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Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells
Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells
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Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells
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Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells
Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells

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Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells
Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells
Journal Article

Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells

2003
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Overview
We have investigated whether there are any differences in the release of urokinase plasminogen activator (uPA) and its inhibitor (PAI-1) from cultured endometrial and endometriotic stromal cells, and whether the release is regulated by epidermal growth factor (EGF) or transforming growth factor β1 (TGFβ1). The cells were isolated from endometriomas and endometrium from women with and without endometriosis. After treatment with EGF or TGF and in untreated controls, incubated media collected at 0, 24, 48 and 72 h were analyzed by ELISA. Stromal cells from all three types of tissues released uPA and PAI-1, but the soluble receptor of uPA was not measurable in any group. The basal release of uPA and PAI-1 from endometriotic cells was higher than from endometrial cells. The uPA release in endometriotic cells was reduced with and without the addition of EGF (p < 0.05) or TGFβ1 (p < 0.05). EGF increased the release of PAI-1 from stromal cells from women without endometriosis (p < 0.05) but decreased the release of PAI-1 from stromal cells from endometriotic women (p < 0.05). TGFβ1 increased the release of PAI-1 from endometriotic cells (p < 0.05) but had no effect in endometrial cells.