Importancia de las acuaporinas placentarias en la fisiopatología de la preeclampsia.

SZPILBARG NATALIA; DAMIANO, ALICIA E

San Javier, Tucuman

Congreso; Reunión Anual de la Sociedad de Biofisica.; 2012

SAB

It has been proposed that intermittent placental perfusion, secondary to deficient trophoblast invasion of the spiral arteries, leads to an ischemia-reperfusion type insult in preeclamptic (PE) placentas. Such variations in oxygenation can further alter placental transport functions. Previously we reported that AQP3 and AQP9 are highly expressed in normal placentas. In subsequent experiments, we found that AQP3 decreased while AQP9 showed an overexpression in PE placentas, with a lack of functionality for water transport. Recently, we found that placental intermittent oxygenation may be responsible for the altered AQPs expression. Moreover, water transport mediated by placental AQPs seems to be independent of its molecular expression, strongly suggesting that AQPs might not have a key role in water transport in human placenta. Recently, AQPs have been associated with cell shrinkage process during apoptosis. Although apoptosis increases progressively throughout pregnancy, it is exaggerated in PE placentas. Our aim was to determine whether alterations in the expression of AQPs in PE placentas are related to apoptosis. Term placental explants were cultured in different O2 tensions. AQP3 and AQP9 molecular expression and water flux were analyzed. After inhibition of AQPs by HgCl2, Hoechst staining, Bax expression, DNA fragmentation and Caspase-3 activity were evaluated. In explants exposed to hypoxia followed by reoxygenation, AQPs expression and functionality showed the same pattern to that previously observed in PE placentas. Interestingly, mercurial inhibition of AQPs resulted in a decrease in all apoptosis parameters studied. Our results suggest that placental AQPs may be involved in apoptosis. It is possible that the reduce transcellular water transport that we observed in PE placentas may be linked to the fact that, after cell shrinkage process, AQPs are inactivated. Therefore, the dysregulation of AQPs in preeclampsia may be one of the causes of the exacerbated apoptotic events which at last lead to the clinical manifestations of this gestational hypertensive disorder.