INVESTIGADORES
SZPILBARG Natalia
congresos y reuniones científicas
Título:
New insights into the role of placental aquaporins and the pathogenesis of preeclampsia.
Autor/es:
SZPILBARG NATALIA; RECA ALEJANDRA; CASTRO-PARODI MAURICIO; MARTÍNEZ NORA; DAMIANO ALICIA ERMELINDA
Lugar:
Mar del Plata
Reunión:
Simposio; VI LatinAmerican Symposium on Maternal-Fetal Interaction & Placenta; 2015
Institución organizadora:
SLIMP
Resumen:
Preeclampsia is a pregnancy complication characterized by hypertensionand proteinuria. Although its etiology is unknown, it is considered as atwo-stage disorder. In the first stage, the reduced placental perfusion in some but not all women, could lead to the second stage where thematernal multisystem disorder is established. However, what links bothstages is not determined yet.Since the placenta plays a central role in this syndrome, alterations inplacental functions may contribute to the pathogenesis of preeclampsia.Accumulated evidence suggests that the expression of a variety of syncytiotrophoblast transporters is reduced or abnormal in preeclampticplacentas. In this regard, we have previously reported that the expression of aquaporins (AQPs) is altered. AQPs are involved not only in several physiological processes but also in multiple and diverse clinicaldysfunctions.In other tissues, it has been proposed that AQPs may participate in cellmigration/invasion processes. Therefore, we evaluated the association ofAQPs with these events during placentation. Our results showed thatinhibition of AQPs significantly reduced the migration and invasion oftrophoblast cells. Thus, we proposed that abnormal expression of theseproteins might lead to a shallow trophoblast invasion characteristic ofpreeclamptic placentas. Consequently, placentation takes place underfluctuations of oxygen tension, which are believed to be a potentstimulus for trophoblast apoptosis. Although apoptosis increases progressively throughout pregnancy, it is exacerbated in preeclampticplacentas. Recently, we have established that intermittent hypoxia altersplacental AQPs expression and increases the apoptosis of the trophoblast.Even more, we found that the blocking of placental AQPs abrogatedthese processes, suggesting that AQPs may also have a role inapoptosis.In conclusion, we propose that the abnormal expression of placental AQPs,at early stages of pregnancy, may produce failures in placentation,resulting in an increase of trophoblast apotosis, which finally triggers the clinical manifestations of preeclampsia.