Immunohistochemical identification of the receptor for urokinase plasminogen activator associated with fibrin deposition in normal and ectopic human placenta

被引:27
作者
Pierleoni, C
Samuelsen, GB
Græm, N
Ronne, E
Nielsen, BS
Kaufmann, P
Castellucci, M
机构
[1] Univ Ancona, Fac Med, Inst Normal Human Morphol, I-60020 Ancona, Italy
[2] Copenhagen Univ Hosp, Rigshosp, Dept Pathol, Copenhagen, Denmark
[3] Copenhagen Univ Hosp, Rigshosp, Finsen Lab, Copenhagen, Denmark
[4] Aachen Tech Univ, Dept Anat, Aachen, Germany
[5] Fac Med Torino 2, Dept Med Sci, Novara, Italy
关键词
D O I
10.1016/S0143-4004(98)91043-8
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The receptor for urokinase plasminogen activator (uPAR) is a key molecule in cell surface-directed plasminogen activation. uPAR binds urokinase plasminogen activator (uPA) and thereby focuses plasminogen activation on the cell surface. Plasmin dissolves fibrin deposits and facilitates cell migration during tissue repair processes by degrading the extracellular matrix. During human implantation and placental development, plasmin is considered important for both trophoblast migration/invasion and for fibrin surveillance. This study examined the expression of uPAR in normal and ectopic human placentae by immunohistochemistry. In first and third trimester normal placentae as well as in tubal ectopic placental tissues, a high uPAR expression was seen in the trophoblast associated with deposits of fibrin-type fibrinoid. Extravillous trophoblast of the basal plate, of the cell islands, and of the cell columns was also positive for uPAR in the first trimester whereas at term the expression of the protein was decreased. Moreover, uPAR immunostaining was observed in decidual cells throughout normal gestation and in endometrial tissues of patients with ectopic pregnancies. These findings suggest that uPAR participates in placental development and in trophoblast invasion particularly in the first trimester of pregnancy and that uPAR is involved in repair mechanisms of the trophoblast and fibrin surveillance. (C) 1998 W. B. Saunders Company Ltd.
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页码:501 / 508
页数:8
相关论文
共 67 条
[1]   Focalized proteolysis: Spatial and temporal regulation of extracellular matrix degradation at the cell surface [J].
Basbaum, CB ;
Werb, Z .
CURRENT OPINION IN CELL BIOLOGY, 1996, 8 (05) :731-738
[2]  
BEHRENDT N, 1991, J BIOL CHEM, V266, P7842
[3]  
BEHRENDT N, 1990, J BIOL CHEM, V265, P6453
[4]  
Benirschke K., 1995, Pathology of the Human Placenta. Pathology of the Human Placenta
[5]  
BILLINGTON WD, 1971, ADV REPROD PHYSL, V5, P39
[6]   Co-ordinated expression of MMP-2 and its putative activator, MT1-MMP, in human placentation [J].
Bjorn, SF ;
Hastrup, N ;
Lund, LR ;
Dano, K ;
Larsen, JF ;
Pyke, C .
MOLECULAR HUMAN REPRODUCTION, 1997, 3 (08) :713-723
[7]   Urokinase-type plasminogen activator is effective in fibrin clearance in the absence of its receptor or tissue-type plasminogen activator [J].
Bugge, TH ;
Flick, MJ ;
Danton, MJS ;
Daugherty, CC ;
Romer, J ;
Dano, K ;
Carmeliet, P ;
Collen, D ;
Degen, JL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (12) :5899-5904
[8]   PLASMINOGEN DEFICIENCY CAUSES SEVERE THROMBOSIS BUT IS COMPATIBLE WITH DEVELOPMENT AND REPRODUCTION [J].
BUGGE, TH ;
FLICK, MJ ;
DAUGHERTY, CC ;
DEGEN, JL .
GENES & DEVELOPMENT, 1995, 9 (07) :794-807
[9]   EXPRESSION OF THE PROLIFERATION MARKERS KI67 AND TRANSFERRIN RECEPTOR BY HUMAN TROPHOBLAST POPULATIONS [J].
BULMER, JN ;
MORRISON, L ;
JOHNSON, PM .
JOURNAL OF REPRODUCTIVE IMMUNOLOGY, 1988, 14 (03) :291-302
[10]   PHYSIOLOGICAL CONSEQUENCES OF LOSS OF PLASMINOGEN-ACTIVATOR GENE-FUNCTION IN MICE [J].
CARMELIET, P ;
SCHOONJANS, L ;
KIECKENS, L ;
REAM, B ;
DEGEN, J ;
BRONSON, R ;
DEVOS, R ;
VANDENOORD, JJ ;
COLLEN, D ;
MULLIGAN, RC .
NATURE, 1994, 368 (6470) :419-424