FIBRONECTIN EXPRESSION CORRELATES WITH U937 CELL-ADHESION TO MIGRATING BOVINE AORTIC ENDOTHELIAL-CELLS IN-VITRO

Citation
Ia. Hauser et al., FIBRONECTIN EXPRESSION CORRELATES WITH U937 CELL-ADHESION TO MIGRATING BOVINE AORTIC ENDOTHELIAL-CELLS IN-VITRO, The American journal of pathology, 143(1), 1993, pp. 173-180
Citations number
25
Categorie Soggetti
Pathology
ISSN journal
00029440
Volume
143
Issue
1
Year of publication
1993
Pages
173 - 180
Database
ISI
SICI code
0002-9440(1993)143:1<173:FECWUC>2.0.ZU;2-L
Abstract
A blood vessel's response to denudation injury will determine its fina l luminal diameter as well as its function. The synthesis, deposition, and remodeling of extracellular matrix components and migration by va scular endothelial cells are major factors in determining luminal diam eter, cellular proliferative and migratory responses, and mononuclear cell adhesion at sites of injury. Previously, we have shown that after in vivo and in vitro denudation injury, endothelial cell migration is dramatically influenced by the amount of fibronectin synthesized and deposited by the responding endothelial cell population. The aim of th is study was to elucidate the roles of fibronectin in modulating monon uclear cell adhesion to the endothelial cell population during in vitr o migration. In this report we demonstrate that U937 cell binding to t he migrating fronts of endothelial cell monolayers is modulated by the amount of fibronectin synthesized and deposited by the endothelial ce lls. Agents which increase fibronectin deposition, such as transformin g growth factor-beta1, elicit greater U937 cell adhesion. Manipulation s that decrease fibronectin deposition, such as transfection and overe xpression of pp60c-src proto-oncogene in endothelial cells, reduce U93 7 cell adhesion. These results suggest that changes in endothelial cel l extracellular matrix synthesis and deposition modulate, in part, the adhesive properties of the vessel wall after injury. In turn, the int ensity and duration of mononuclear cell adhesion at sites of vessel wa ll injury determines, in part, the vessel wall response.