Abstract #1504468: Estrogen Attenuates Ferroptosis via Estrogen Receptor (ER) β/ERα/Lipocalin 2 Pathway in Endometriosis

Endometriosis is an estrogen-dependent gynecologic disease, which characterized by the elevated ratio of ERβ/ERα expression. Retrograde menstruation leads to ectopic erythrocytes deposition and iron overload at pelvic cavity in endometriosis. Lipocalin 2 (LCN2) a secretory protein that plays important role during transport metabolism. To date, relationship estrogen homeostasis not well studied yet. The aim our study was investigate regulating metabolism Sixty-eight women with endometriosis forty-three without (controls) were included, their serum levels estrodiol LCN2 determined for via ELISA. Primary cultures ESCs obtained vitro. expression receptor (ER) α, ERβ, examined qPCR, western blot, ChIP used how ER regulated LCN2. Cell viability assessed Counting Kit-8 assay. Reactive oxygen species production evaluated dihydroethidium staining. In addition, intracellular ferrous level (Fe2+ ) using assay kit. Ferroptosis Cyclooxygenase-2(COX-2), Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4), glutathione peroxidase (GPX4) ferritin heavy chain 1(FTH1). Elevated found compared those without. A positive correlation E2 observed group but controls. dose-dependently increased ESCs. This also seen presence ERα antagonist alone ERβ alone. Interestingly, bind promoter attenuated Moreover, E2-induced resulted concentrations. Importantly, GPX4 FTH1 expression, COX-2 ACSL4 levels, turn inhibited ferroptosis inhibition effect can be partly reversed or overexpression ERα. Our studies demonstrate upregulated may inhibit ERβ/ERα/ pathway, potentially endometriotic tissue survival progression, ERβ/ERα/LCN pathway potential target treatment.