CONICET | Buscador de Institutos y Recursos Humanos

Preeclampsia is a pregnancy complication characterized by hypertension and proteinuria. Although its etiology remains uncertain, it is considered as a two-stage disorder. In the first stage, the reduced placental perfusion, in some, but not in all women, could lead to the second stage where the maternal multisystem disorder is established. However, what links both stages is not determined yet.Consequently, it is well-accepted that the placenta plays an essential role in the pathophysiology of this syndrome. Accumulated evidence suggests that an abnormal placentation and an altered expression of a variety of trophoblast transporters were associated to preeclampsia. In this regard, we have previously reported that the expression and function of aquaporins (AQPs) are altered in preeclamptic placentas. However, preeclampsia is not known to be associated with an altered feto-maternal water flux. Recently, AQPs were proposed to have cellular unexpected roles. In this context, we found that placental AQPs may be involved in the apoptosis of the trophoblast. Thus, their dysregulation may be associated to the increase of the apoptotic events observed in preeclampsia. However, our findings are related to term placentas when this disorder is well established. Thus, we evaluated the roles of AQPs during the early stages of placental development. Our findings showed that the inhibition of AQP3 significantly attenuates migration of trophoblast cells. In all cases, metalloproteinases expression and function was not modified and invasion process was unaltered. Therefore, we proposed that abnormal expression of placental aquaporins may produce failures in placentation, resulting in an increase of trophoblast apoptosis which finally triggers the clinical manifestations of preeclampsia.