IQUIBICEN   23947
INSTITUTO DE QUIMICA BIOLOGICA DE LA FACULTAD DE CIENCIAS EXACTAS Y NATURALES
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
The transcription factor NFB is involved in estradiol leptin induction in placental cells.
Autor/es:
MARIA FERNANDA CAMISAY; SCHANTON, MALENA; VÍCTOR SÁNCHEZ MARGALET; BERNARDO MASKIN; ANTONIO PÉREZ PÉREZ; VARONE, CECILIA; ALEJANDRA ERLEJMAN
Lugar:
Tokio
Reunión:
Congreso; International Federation of Placenta Associations IFPA; 2018
Resumen:
TitleThe transcription factor NFB is involved in estradiol leptin induction in placental cells.Malena Schanton, María Fernanda Camisay, Antonio Pérez-Pérez, Bernardo Maskin, Víctor Sánchez Margalet, Alejandra Erlejman and Cecilia VaroneObjectivesLeptin plays an important role in reproduction mainly it has been suggested to have functions in the placenta during gestation, where leptin and leptin receptors expression were detected. The mechanisms involved in the regulation of placental leptin expression are not fully understood. Previous results from our lab demonstrated that estradiol (E2) regulates leptin expression involving genomic and non-genomic effects. In the present work, we analyzed the influence of the transcription factor NFB on E2 induction of leptin expression in the human placenta.Methods: BeWo cells, cultured and human placental explants were used. Western blot, qRT-PCR, immunocytochemistry, immunoprecipitation and transfection assays were carried out. All procedures were approved by ethical review committee at the Alejandro Posadas National Hospital.Results:We find that basal and induced leptin expression is diminished by sulfasalazine treatment, an inhibitor of the I. Moreover through transient transfection analysis we observed that the overexpression of p65 subunit increases basal transcriptional activity of leptin promoter. On the other hand the overexpression of p65 subunit in BeWo-Sh2 cells that have diminished ER levels by siRNA strategy produces a significant decrease in basal leptin promoter activity. These results suggest that the effect of p65 overexpression is ER dependent. The overexpression of p65would not be affecting estradiol leptin induction neither in the presence or the absence of ERThe subcellular localization of ER and p65 subunit has been evaluated in BeWo cells by immunofluorescence assay. Their possible interaction was assessed by coimmunoprecipitation. We have found that both proteins are located in the cytoplasm and when they are overexpressed, they migrate to the nucleus. They probably interact forming a complex as p65 could be revealed in ER immunoprecipitate. ConclusionAll 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.