Session: MON 561-585-Ovarian & Uterine Function II
Poster Board MON-582
Methods: Human eSF from participants without uterine pathology (n=5) and from patients with severe (n=5) and mild (n=4) endometriosis were obtained from the NIH UCSF Endometrial Tissue and DNA Bank. Toxicity experiments with TSA concentrations of 250 nM, 500 nM, 1μM, 10 μM, and 100 μM for 12hrs, 24hrs, 48hrs, 72hrs and 96hrs determined 1μM TSA for 72hrs as the maximum-nontoxic treatment regimen based on cellular proliferation assays. Subsequently, cells were treated with E2+P4, vehicle, TSA, or E2+P4plus TSA for 15 days, wherein TSA was administered as a single 3-day treatment or multiple 3-day treatments. Single treatments were applied at day 0 to 3, 6 to 9, or 12 to15. Multiple treatments were applied at day 0 to 3, 6 to 9, and 12 to15 (total 9 days). Decidualization was assessed by IGFBP1 protein level by ELISA.
Results: In controls, E2+P4 induced decidualization after 15 days while vehicle and TSA in single or multiple treatments did not. Also, E2+P4 plus TSA, in single or multiple treatments, did not affect decidualization. Some endometriosis samples decidualized and some did not, independent of stage. In the non-decidualizing group, TSA, alone or together with hormones (in single or multiple treatments) did not rescue decidualization. However, in decidualizing endo samples, multiple treatments of E2+P4plus TSA (but not single treatments), resulted in significantly decreased decidualization, while it was ineffective in controls.
Conclusion: Our data indicate that decidualizing or non-decidualizing endometrium in women with disease represent two subtypes with different histone modifications that is not reflective of disease stage. Further investigation of epigenetic regulation of decidualization in normal and disease endometrium is warranted to better understand the associated sub-fertility in patients with endometriosis.
Nothing to Disclose: SH, JCI, LCG
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