SYNCYTIOTROPHOBLAST STRESS PROMOTES THE RELEASE OF AQP-POSITIVE EXTRACELLULAR VESICLES

SIERRA, MATÍAS; FERNANDEZ, NAZARENA; BERTON, MAGALÍ; CASTRO-PARODI MAURICIO; FERREIROS, ALBERTO; COROMINAS ANA; CASALE, ROBERTO; SZPILBARG NATALIA; DAMIANO ALICIA E

Mar del Plata

Congreso; Reunion Anual de las Sociedades de Biociencias; 2022

SAIC-SAI-SAFIS

Introduction: Preeclampsia is a gestational disorder unique to human pregnancy. Although its etiology remains unclear, this syndrome is associated with placental insufficiency, which increases syncytiotrophoblast stress and the release of extracellular vesicles (EVs). This cellular stress may affect placental transport functions altering the expression of different proteins as aquaporins (AQPs). We previously reported that placental AQPs may have a key role during placentation, and we found an abnormal expression of AQP3, AQP4, andAQP9 in preeclamptic placentas. Recent evidence shows that EVs not only may reflect the state of the tissue from which they come but also, can modulate cell communication. However, the significance of placenta AQP-positive EVs was not studied yet. We hypothesized that syncytiotrophoblast stress promotes the release of AQP-positive EVs that are involved in the etiology of preeclampsia. Objective: To study AQP3, AQP4, and AQP9 expressions in EVs isolated fromplacenta explants exposed to stress. Methods: Normal placental explants were cultured with 100 μM of CoCl2 to induce syncytiotrophoblast stress. After incubations, a histological examination of the explants was performed to evaluate tissue integrity and quantify syncytial nuclear aggregates (SNA). EVs from the culture medium were isolated by differential centrifugation and analyzed in Zetasizer Nano-ZSP equipment. AQP3, AQP4, AQP9, and PLAP expressionwere assessed by Western blot. Results: CoCl2 treatment enhanced the number of SNA (p