Hypoxia/reoxygenation may alter the expresion of aquaglyceroporins in human placenta.

SZPILBARG N, DIETRICH, V, CASTRO-PARODI M, ZOTTA E, FARINA M, DAMIANO AE.

Geilo

Congreso; International Federation of Placenta Associations (IFPA); 2011

It has been proposed that intermittent placental perfusion, secondary to deficient trophoblast invasion of the endometrial arteries, leads to an ischemia-reperfusion [hypoxia-reoxygenation (H/R)] type insult in preeclamptic placentas (PE). Such variations in oxygenation can further alter the syncyciotrophoblast transport functions. We observed that, in preeclamptic placentas, the molecular expression of aquaporin-3 (AQP3) decreases, while that corresponding to aquaporin-9 AQP9 increases. However, a lack of water transport activity mediated by AQPs was observed. It has also been proposed that H/R leads to an increase in apoptosis in human placenta. Apoptosis starts with the decrease on cell volume (AVD). Although the role of AQPs on apoptosis is related with the AVD, the exact mechanism that triggers the changes in cell volume is still unknown. OBJECTIVES: To establish the effect of H/R on AQP9 and AQP3 expression in human placenta and their possible role in the programmed cell death processes observed. METHODS: Explants from normal placenta were cultured in normoxia, hypoxia, and H/R. Some explants were treated with HgCl2, a general inhibitor of AQPs. AQP3 and AQP9 expression was analyzed by semiquantitative RT-PCR, Western blot, and immunohistochemistry. Apoptosis was evaluated by DNA fragmentation and Bax expression. RESULTS: In explants cultured under H/R conditions we observed that AQP9 expression increased significantly while AQP3 decreased compared with the control, a similar pattern to that observed in PE placentas. Furthermore, in all cases DNA fragmentation was inhibited after treatment with HgCl2. Even though Bax expression increased under H/R treatment it decreased dramatically after AQP blocking. CONCLUSIONS: Our findings show that changes in oxygenation may alter AQPs expression and increase apoptosis indexes in human placenta. We also suggest that AQPs are involved in this event and their inhibition may prevent apoptosis processes.