CONICET | Buscador de Institutos y Recursos Humanos

NFB signalling on placental leptin expression induced by E2.Malena Schanton, María Fernanda Camisay, Antonio Pérez-Pérez, Bernardo Maskin, Víctor Sánchez Margalet, Alejandra Erlejman and Cecilia Varone. Leptin is a key hormone in placental physiology. It regulates trophoblast proliferation, inhibits apoptosis, stimulates protein synthesis, and regulates fetal growth and development. The mechanisms involved in the regulation of placental leptin expression are not fully understood. Previous results from our lab demonstrated that estradiol (E2) induces leptin expression involving genomic and non-genomic effects. In this study we aimed to analyze the effect of the transcription factor NFB on E2 induction of leptin expression in human placental cells. BeWo cells cultured under standard conditions, as well as human placental explants were used. Western blot, immunoprecipitation and immunocytochemistry were carried out. We found that E2 treatment did not modify p65 expression. However E2 increased IKBphosphorylation suggesting that the transcription factor NFB, might be affecting estradiol leptin induction. We also evaluated the localization of ER and p65 NFB subunit in BeWo cells by immunofluorescence assay. We have found that both proteins are located in the cytoplasm and when they are overexpressed, they migrate to the nucleus. We also analyzed the interaction between ERand p65 by immunoprecipitation. We observed that they probably interact forming a complex as p65 could be revealed in ER immunoprecipitation. All these findings suggest that leptin expression is tightly regulated and improve the comprehension of the mechanisms whereby E2 regulates leptin expression probably involving a cooperative effect between ER and NFB.