested from monocytes cultured for 18 h, or by maximal concentrations of TNF. The induction of E-selectin in monocyte/endothelium co-cultures was inhibited by mAb to CD11b, but not by those directed against VLA-4 or L-selectin. Extracellular matrix molecules may also play a role in adhesion-dependent cellular activation, as inclusion of soluble collagen type I led to significant reduction in E-selectin expression in monocyte/endothelium co-cultures. We conclude that adhesive interactions between monocytes and endothelial cells provide a source of signals which influence the activation state of the endothelium, and consequently, the continued influx of inflammatory cells.

journal_name

Eur J Immunol

journal_title

European journal of immunology

authors

Noble KE,Panayiotidis P,Collins PW,Hoffbrand AV,Yong KL

doi

10.1002/eji.1830261221

subject

Has Abstract

pub_date

1996-12-01 00:00:00

pages

2944-51

issue

eissn

0014-2980

issn

1521-4141

journal_volume

pub_type

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Monocytes induce E-selectin gene expression in endothelial cells: role of CD11/CD18 and extracellular matrix proteins.