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Altered expression of plasminogen activator inhibitor type 1 in placentas
from pregnant women with preeclampsia and/or intrauterine fetal growth
retardation
A Estelles, J Gilabert, M Keeton, Y Eguchi, J Aznar, S Grancha, F Espna, DJ Loskutoff and RR Schleef
Centro Investigacion and Centro Maternal, Hospital La Fe, Valencia, Spain.
Elevated plasma levels of type 1 plasminogen activator inhibitor (PAI- 1)
have been implicated in mediating the fibrin deposition and occlusive
lesions that occur within the placental vasculature in preeclampsia (PE)
and intrauterine growth retardation (IUGR). In this report we identify the
cells within the normal-appearing villous tissue that are responsible for
the local production of PAI-1 in women with PE and IUGR. Levels for another
fibrinolytic inhibitor (ie, type 2 plasminogen activator inhibitor [PAI-2])
were determined for comparative purposes. Elevated levels of PAI-1 were
detected in placenta extracts from PE/IUGR patients (121 +/- 38 ng/mg, n =
8) when compared with the levels in placenta extracts from normal women (43
+/- 17 ng/mg, n = 10) or women with IUGR but not PE (51 +/- 22 ng/mg, n =
11). Immunohistochemical analysis of paraffin sections showed an increased
immunoreactivity for PAI-1 in the placental villous syncytiotrophoblasts
from PE/IUGR women compared with the immunostaining of placental samples
from the normal or IUGR group. In contrast, antigen levels and
immunostaining for PAI-2 were reduced in the placentas harvested from not
only the PE/IUGR women (209 +/- 144 ng/mg) but also the IUGR group (169 +/-
106 ng/mg) in comparison with the PAI-2 levels in normal placentas (535 +/-
98 ng/mg). To document that the increased immunoreactivity for PAI-1 in
PE/IUGR syncytiotrophoblasts was mediated by an increased production of
PAI-1 within these cells, in situ hybridization analysis was performed. A
strong positive signal for PAI-1 mRNA in villous syncytiotrophoblasts from
PE patients (n = 5) was obtained after 2 weeks of exposure to the NTB2
emulsion in comparison with the weak signal for PAI-1 mRNA that required a
10-week exposure of the normal placenta sections (n = 10). Northern
blotting for PAI-1 mRNA showed that both transcripts (ie, 3.2 and 2.3 kb)
were elevated in samples of two PE patients in comparison with the PAI-1
mRNA transcripts present in a normal placenta and an IUGR placental sample.
These results show increased PAI-1 and mRNA levels in placentas from PE
patients and raise the possibility that localized elevated levels of PAI-1
may play a role in the initiation of placental damage, as well as in the
thrombotic complications associated with this disease.
Volume 84,
Issue 1,
pp. 143-150,
07/01/1994
Copyright © 1994 by The American Society of Hematology
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