INVESTIGADORES
DAMIANO Alicia Ermelinda
congresos y reuniones científicas
Título:
Hypoxia may regulate AQP9 expression in human placenta
Autor/es:
DAMIANO ALICIA E; CASTRO-PARODI MAURICIO; LEVI LORENA; FRANCHI ANA; IBARRA CRISTINA; FARINA MARIANA
Lugar:
Seggau Castle, Austria
Reunión:
Congreso; International Federation of Placental Associations Meeting 2008 / 12th European Placental Group Conference; 2008
Institución organizadora:
International Federation of Placental Associations
Resumen:
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-1alfa (HIF-1alfa) 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.