| First Author | Rusidzé M | Year | 2022 |
| Journal | Development | Volume | 149 |
| Issue | 19 | PubMed ID | 36239412 |
| Mgi Jnum | J:330449 | Mgi Id | MGI:7377806 |
| Doi | 10.1242/dev.200683 | Citation | Rusidze M, et al. (2022) Loss of function of the maternal membrane oestrogen receptor ERalpha alters expansion of trophoblast cells and impacts mouse fertility. Development 149(19):dev200683 |
| abstractText | The binding of 17beta-oestradiol to oestrogen receptor alpha (ERalpha) plays a crucial role in the control of reproduction, acting through both nuclear and membrane-initiated signalling. To study the physiological role of membrane ERalpha in the reproductive system, we used the C451A-ERalpha mouse model with selective loss of function of membrane ERalpha. Despite C451A-ERalpha mice being described as sterile, daily weighing and ultrasound imaging revealed that homozygous females do become pregnant, allowing the investigation of the role of ERalpha during pregnancy for the first time. All neonatal deaths of the mutant offspring mice resulted from delayed parturition associated with failure in pre-term progesterone withdrawal. Moreover, pregnant C451A-ERalpha females exhibited partial intrauterine embryo arrest at about E9.5. The observed embryonic lethality resulted from altered expansion of Tpbpa-positive spiral artery-associated trophoblast giant cells into the utero-placental unit, which is associated with an imbalance in expression of angiogenic factors. Together, these processes control the trophoblast-mediated spiral arterial remodelling. Hence, loss of membrane ERalpha within maternal tissues clearly alters the activity of invasive trophoblast cells during placentogenesis. This previously unreported function of membrane ERalpha could open new avenues towards a better understanding of human pregnancy-associated pathologies. |
