Contribution of aquaporins in the transamniotic water flux.

We explored the contribution of each aquaporin (AQP) expressed in human amnion in the transcellular water flux across the human amnion. Human amnion was placed between two lucite chambers and net water transport (Jw) was recorded by applying a hydrostatic (7 cm H2O) and an osmotic (40 mOsm PEG 8000) pressure gradients. The hydrostatic (Phydr) and osmotic (POsm) permeabilities were calculated before and after the blocking of AQPs. Phdr showed no significant difference after the blocking of AQPs, while POsm was dramatically reduced. Interestingly, we also found that the blocking of AQP1 produced the highest decrease of POsm (80 ± 1%). Our results strongly suggested that AQP1 seems to contribute more to the maintenance of AF volume homeostasis.

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

Accumulated evidence suggests that an abnormal placentation and an altered expression of a variety of trophoblast transporters are 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 processes required 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 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 apoptotic 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 leading to the clinical manifestations of preeclampsia.