Does plasminogen activator inhibitor-1 (PAI-1) control trophoblast invasion? A study of fetal and maternal tissue in intrauterine, tubal and molar pregnancies

被引:42
作者
Floridon, C
Nielsen, O
Holund, B
Sweep, F
Sunde, L
Thomsen, SG
Teisner, B
机构
[1] Odense Univ Hosp, Dept Pathol, DK-5000 Odense C, Denmark
[2] Univ Med Ctr Nijmegen, Dept Clin Endocrinol, Nijmegen, Netherlands
[3] Aarhus Univ Hosp, Inst Human Genet, Aarhus, Denmark
[4] Odense Univ Hosp, Dept Obstet & Gynaecol, DK-5000 Odense, Denmark
[5] Odense Univ, Dept Immunol & Microbiol, DK-5230 Odense M, Denmark
关键词
D O I
10.1053/plac.2000.0573
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Urokinase plasminogen activator, its receptor and the inhibitor PAI-1 are believed to central proteolysis and remodelling of maternal tissue during trophoblast invasion. This system appears to be strictly regulated in normal intrauterine pregnancies whereas tubal and molar pregnancies seem to be characterized by an uncontrolled. excessive placental invasion. This study evaluates subcellular PAI-1 by immunohistochemistry in the villous placenta, in the basal plate and placental bed, and in the decidual compartments of normal, tubal and molar pregnancies. PAI-1 was present in villous syncytiotrophoblasts and co-localized focally with fibrin-type fibrinoid on the surface of the chorionic villi. Basal plate and placental bed extravillous interstitial trophoblasts, as well as vascular trophoblasts, were also PAI-1 positive. In the decidua parietalis, PAI-1 was observed in the cytoplasm of the non-invaded decidual cells. In the decidua basalis comprising the basal plate, PAI-1 was seen to be membrane-associated or confined to the extracerlular matrix (ECM) facing the invasive front of anchoring villi. The ECM of decidua capsularis and chorion laeve displayed the most pronounced PAI-1 expression towards the maternal interface. In contrast, the majority of placental bed decidual cells adjacent to the interstitial and vascular trophoblasts were PAI-1 negative. Only a few stromal cells distant from the implantation site were PAI-1 positive in the tubal pregnancies and decidualization was not present. Likewise, excessive decidual necrosis and fibrinoid deposition devoid of PAI-1 was a common finding in complete molar pregnancies. These results suggest that PAI-1 defines specific extravillous invasive trophoblasts within the maternal decidua. Moreover, maternal cellular lack of PAI-1 in tubal pregnancies and excessive decidual necrosis in molar pregnancies indicate an uncontrolled placental invasion. The present data indicate that trophoblast invasion is primarily regulated by signals from decidual cells. (C) 2000 Harcourt Publishers Ltd.
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页码:754 / 762
页数:9
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