Abstract
Essential features of endometrial physiology involve the extracellular matrix (ECM). In the pathogenesis of endometriosis, interactions of endometriosis cells with ECM can be postulated. Two systems of secreted proteases in the endometrium, the plasmin(ogen) activator/inhibitor and the matrix metalloproteinases and their inhibitors were examined in cell cultures of uterine endometrial cells from women with and without endometriosis. Soluble urokinase receptor secretion is increased, and mRNA transcription of tissue inhibitor of metalloproteinases-2 (TIMP-2) is upregulated by progestin in endometriosis. These findings are compatible with an altered ECM turnover in the endometrium of these patients that may explain a higher invasive potential of retrogradely menstruated endometrial fragments.
MeSH terms
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Cells, Cultured
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Endometriosis / etiology
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Endometriosis / pathology
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Endometriosis / physiopathology*
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Endometrium / cytology
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Endometrium / pathology*
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Endometrium / physiology
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Endometrium / physiopathology*
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Endopeptidases / genetics
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Endopeptidases / metabolism*
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Extracellular Matrix / pathology
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Extracellular Matrix / physiology*
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Female
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Gene Expression Regulation*
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Humans
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Plasminogen Activator Inhibitor 1 / genetics
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Plasminogen Activator Inhibitor 1 / metabolism
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Plasminogen Activator Inhibitor 2 / genetics
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Plasminogen Activator Inhibitor 2 / metabolism
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Tissue Inhibitor of Metalloproteinase-2 / genetics
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Transcription, Genetic
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Urokinase-Type Plasminogen Activator / genetics
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Urokinase-Type Plasminogen Activator / metabolism
Substances
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Plasminogen Activator Inhibitor 1
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Plasminogen Activator Inhibitor 2
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Tissue Inhibitor of Metalloproteinase-2
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Endopeptidases
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Urokinase-Type Plasminogen Activator