The journal of obstetrics and gynaecology research · 2025
Estradiol regulates MBOAT1-mediated ferroptosis and participates in the progression of endometriosis.
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Fang Yu-Qing, Li Yan-Hui, Li Jing-Yi, Wang Xiu-Ping, Zhang Han-Ke, Wang Hua-Jing, Liu Yi, Zhang Ling
Аннотация
AIM: Endometriosis is an estrogen-dependent disease with unclear pathogenesis. Recent evidence suggests that ferroptosis plays an important role in the development of endometriosis. In this study, we aimed to explore whether membrane-bound O-acyltransferase domain-containing 1 (MBOAT1) is a key factor by which estradiol (E2) regulates ferroptosis in endometriosis.
METHODS: The expression of estrogen receptors (ESR1 and ESR2) and MBOAT1 was examined by western blotting in endometrium and primary endometrial stromal cells (ESCs). We measured iron content, MDA, and GSH levels using corresponding assay kits and assessed the level of ROS by flow cytometry to evaluate ferroptosis. We treated primary ESCs and human ESCs (T HESCs) with or without RSL3, E2, and an estrogen receptor inhibitor, fulvestrant (Ful), to verify the regulatory relationship between E2 and ferroptosis. In addition, endometriosis model mice were constructed and treated with an intraperitoneal injection of 5 mg/kg Ful once a day for 2 weeks.
RESULTS: Ectopic ESCs (EESCs) showed increased expression of ESR1, ESR2, and MBOAT1. Meanwhile, EESCs demonstrated resistance to ferroptosis compared with normal ESCs (NESCs). Compared with NESCs, EESCs showed significant resistance to RSL3-induced ferroptosis. E2 could up-regulate the expression of MBOAT1 and alleviate RSL3-induced ferroptosis in NESCs, while Ful could down-regulate the expression of MBOAT1 and accelerate RSL3-induced ferroptosis in EESCs. Furthermore, Ful treatment significantly decreased the number and size of ectopic lesions in endometriosis mice by promoting ferroptosis.
CONCLUSION: E2 affected ferroptosis by regulating the expression of MBOAT1 and further participated in the progression of endometriosis.
METHODS: The expression of estrogen receptors (ESR1 and ESR2) and MBOAT1 was examined by western blotting in endometrium and primary endometrial stromal cells (ESCs). We measured iron content, MDA, and GSH levels using corresponding assay kits and assessed the level of ROS by flow cytometry to evaluate ferroptosis. We treated primary ESCs and human ESCs (T HESCs) with or without RSL3, E2, and an estrogen receptor inhibitor, fulvestrant (Ful), to verify the regulatory relationship between E2 and ferroptosis. In addition, endometriosis model mice were constructed and treated with an intraperitoneal injection of 5 mg/kg Ful once a day for 2 weeks.
RESULTS: Ectopic ESCs (EESCs) showed increased expression of ESR1, ESR2, and MBOAT1. Meanwhile, EESCs demonstrated resistance to ferroptosis compared with normal ESCs (NESCs). Compared with NESCs, EESCs showed significant resistance to RSL3-induced ferroptosis. E2 could up-regulate the expression of MBOAT1 and alleviate RSL3-induced ferroptosis in NESCs, while Ful could down-regulate the expression of MBOAT1 and accelerate RSL3-induced ferroptosis in EESCs. Furthermore, Ful treatment significantly decreased the number and size of ectopic lesions in endometriosis mice by promoting ferroptosis.
CONCLUSION: E2 affected ferroptosis by regulating the expression of MBOAT1 and further participated in the progression of endometriosis.