Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

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

Noble, Karen E., Panayiotidis, Panayiotis, Collins, Peter William, Hoffbrand, A. Victor and Yong, Kwee L. 1996. Monocytes induce E-selectin gene expression in endothelial cells: role of CD11/CD18 and extracellular matrix proteins. European Journal of Immunology 26 (12) , pp. 2944-2951. 10.1002/eji.1830261221

Full text not available from this repository.

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.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: Q Science > QH Natural history > QH426 Genetics
R Medicine > R Medicine (General)
Uncontrolled Keywords: Monocyte; Endothelium; E-selectin
Publisher: Wiley
ISSN: 1521-4141
Last Modified: 04 Jun 2017 06:28
URI: http://orca.cf.ac.uk/id/eprint/60480

Citation Data

Cited 25 times in Google Scholar. View in Google Scholar

Cited 25 times in Scopus. View in Scopus. Powered By Scopus® Data

Cited 23 times in Web of Science. View in Web of Science.

Actions (repository staff only)

Edit Item Edit Item