title: A biological model for the regulation of peri-implantational hemostasis and menstruation.
abstract: OBJECTIVE
  To delineate the physiologic mechanisms whereby the human endometrium maintains hemostasis during endovascular trophoblast invasion but permits menstrual hemorrhage.
  
  
  METHODS
  Experimental results are presented that are relevant to developing a comprehensive biological model for studying peri-implantational hemostasis and menstruation.
  
  
  RESULTS
  A marked increase in the expression of tissue factor (TF) and type-1 plasminogen activator inhibitor (PAI-1) and an inhibition of tissue-type and urokinase-type plasminogen activators (tPA and uPA, respectively), matrix metalloproteinases (MMP), and endothelin-1 (ET-1) expression accompany progestin-induced decidualization of estrogen-primed endometrial stromal cells both in vivo and in vitro. The presence of these important regulators of hemostasis, fibrinolysis, extracellular matrix (ECM) turnover, and vascular tone in decidualized human stromal cells and decidual cells isolated from gestational endometrium suggests a mechanism to explain the absence of hemorrhage during invasion of the endometrial vasculature by trophoblasts. Conversely, progesterone withdrawal reduces TF and PAI-1 expression and increases tPA, uPA, MMP, and ET-1 expression accounting for the hemorrhage, enhanced fibrinolysis, ECM degradation, and ischemic spiral arterial vascular injury characterizing menstruation.
  
  
  CONCLUSIONS
  Perivascular decidualized endometrial stromal cells are spatially and temporally positioned to promote endometrial hemostasis during implantation but, paradoxically, promote the hemorrhage of menstruation via their hormone-regulated expression of hemostatic, proteolytic, and vasoactive proteins.
authors.affiliation: Department of Obstetrics and Gynecology, New York University School of Medicine, New York, USA.
authors.forename: C J
authors.initials: CJ
authors.lastname: Lockwood
authors.forename: F
authors.initials: F
authors.lastname: Schatz
mesh_terms: D010064:Embryo Implantation; D004717:Endometrium / Q000502:physiology*; D016232:Endothelins / Q000096:biosynthesis; D004967:Estrogens / Q000502:physiology; D005260:Female; D005342:Fibrinolysis; D015870:Gene Expression; D006487:Hemostasis; D006706:Homeostasis; D006801:Humans; D008598:Menstruation / Q000502:physiology*; D008666:Metalloendopeptidases / Q000096:biosynthesis; D008954:Models, Biological; D017395:Plasminogen Activator Inhibitor 1 / Q000096:biosynthesis; D011247:Pregnancy; D011372:Progestins / Q000502:physiology; D013925:Thromboplastin / Q000096:biosynthesis; D010959:Tissue Plasminogen Activator / Q000096:biosynthesis; D014327:Trophoblasts / Q000502:physiology; D014568:Urokinase-Type Plasminogen Activator / Q000096:biosynthesis
chemical_list: D016232:Endothelins; D004967:Estrogens; D017395:Plasminogen Activator Inhibitor 1; D011372:Progestins; D013925:Thromboplastin; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator; D008666:Metalloendopeptidases