NEW INSIGHTS INTO THE ROLE OF PLACENTAL AQUAPORINS AND THE PATHOGENESIS OF PREECLAMPSIA

SZPILBARG NATALIA; MARTÍNEZ NORA; DI PAOLA MAURICIO; REPPETTI JULIETA; MEDINA YOLLYSETH; SEHAYIAN ABRIL; CASTRO-PARODI MAURICIO; DAMIANO ALICIA ERMELINDA

FRONTIERS IN PHYSIOLOGY

Frontiers Editorial Office

Lugar: Lausanne; Año: 2018 vol. 9

1664-042X

Accumulated evidence suggests that an abnormal placentation and an altered expression of a variety of trophoblast transportersare associated to preeclampsia. In this regard, 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 that may participate in relevant processesrequired for a normal placental development, such as cell migration and apoptosis.Recently we reported that a normal expression of AQP3 is required for the migration of extravillous trophoblast (EVT) cells. Thus,alterations in this protein might lead to an insufficient transformation of the maternal spiral arteries resulting in fluctuations ofoxygen tension, a potent stimulus for oxidative damage and trophoblast apoptosis. In this context, the increase of oxygen andnitrogen reactive species could nitrate AQP9, producing the accumulation of a non-functional protein affecting the survival of thevillous trophoblast (VT). This may trigger the exacerbated release of apoptotic VT fragments into maternal circulation producingthe systemic endothelial dysfunction underlying the maternal syndrome.Therefore, our hypothesis is that the alteration in the expression of placental AQPs observed at the end of gestation may takeplace during the trophoblast stem cell differentiation, disturbing both EVT and VT cells development, or during the VTdifferentiation and turnover. In both situations, VT is affected and at last the maternal vascular system is activated leading to theclinical manifestations of preeclampsia.