IFIBIO HOUSSAY   25014
INSTITUTO DE FISIOLOGIA Y BIOFISICA BERNARDO HOUSSAY
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
New insights into the pathogenesis of preeclampsia: the role of placental aquaporins
Autor/es:
SZPILBARG NATALIA; FARINA MARIANA; MARTINEZ, NORA; MASKIN BERNARDO; DAMIANO, ALICIA E; RECA ALEJANDRA; CASTRO-PARODI MAURICIO
Lugar:
Puerto Varas
Reunión:
Simposio; VII LatinAmerican Symposium on Maternal-Fetal Interaction & Placenta; 2017
Institución organizadora:
SLIMP
Resumen:
Although the etiology of preeclampsia remains uncertain, it is well-known that the placenta plays a central role in the pathophysiology of this syndrome. Abnormal syncytiotrophoblast differentiation and altered expression of a variety of trophoblast transporters were associated with preeclampsia. Although differentiation into syncytium results in a decrease of caveolin-1 and a marked reduction of caveolas, in placentas from women with preeclampsia we found no expression of caveolin-1 which correlated to changes in the membrane lipid composition of trophoblast. Caveolin-1/caveolas domains orchestrate different cellular events such as migration. In addition, we previously reported that the expression and function of aquaporins (AQPs) are also altered in the placenta from preeclampsia. However, preeclampsia is not known to be associated with an altered foeto-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 and their dysregulation may be associated to an increase of the apoptotic events in preeclampsia. However, our findings are related to term placentas when this disorder is well established. Therefore, we evaluated the roles of AQPs and caveolin-1/caveolas during the early stages of placental development. Our results showed that inhibition of AQPs and the lipid raft disruption significantly attenuates migration of trophoblast cells. In all cases, metalloproteinases expression and function was not modified and invasion process was unaltered. Thus, we proposed that abnormal expression of these proteins may produce failures in placentation, resulting in an increase of trophoblast apoptosis which finally triggers the clinical manifestations of preeclampsia.