INVESTIGADORES
SZPILBARG Natalia
congresos y reuniones científicas
Título:
NEW INSIGHTS INTO THE PATHOGENESIS OF PREECLAMPSIA: THE ROLE OF PLACENTAL AQUAPORINS
Autor/es:
MARTÍNEZ NORA; RECA ALEJANDRA; SZPILBARG NATALIA; MASKIN BERNARDO; CASTRO-PARODI MAURICIO; FARINA MARIANA; DAMIANO ALICIA ERMELINDA
Lugar:
Puerto Varas
Reunión:
Congreso; SLIMP 2017; 2017
Institución organizadora:
SLIMP
Resumen:
Although the etiology of preeclampsia remains uncertain, it is well-knownthat the placenta plays a central role in the pathophysiology of this syndrome.Abnormal syncytiotrophoblast differentiation and altered expressionof a variety of trophoblast transporters were associated withpreeclampsia. Although differentiation into syncytium results in adecrease of caveolin-1 and a marked reduction of caveolas, in placentasfrom women with preeclampsia we found no expression of caveolin-1which correlated to changes in the membrane lipid composition oftrophoblast. Caveolin-1/caveolas domains orchestrate different cellularevents such as migration. In addition, we previously reported that theexpression and function of aquaporins (AQPs) are also altered in theplacenta from preeclampsia. However, preeclampsia is not known to beassociated with an altered foeto-maternal water flux. Recently, AQPs wereproposed to have cellular unexpected roles. In this context, we found thatplacental AQPs may be involved in the apoptosis of the trophoblast andtheir dysregulation may be associated to an increase of the apoptoticevents in preeclampsia. However, our findings are related to term placentaswhen this disorder is well established. Therefore, we evaluated theroles of AQPs and caveolin-1/caveolas during the early stages of placentaldevelopment. Our results showed that inhibition of AQPs and the lipid raftdisruption significantly attenuates migration of trophoblast cells. In allcases, metalloproteinases expression and function was not modified andinvasion process was unaltered. Thus, we proposed that abnormalexpression of these proteins might produce failures in placentation,resulting in an increase of trophoblast apoptosis, which finally triggers theclinical manifestations of preeclampsia.