A Potential Mechanism of Breakthrough Bleeding Associated with Progestin: Involvement in Alteration of Endometrial Endothelial Cells
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Progestin combined with estradiol increased urokinase-type plasminogen activator and inhibited apoptosis and cell death in endometrial endothelial cells, potentially explaining breakthrough bleeding.
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Abstract
OBJECTIVE: To explore the potential mechanism of breakthrough bleeding associated with progestin with in vitro methods. METHODS: The isolation and culture of human endometrial endothelial cells (HEECs) was performed with the method established in our laboratory. The content and activity of urokinase-type plasminogen activator (uPA) and the content of plasminogen activator inhibitor-1 (PAI-1) in cell supernatants after incubated with different concentrations of progesterone (0-5 micromol/L) and 17beta-estradiol (0, 0.1, or 1 nmol/L) were measured by method of ELISA. Apoptosis rate of HEECs was measured by flow cytometry. Viable cell count was measured by MTT. RESULTS: The increased level of progesterone (0.5-5 micromol/L) combined with 17beta-estradiol elevated content and activity of uPA while the production of PAI-1 remained unchanged. The apoptosis of HEECs was inhibited along with the increment of total viable cell counts at higher concentrations of progesterone with 17beta-estradiol. CONCLUSION: The inhibition of apoptosis and increased content and activity of uPA may contribute to the occurrence of irregular bleeding associated with progestin use to some extent
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