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Monocytes enhance the bidirectional release of type I plasminogen activator
inhibitor by endothelial cells
BC Hakkert, JM Rentenaar and JA van Mourik
Central Laboratory of The Netherlands Red Cross Blood Transfusion Service,
Amsterdam.
Human umbilical vein endothelial cells cultured on a collagen lattice were
used to study the effects of the interaction between human monocytes and
endothelial cells on the production of type 1 plasminogen activator
inhibitor (PAI-1) by endothelial cells. The effects of adherence and
transendothelial migration of monocytes on endothelial PAI-1 release were
compared with those of other leukocytes, conditioned media from monocytes,
and interleukin-1 beta (IL-1 beta). Because the cell culture system used
allows simultaneous analysis of the lumenal and the subendothelial
compartment of endothelial cell monolayers, we also studied into which
direction PAI-1 is released by endothelial cells. Under quiescent
conditions, the net amount of PAI-1 accumulated at the lumenal side was
twofold higher than that accumulated at the subendothelial side (about 2.0
micrograms PAI-1/10(6) cells and 1.1 microgram PAI-1/10(6) cells,
respectively, in 24 hours), as analyzed by a quantitative immunoradiometric
assay (IRMA). Direct cell-cell contact between highly purified monocytes
and endothelial cells strongly enhanced the PAI-1 release by endothelial
cells in a dose-dependent way, whereas lymphocytes and neutrophils did not
affect endothelial PAI- 1 production. The monocyte-mediated increase was
first detected after 12 hours of incubation and lasted for at least 48
hours. In the presence of two monocytes per endothelial cell, the increases
of PAI-1 at the lumenal side and at the subendothelial side were 87% and
32% in 24 hours, respectively. The effect of IL-1 beta on PAI-1 release by
endothelial cells closely resembled that observed for monocytes.
Monocyte-conditioned medium contained heat-labile product(s) which also,
although to a much lesser extent than intact monocytes, enhanced
endothelial PAI-1 release. Similarly, monocytes cultured on top endothelial
cell separated by a microporous filter enhanced the release of PAI-1 to a
lesser extent. Thus, these findings indicate that monocytes enhance
endothelial PAI-1 release by mechanisms that are, at least in part,
dependent on cell-cell contact.
Volume 76,
Issue 11,
pp. 2272-2278,
12/01/1990
Copyright © 1990 by The American Society of Hematology
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