Hypoxia may regulate AQP9 expression in human placenta

DAMIANO AE, CASTRO- PARODI M, LEVI L, FRANCHI A, IBARRA C, FARINA M.

Seggau Castle, Austria

Congreso; International Federation of Placenta Association (IFPA) Meeting: Placenta–Established hypotheses and current concepts; 2008

Preeclampsia is a gestational disorder and it is a important cause of maternal and perinatal morbidity and death. It is characterized by abnormal trophoblast invasion of the spiral arteries leading to a relatively hypoxic trophoblast tissue, attenuating considerably the syncyciotrophoblast synthesis and transport functions. We previously observed in preeclamptic placenta an increase of AQP-9 protein expression, with a lack of functionality. Up to now, the mechanisms of AQP-9 regulation and its rol in human placenta remain unknown. OBJECTIVE: Our aim is to identify the mechanisms implicated in the regulation of the expression of AQP-9. We hypothesized that generated hypoxia-ischemia and/or the augmented hypoxia inducible factor-1á (HIF-1á) observed in this syndrome could be responsible for the up-regulation in AQP9 protein. METHODS: Explants from normal term placenta were incubated in normoxia, hypoxia, and in hypoxia/reoxygenation. Semiquantitative Western blot analysis and immunohistochemistry were performed to study AQP9 and HIF-1a expression. RESULTS: Explants exposed to hypoxia showed an increased of the glycosilated form AQP9. They also expressed HIF-1a. AQP9 was localized in the apical and basal membranes and in citoplasmatic regions. Explants exposed hypoxia/reoxygenation showed a similar expression of AQP9. In both cases, it was located in the apical and basal membranes. CONCLUSIONS: Our results provide new evidence to suggest that hypoxia and HIF-1a would be the responsible for AQP9 over-expression in preeclampsia. Further studies are required to clarify the regulation of AQP9 in human placenta.