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| Our novel discoveries have shown that eutopic endometrial tissue, retrogradely shed menstrual tissue and ectopic endometriotic lesions from women with endometriosis, but not women without endometriosis, produce a uniquely glycosylated form of haptoglobin (eHp). eHp binds to peritoneal macrophages and reduces phagocytic function while eliciting secretion of inflammatory cytokines. This feed forward loop between the endometrium/endometriotic lesions and immune cells in women with endometriosis helps explain why only some women get endometriosis while most women have retrograde menstruation. Mechanisms to block eHp production and/or function may be developed into novel therapeutic approaches to prevent endometriosis and reduce or eliminate endometriotic lesions and the pain and subfertility they cause. |
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Most recently, our endometriosis research team has discovered that tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) produced by endometriotic lesions and interferes with normal ovarian function, embryo implantation and development and endometrial receptivity for embryo implantation. We are currently modulating TIMP-1 in an animal model for endometriosis and have found that TIMP-1 treatment reduces fecundity in control animals while a TIMP-1 blocking agent restores fecundity in rats with endometriosis. |
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We are currently exploring how the reproductive anomalies associated with endometriosis are multigenerational. Epigenetic modifications appear to methylate targeted genes and alter their expression thereby affecting in these mechanisms. |
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