A biological model for the regulation of peri-implantational hemostasis and menstruation.
作者： Charles J. Lockwood , Frederick Schatz
DOI: 10.1177/107155769600300401
关键词: Andrology 、 Plasminogen activator 、 Decidual cells 、 Extracellular matrix 、 Decidualization 、 Biology 、 Stromal cell 、 Endocrinology 、 Hemostasis 、 Fibrinolysis 、 Endometrium 、 Internal medicine
摘要: Objective To delineate the physiologic mechanisms whereby human endometrium maintains hemostasis during endovascular trophoblast invasion but permits menstrual hemorrhage. Methods Experimental results are presented that relevant to developing a comprehensive biological model for studying peri-implantational and menstruation. Results A marked increase in expression of tissue factor (TF) type-1 plasminogen activator inhibitor (PAI-1) an inhibition tissue-type urokinase-type activators (tPA uPA, respectively), matrix metalloproteinases (MMP), endothelin-1 (ET-1) accompany progestin-induced decidualization estrogen-primed endometrial stromal cells both vivo vitro. The presence these important regulators hemostasis, fibrinolysis, extracellular (ECM) turnover, vascular tone decidualized decidual isolated from gestational suggests mechanism explain absence hemorrhage vasculature by trophoblasts. Conversely, progesterone withdrawal reduces TF PAI-1 increases tPA, MMP, ET-1 accounting hemorrhage, enhanced ECM degradation, ischemic spiral arterial injury characterizing Conclusion Perivascular spatially temporally positioned promote implantation but, paradoxically, menstruation via their hormone-regulated hemostatic, proteolytic, vasoactive proteins.
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