May insufficient oxygenation be responsible for the molecular changes in syncyciotrophoblast transport proteins in preeclampsia?

SZPILBARG NATALIA; DIETRICH VALERIA; ZOTTA ELSA; FARINA MARIANA; DAMIANO ALICIA E

Santiago

Congreso; International Federation of Placenta Associations Meeting 2010; 2010

International Federation of Placenta Associations

Increasing evidence indicates that O2 is a key regulator of trophoblast differentiation, and contributes to placental disease such as preeclampsia. It has been proposed that intermittent placental perfusion, secondary to deficient trophoblast invasion of the endometrial arteries, leads to an ischemia-reperfusion [hypoxia-reoxygenation] type insult in preeclamptic placentas. Such variations in oxygenation can further alter the syncyciotrophoblast transport functions.We have previously reported that AQP9 protein expression increased in preeclamptic placentas while AQP3 and CFTR decreased. Consistent with earlier reports, we also demonstrated that alterations in CFTR protein may affect transcellular water transport. Here, we are focused on establishing if different O2 tensions may alter the expression of AQP3, AQP9 and CFTR in human placentas. In placental explants we demonstrated that changes in oxygen tension may be responsible for the dysregulation of these proteins.We found that the expression of these proteins in explants cultured under hypoxia-reoxygenation conditions showed a similar pattern to that observed in preeclamptic placentas, suggesting that insufficient oxygenation may be responsible for the altered expression of these transport proteins in preeclampsia.