Placental apoptosis induced by hypoxia is counteracted by leptin

NATALY DE DIOS; CASALE, ROBERTO; MALENA SCHANTON; JULIETA MAYMO; RODRIGO RIEDEL; CECILIA VARONE

capital federal

Congreso; Reunión anual de sociedades de biociencias SAIC. SAI. SAFIS 2020; 2020

Leptin acts as a regulatory hormone in the maternal fetal interface. We demonstrated that leptin promotes proliferation and survival of trophoblastic cells. Moreover, leptin prevents cellular stress under hypoxic condition in trophoblastic cells. In this sense, Leptin is in- cremented in different pregnancy pathologies such as preeclamp- sia. In this work we aimed to elucidate the mechanisms involved in Leptin antiapoptotic effect on placental apoptosis induced by cobalt chloride (CoCl2). This agent stabilizes HIF-1α transcription factor. We used Swan-71 cells, a cytotrophoblast human cell line and hu- man term placental explants cultured under normoxia and hypoxia conditions. Swan-71 cells and placental explants were treated with CoCl2 (50 or 100 μM) in presence or absence of leptin (100 ng/ml). The expression of HIF-1α, p53, Caspase-3, cPARP and Mdm2 was determined by Western blot. Apoptosis was determined by the visu- alization of apoptotic nuclei by IF. All procedures were approved by ethical review committee at the Alejandro Posadas National Hos- pital.We observed that HIF-1α stabilization increased apoptosis (1.54 ±0.1) in Swan-71 cells. Treatment with CoCl2 increased (1.8 ± 0.5) PARP-1 and (1.7 ± 0.2)Caspase-3 levels indicating that apoptosis was induced. Leptin treatment diminished this effect (p