NFΚB SIGNALLING ON PLACENTAL LEPTIN EXPRESSION INDUCED BY ESTRADIOL

CAMISAY M.F.; SANCHEZ MARGALET V.; PERÉZ PERÉZ A.; ERLEJMAN A.G.; SHANTON M.; MASKIN B.; VARONE C.

Mar del Plata

Congreso; LXIII Reunión anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2018

Sociedad Argentina de Investigación Clínica

Leptin is a key hormone in placental physiology. It regulates trophoblastproliferation, inhibits apoptosis, stimulates protein synthesis,and regulates fetal growth and development. The mechanisms involvedin the regulation of placental leptin expression are not fullyunderstood. Previous results from our lab demonstrated that estradiol(E2) induces leptin expression involving genomic and non-genomiceffects. In this study we aimed to analyze the effect of the transcriptionfactor NFκB on E2 induction of leptin expression in humanplacental cells. BeWo cells cultured under standard conditions, aswell as human placental explants were used. Western blot, immunoprecipitationand immunocytochemistry were carried out. We foundthat E2 treatment did not modify p65 expression. However E2 increasedIκBα phosphorylation suggesting that the transcription factorNFκB, might be affecting estradiol leptin induction. We also evaluatedthe localization of ERα and p65 NFκB subunit in BeWo cellsby immunofluorescence assay. We have found that both proteinsare located in the cytoplasm and when they are overexpressed, theymigrate to the nucleus. We also analyzed the interaction betweenERα and p65 by immunoprecipitation. We observed that they probablyinteract forming a complex as p65 could be revealed in ERα immunoprecipitation.All these findings suggest that leptin expressionis tightly regulated and improve the comprehension of the mechanismswhereby E2 regulates leptin expression probably involving acooperative effect between ERα and NFκB.