Placental apoptosis induced by chemical hypoxia is counteracted by leptin

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

virtual

Congreso; LXV REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC); 2020

SAIC-SAI-SAFIS

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 incremented in different pregnancy pathologies such as preeclampsia. 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 human 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 visualization of apoptotic nuclei by IF. All procedures were approved by ethical review committee at the Alejandro Posadas National Hospital. 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