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Characterization of the interactions between procoagulant albumin and human
endothelial cells
KJ Faucette, LA Fitzgerald, L Liu, CJ Parker and GM Rodgers
Department of Pediatrics, University of Utah Medical Center, Salt Lake City
84132.
Normal human plasma contains procoagulant albumin (PC-Al), an anionic form
of albumin that induces tissue factor (TF) activity in human umbilical vein
endothelial cells (HUVEC) and monocytes. In this study, we investigated
both the interactions between HUVEC and PC-Al and the mechanism by which
PC-Al induces TF activity. Binding of PC-Al to HUVEC was specific and
reversible. Further studies indicated that membrane- bound PC-Al was not
internalized by HUVEC. A potential receptor on HUVEC was suggested by
studies in which the capacity of a variety of reagents to inhibit the
activity of PC-Al was quantitated. Induction of TF activity by PC-Al was
antagonized by dextran sulfate, heparin, fucoidan, and concanavalin A but
not by ovalbumin, polyglutamic acid, or polyvinyl sulfate. This competition
profile bears similarities to those reported for scavenger receptors that
have been identified on both HUVEC and monocytes. Involvement of protein
kinase C (PKC) in the PC-Al-induced enhancement of TF activity was
suggested by experiments in which staurosporine, an inhibitor of PKC,
suppressed the activity of PC-Al. The induction of TF activity by PC-Al was
further characterized by using a quantitative polymerase chain reaction
assay. Increased TF mRNA was first seen after 1 hour of incubation with
PC-Al. Maximal observed expression occurred at 2 hours, but at 5 hours,
expression had significantly decreased. Monocytes could also be induced to
express TF mRNA after a 2-hour incubation with PC-Al. These results suggest
that the functionally relevant binding of PC-Al to HUVEC may be mediated
through interactions with a membrane constituent that has some of the
properties of a scavenger receptor and that this interaction augments TF
activity by enhancing transcription of TF mRNA, at least in part, by a
mechanism that is dependent on activation of PKC.
Volume 82,
Issue 9,
pp. 2684-2692,
11/01/1993
Copyright © 1993 by The American Society of Hematology
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