RESUMO
INTRODUCTION: Plasminogen activators and inhibitors were quantitated in cultured human endometrial and trophoblast cells under the influence of ovarian steroids in order to investigate the role of the fibrinolytic system for trophoblast invasion and anchorage. MATERIALS AND METHODS: Plasminogen activators (t-PA and u-PA) and their inhibitors (PAI-1 and PAI-2) secretions were assayed in cultures of epithelial, stromal, and trophoblast cells. These cells were also cultured on a fibrin substrate for microscopic examination of the fibrinolytic degradation. RESULTS: The u-PA from epithelial cells was predominant among PAs and PAI-1 in endometrial cells. Estradiol (E2) enhanced t-PA production in stromal cells and PAI-1 production in epithelial cells. Progesterone (P4) suppressed u-PA production in epithelial cells and enhanced PAI-1 production in both epithelial and stromal cells. Trophoblasts produced PAI-1, PAI-2, and small quantities of t-PA and u-PA, none of which were notably influenced by E2 or P4. The PAI-1 production in trophoblasts was more than four-fold greater than the u-PA production in epithelial cells. Epithelial and stromal cells initially grew on fibrin substrate but were gradually detached from the substrate with fibrinolytic degradation, with the exception of the stromal cells grown in the presence of P4 (or E2+P4). Trophoblasts grew well on fibrin substrate without fibrinolytic degradation both in the presence and absence of the steroids tested. CONCLUSIONS: Fibrinolytic balance seemed to be basically maintained between the endometrial PAs and the relative excess of trophoblasts-derived PAI-1. This balance might be regulated principally by P4 and focally by E2 in the endometrial tissue for placental implantation.
