Placental leptin expression is mediated by NFkB signaling.

SCHANTON MALENA; BERNARDO MASKIN; YESICA GAMBINO; CECILIA VARONE; A. PEREZ PEREZ; V. SANCHEZ MARGALET

Puerto Varas

Congreso; SLIMP 2017-Latin american society for maternal fetal interaction and placental; 2017

Leptin is a key hormone in placental physiology. Previous results demonstrated that estradiol (E2) regulates leptin expression involving genomic and non-genomic effects. Objectives: Considering there is a potential binding site for NFκB between -2850 and -2838bp at the promoter sequence of leptin gene, and taking into account the interaction between ERs and the NFκB factor, we analyzed the involvement of this transcription factor in the effects of E2 on placental leptin expression. Methods: BeWo cells were transiently transfected with the Rel A vector which express the subunit p65, responsible for the activity of NFκB dimers. We performed experiments with placental explants and BeWo cells treated with E2 for 48 hours in presence of sulfasalazine (an Ikk inhibitor), also BeWo-Sh2, were treated with doxycycline, western blot and qRT-PCR were used to explore protein and transcript expression.Results: The expression of subunits p65 decreased significantly E2 effects on the transcriptional activity of pL1951 vector. We saw a markedly activity reduced of the basal leptin promoter. Similar results it´s seen with the BeWo-Sh2, which presents reduced level of Erα protein. Suggesting that the overexpression of Rel A would inhibit the interaction of others factors with their response element on the leptin promoter, for example ERs receptors. Conclusion: The treatment with the drug reduces E2 action over the endogenous leptin expression, suggesting the participation of the NFκB dimers in the regulatory effect from this steroid. These provide new evidence about the mechanisms by which the E2 regulates the expression of placental leptin.