{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Arlier S"],"funding":["Eunice Kennedy Shriver National Institute of Child Health and Human Development","NICHD NIH HHS","NIH/NICHD"],"pagination":["10532"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10341894"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(13)"],"pubmed_abstract":["Progestin-only long-acting reversible-contraceptive (pLARC)-exposed endometria displays decidualized human endometrial stromal cells (HESCs) and hyperdilated thin-walled fragile microvessels. The combination of fragile microvessels and enhanced tissue factor levels in decidualized HESCs generates excess thrombin, which contributes to abnormal uterine bleeding (AUB) by inducing inflammation, aberrant angiogenesis, and proteolysis. The- zinc finger and BTB domain containing 16 (ZBTB16) has been reported as an essential regulator of decidualization. Microarray studies have demonstrated that <i>ZBTB16</i> levels are induced by medroxyprogesterone acetate (MPA) and etonogestrel (ETO) in cultured HESCs. We hypothesized that pLARC-induced ZBTB16 expression contributes to HESC decidualization, whe"],"journal":["International journal of molecular sciences"],"pubmed_title":["Enhanced ZBTB16 Levels by Progestin-Only Contraceptives Induces Decidualization and Inflammation."],"pmcid":["PMC10341894"],"funding_grant_id":["RO1 HD 033937","R01 HD033937"],"pubmed_authors":["Semerci N","Lockwood CJ","Guzeloglu-Kayisli O","Ozmen A","Larsen K","Schatz F","Arlier S","Kayisli UA"],"additional_accession":[]},"is_claimable":false,"name":"Enhanced ZBTB16 Levels by Progestin-Only Contraceptives Induces Decidualization and Inflammation.","description":"Progestin-only long-acting reversible-contraceptive (pLARC)-exposed endometria displays decidualized human endometrial stromal cells (HESCs) and hyperdilated thin-walled fragile microvessels. The combination of fragile microvessels and enhanced tissue factor levels in decidualized HESCs generates excess thrombin, which contributes to abnormal uterine bleeding (AUB) by inducing inflammation, aberrant angiogenesis, and proteolysis. The- zinc finger and BTB domain containing 16 (ZBTB16) has been reported as an essential regulator of decidualization. Microarray studies have demonstrated that <i>ZBTB16</i> levels are induced by medroxyprogesterone acetate (MPA) and etonogestrel (ETO) in cultured HESCs. We hypothesized that pLARC-induced ZBTB16 expression contributes to HESC decidualization, whe","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jun","modification":"2025-07-02T03:04:52.265Z","creation":"2025-04-19T15:59:33.587Z"},"accession":"S-EPMC10341894","cross_references":{"pubmed":["37445713"],"doi":["10.3390/ijms241310532"]}}