Abstract
17β-estradiol following binding to estrogen receptor alpha (ERα) exerts a critical role in the control of reproduction, acting through both nuclear and membrane-initiated signaling. To study the physiological role of membrane ERα in the reproductive system, we used the C451A-ERα mouse model with selective loss-of-function of membrane ERα. Despite C451A-ERα mice being described as sterile, daily weighing and ultrasound imaging revealed that homozygous females do get pregnant, allowing to investigate the role of ERα during pregnancy for the first time. Total neonatal deaths of the mice offspring resulted from delayed parturition associated with failure in pre-term progesterone withdrawal. Moreover, pregnant C451A-ERα females exhibit partial intrauterine embryo arrest at about E9.5. The observed embryonic lethality results from altered expansion of Tpbpa-positive spiral artery-associated trophoblast giant cells (SpA-TGCs) into the utero-placental unit, associated with the imbalance expression of angiogenic factors, together controlling the trophoblast-mediated spiral arterial remodeling. Hence, maternal loss of membrane ERα function clearly alters the activity of invasive trophoblast cells during placentogenesis. This novel function of membrane ERα could open new avenues towards a better understanding of human pregnancy-associated pathologies.
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