Possible role of AQP3 in the etiology of preeclampsia

SZPILBARG, NATALIA

Santiago de Chile

Congreso; Joint meeting SCHCF + ALACF 2020; 2020

Sociedad chilena de Ciencias Fisiológicas + Asociación Latinoamericana de Ciencias Fisiológicas

Preeclampsia affects 7?10% of pregnancies worldwide. It is characterized by hypertension and proteinuria after 20 weeks of gestation. The most severe form develops before 34 weeks of gestation and is associated with intrauterine growth restriction, alterations in trophoblast migration processes, and incomplete perfusion of the placenta. Furthermore, trophoblast apoptosis levels are elevated, leading to the development of clinical symptoms. Aquaporin-3 (AQP3) is expressed in human placenta from the onset to term gestation. Our objective was to study AQP3 expression in preeclamptic placentas and its role in processes related to the pathophysiology of preeclampsia, such as trophoblast migration in the first trimester and trophoblast apoptosis in the third trimester of pregnancy. Furthermore, we studied the possible association of AQP3 with caveolin-1 in the first trimester, since this protein is essential to generate the appropriate membrane domains for cell migration.This project was approved by the ethics committee of the Hospital Nacional ¨Prof. Dr. Alejandro Posadas¨ in Buenos Aires. AQP3 expression was analyzed in normal and preeclamptic term placentas. Additionally, an in vitro model of preeclampsia was used for apoptosis experiments in the third trimester. Finally, Swan 71 cell line was used for migration experiments and AQP3 and caveolin-1 association experiments in first trimester. The results showed that AQP3 is reduced in term preeclamptic placentas and that it participates in trophoblast migration and apoptosis in the first and third trimester respectively. Additionally, AQP3 colocalized with caveolin-1 in the first trimester, suggesting that this interaction may be necessary during placentation.In conclusion, further experiments are necessary to determine if the reduction of AQP3 comes from the beginning of pregnancy, being one possible cause of insufficient trophoblast migration in preeclampsia, or if it is a consequence of the increase in apoptotic levels as an attempt by the trophoblast to reduce damage.