Artículos de revistas
Multiparity upregulates placental plasminogen and urokinase-type plasminogen activator
Fecha
2017-04Registro en:
Cortina, María Eugenia; Litwin, Silvana; Rial Hawila, María Rocío; Miranda, Silvia Esther; Multiparity upregulates placental plasminogen and urokinase-type plasminogen activator; Wiley Blackwell Publishing, Inc; American Journal of Reproductive Immunology; 77; 4; 4-2017; 1-10; e12633
1046-7408
CONICET Digital
CONICET
Autor
Cortina, María Eugenia
Litwin, Silvana
Rial Hawila, María Rocío
Miranda, Silvia Esther
Resumen
Problem: Multiparity increased the number of trophoblast cells in decidua of both low and high fetal loss mouse models. However, they differ in fetal survival rate and maternal thymocyte subpopulations, suggesting that trophoblast invasiveness is not equivalent. Our aim was to explore the involved mechanism. Method of study: We studied placentae from primiparous and multiparous females of low and high fetal loss models. We investigated invasiveness in vitro, expression of plasminogen, and its activators: tissue type (tPA)‐urokinase type (uPA), and activity and expression of matrix metalloproteinases (MMP)‐2 and MMP‐9. Results: Placental invasiveness is upregulated by multiparity, but lesser in the high fetal loss model. Multiparous animals showed elevated expression of plasminogen and uPA. However, the high fetal loss combination showed higher expression of a short and less active fragment of uPA (LMW‐uPA). MMP‐2, MMP‐9, and tPA were unaffected. Conclusion: uPA would participate in the increased multiparity‐associated placental invasiveness.