La hipoxia regularia la expresión de CFTR en placenta humana.

SZPILBARG NATALIA; RECA ALEJANDRA; DIETRICH VALERIA; ZOTTA ELSA; DAMIANO ALICIA E

Buenos Aires

Jornada; XII Jornadas anuales de la Sociedad Argentina de Biología; 2010

SAB

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 have previously reported that CFTR (cystic fibrosis transmembrane conductance regulator) is significantly reduced in PE. Our aim is to identify the mechanisms implicated in the regulation of CFTR expression. We hypothesized that generated hypoxia-ischemia observed in preeclampsia may be responsible for the down-regulation in CFTR protein. Explants from normal placenta were cultured in normoxia, hypoxia, and H/R. CFTR expression was analyzed by semiquantitative RT-PCR, Western blot, and immunofluorescence. We observed that CFTR expression decreased significantly in explants cultured under hypoxia conditions. However, H/R treatment did not restore CFTR expression. Immunofluorescence experiments also showed the same results. Our findings provide new evidence suggesting that H/R may be the responsible for CFTR reduced expression in preeclampsia. Further studies are required to clarify the regulation of CFTR in human placenta.