New Insights Into the Role of Placental Aquaporins and the Pathogenesis of Preeclampsia

SZPILBARG N.; MARTÍNEZ N.; DI PAOLA M.; REPPETTI J.; MEDINA Y.; SEYAHIAN A.; CASTRO PARODI M.; DAMIANO A. E.

VASCULAR DYSFUNCTION BEYOND PATHOLOGICAL PREGNANCIES. AN INTERNATIONAL EFFORT ADDRESSED TO FILL THE GAPS IN LATIN AMERICA

Frontiers Media SA

Año: 2019; p. 79 - 85

New Insights Into the Role ofPlacental Aquaporins and thePathogenesis of PreeclampsiaNatalia Szpilbarg1, Nora A. Martínez1, Mauricio Di Paola1,2, Julieta Reppetti1,Yollyseth Medina1, Abril Seyahian1, Mauricio Castro Parodi2 and Alicia E. Damiano1,2*on behalf of Red Iberoamericana de alteraciones Vasculares Asociadas aTrastornos del Embarazo (RIVATREM)1 Laboratorio de Biología de la Reproducción, Instituto de Fisiología y Biofísica Bernardo Houssay (IFIBIO)-UBA-CONICET,Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina, 2 Cátedra de Biología Celular y Molecular,Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires,ArgentinaAccumulated evidence suggests that an abnormal placentation and an alteredexpression of a variety of trophoblast transporters are associated to preeclampsia. In thisregard, an abnormal expression of AQP3 and AQP9 was reported in these placentas.Recent data suggests that placental AQPs are not only water channel proteins and thatmay participate in relevant processes required for a normal placental development, suchas cell migration and apoptosis. Recently we reported that a normal expression of AQP3is required for the migration of extravillous trophoblast (EVT) cells. Thus, alterations inthis protein might lead to an insufficient transformation of the maternal spiral arteriesresulting in fluctuations of oxygen tension, a potent stimulus for oxidative damage andtrophoblast apoptosis. In this context, the increase of oxygen and nitrogen reactivespecies could nitrate AQP9, producing the accumulation of a non-functional proteinaffecting the survival of the villous trophoblast (VT). This may trigger the exacerbatedrelease of apoptotic VT fragments into maternal circulation producing the systemicendothelial dysfunction underlying the maternal syndrome. Therefore, our hypothesis isthat the alteration in the expression of placental AQPs observed at the end of gestationmay take place during the trophoblast stem cell differentiation, disturbing both EVT andVT cells development, or during the VT differentiation and turnover. In both situations,VT is affected and at last the maternal vascular system is activated leading to the clinicalmanifestations of preeclampsia.Keywords: extravillous trophoblast, villous trophoblast, AQP3, AQP9, human placenta, preeclampsia