The SP1 Transcription Factor is involved in the Regulation of Placental Leptin Expression

MALENA SCHANTON; AYELÉN TORO; JULIETA L. MAYMÓ; ANTONIO PÉREZ PÉREZ; YÉSICA GAMBINO; BERNARDO MASKIN; VÍCTOR SÁNCHEZ MARGALET; CECILIA L. VARONE

Simposio; VI SLIMP- Latin American Symposium on Maternal Fetal Interaction & Placenta; 2015

Objectives: 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) regulates leptin expression involving genomic and non genomic effects. SP1 is a ubiquitous transcription factor. In the leptin promoter there were found several potential binding sites for SP1. One of them is present in the region identificated as PLE (enhancer of the placental leptin) involved in E2 effect. In the present study, we analyzed the effect of SP1 in the induction of leptin expression by E2 in human placental cells.Methods: BeWo cells were cultured under standard conditions. BeWo cells were transiently transfected with different reporter vectors and expression vectors for SP1 or ER.Results: We observed that SP1 overexpression increased basal leptin promoter activity. This effect was not enhanced by E2. On the other hand SP1 augmented leptin promoter activity of the reporter which contains the promoter region of the leptin gene between -1951 and -1887 bp but not when in this region SP1 element is mutated. SP1 effect is ERdependent as it had no activity in cells that had been knocked down with an ER siRNA.Conclussions: All these findings suggest that leptin expression is tightly regulated and improve the comprehension of the mechanisms whereby E2 regulates leptin expression involving SP1 transcription factor.