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

NATALIA SZPILBARG; NORA A MARTINEZ; MAURICIO DI PAOLA; JULIETA REPPETTI; YOLLYSETH MEDINA; ABRIL SEYAHIAN; MAURICIO CASTRO PARODI; ALICIA DAMIANO

Frontiers in Physiology

Frontiers mEDIA s:a:

Año: 2018 vol. 9 p. 1 - 7

1664-042X

Accumulated evidence suggests that an abnormal placentation and an altered expression of a variety of trophoblast transporters are associated to preeclampsia. In this regard, we have previously reported an abnormal expression of AQP3 and AQP9 in these placentas. Described evidence suggests that placental AQPs are not only simple transporting proteins and that may participate in relevant processes required for a normal placental development, such as cell migration and apoptosis.Recently we reported that inhibition of AQP3 significantly reduced the migration of extravillous trophoblast (EVT) cells. This might lead to a shallow trophoblast invasion and poor remodeling of the maternal spiral arteries resulting in fluctuations of oxygen tension, a potent stimulus for oxidative damage and trophoblast apoptosis. In this context, the increase of oxygen and nitrogen reactive species could nitrate AQP9, producing the accumulation of a non-functional protein affecting the survival of the villous trophoblast (VT). This may trigger the exacerbated release of necrotic and aponecrotic VT fragments into maternal circulation producing the 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 take place during the trophoblast stem cell differentiation, disturbing both EVT and VT cells development, or during the VT differentiation and turnover. In both situations, VT is affected and at last the maternal vascular system is activated resulting in the development of the clinical symptoms of preeclampsia.