Expression of CFTR in preeclamptic placentas

LEVI LORENA; CASTRO-PARODI MAURICIO; DIETRICH VALERIA; MASKIN BERNARDO; ZOTTA ELSA; DAMIANO ALICIA E

Seggau Castle, Austria

Congreso; International Federation of Placental Associations Meeting 2008 / 12th European Placental Group Conference; 2008

International Federation of Placental Associations

INTRODUCTION: Preeclampsia (PE) is a hypertensive disorder unique to human pregnancy. Its cause remains unknown but altered placental villous angiogenesis and poorly developed fetoplacental vasculature can affect the transport functions of the syncytiotrophoblast (hST).Previously, we reported an increase AQP9 molecular expression in preeclamptic placentas, with a decrease of water unidirectional fluxes. There is strong evidence that cystic fibrosis transmembrane conductance regulator (CFTR) regulates AQP9 functionality. OBJECTIVE: Here, we investigated if AQP9 lack of activity in PE is associated with alterations in CFTR expression. METHODS: We determined the expression and co-localization of CFTR and AQP9 in normal and preeclamptic placentas by Western Blot and immunohistochemistry. Water uptake experiments were performed using explants from human normal term placentas, treated with CFTR inhibitors. RESULTS: In PE, we demonstrated by molecular biology that CFTR expression decreased in preeclamptic placentas and it did not co- localize with AQP9. Fuctional experiments showed that water uptake decreased after inhibition of CFTR. CONCLUSIONS: These results suggest that the CFTR expression is needed to regulate AQP9 activity.