AQP9 protein expression in human placenta is regulated by hypoxia

CASTRO-PARODI M; MARINO GI; LEVI L; NOVAK M; FARINA M; DAMIANO AE.

Rosario, Santa Fe

Congreso; XLII Reunón Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2006

Sociedad Argentina de Investigación Bioquímica y Biología Molecular

Normal fetal growth and development is critically dependent on sufficient transport of nutrients, metabolites, ions and water across the placenta. Previously we have reported the expression of aquaglyceroporins (AQP3, AQP7 and AQP9) in human placenta. In particular, we observed over expression of AQP9 in preeclamptic placentas. 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. We have recently reported that AQP9 mRNA expression increased after the induction of HIF-1á, but water uptake decreased. In this work we investigate whether AQP9 protein is regulated by HIF-1a or by other conditions associated to hypoxia. Explants from normal placenta were cultured in normoxia, hypoxia, and chemical hypoxia generated by CoCl2, an HIF-1á inducer. Semiquantitative Western blot and immunohistochesmistry were performed. The biochemical viability of the explants was determined by â-hCG. In hypoxia conditions AQP9 protein expression was higher that in normoxia. Interestingly after CoCl2 treatment AQP9 protein level significantly decreased. Our results provide new evidence to suggest that hypoxia but not 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.