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Cell-surface plasminogen activation causes a retraction of in vitro
cultured human umbilical vein endothelial cell monolayer
G Conforti, C Dominguez-Jimenez, E Ronne, G Hoyer-Hansen and E Dejana
Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy.
Vascular endothelium forms a dynamic interface between blood and underlying
tissues. Endothelial monolayer integrity is required for controlled
vascular permeability and to preclude exposure of subendothelial cell
matrix to circulating cells. Recent studies have established that cultured
human umbilical vein endothelial cells (ECs) express receptors for
plasminogen (plg) and urokinase-like plasminogen activator (uPA). In the
present study, we provide evidence that in EC, uPA receptor is present in
focal contacts and at cell-cell contact sites. In these cells, addition of
plg and uPA to confluent EC generates a retraction of the monolayer that is
evidenced by loss of cell-cell contacts and increase in monolayer
permeability. The phenomenon is reversible even after 6 hours of plg-uPA
treatment. Inhibition of plg-uPA effect is obtained with plasmin
inhibitors, as well as reagents that block binding of uPA or plg to the
cell surface. The retractive effect of plg-uPA is concomitant to surface
activation of plasminogen and to the loss of cell-cell activation of plg
can induce EC retraction, possibly by causing proteolysis at specific cell-
cell contacts and cell-matrix sites. This process may be important in
mediating the passage of metastatic tumor cells through an intact EC
monolayer as well as in regulating contacts between circulating cells and
endothelium.
Volume 83,
Issue 4,
pp. 994-1005,
02/15/1994
Copyright © 1994 by The American Society of Hematology
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