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Blood, Vol. 92 No. 3 (August 1), 1998:
pp. 939-945
Apposition-Dependent Induction of Plasminogen Activator
Inhibitor Type 1 Expression: A Mechanism for Balancing Pericellular
Proteolysis During Angiogenesis
Eran Bacharach,
Ahuva Itin, and
Eli Keshet
From the Department of Molecular Biology, The Hebrew University,
Hadassah Medical School, Jerusalem, Israel.
Plasminogen-activator inhibitor type I (PAI-1), the primary
inhibitor of urinary-type plasminogen activator, is thought to play an
important role in the control of stroma invasion by both endothelial
and tumor cells. Using an in vitro angiogenesis model of capillary
extension through a preformed monolayer, in conjunction with in situ
hybridization analysis, we showed that PAI-1 mRNA is specifically
induced in cells juxtaposed next to elongating sprouts. To further
establish that PAI-1 expression is induced as a consequence of a direct
contact with endothelial cells, coculture experiments were performed.
PAI-1 mRNA was induced exclusively in fibroblasts (L-cells) contacting
endothelial cell (LE-II) colonies. Reporter gene constructs driven by a
PAI-1 promoter and stably transfected into L-cells were used to
establish that both mouse and rat PAI-1 promoters mediate
apposition-dependent regulation. This mode of PAI-1 regulation is not
mediated by plasmin, as an identical spatial pattern of expression was
detected in cocultures treated with plasmin inhibitors. Because
endothelial cells may establish direct contacts with fibroblasts only
during angiogenesis, we propose that focal induction of PAI-1 at the
site of heterotypic cell contacts provides a mechanism to negate
excessive pericellular proteolysis associated with endothelial cell
invasion.
© 1998 by The American Society of Hematology.
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