PLACENTAL APOPTOSIS ENHANCED BY HIF1 ALPHA STABILIZATION IS COUNTERACTED BY LEPTIN

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

Mar del Plata

Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2019

SAIC

Abstract/Resumen: Leptin is a pleiotropic hormone producedby the placenta where it plays important regulatory functions.We have previously demonstrated that leptin promotesproliferation and survival of trophoblastic cells. Moreover, leptinprevents cellular stress under hypoxic condition in trophoblasticcells. In this work we aimed to study the mechanisms thatmediate the effect of leptin in placental apoptosis induced bycobalt chloride (CoCl2), a hypoxia mimicking agent that stabilizesHIF-1 alpha transcription factor expression. For this study we useSwan-71 cells, a first trimester trophoblastic human cell line,cultured under standard conditions, as well as human termplacental explants. Swan-71 cells and placental explants weretreated with CoCl2 (50 or 100 μM). The expression of HIF-1alpha, p53, Caspase-3 and cPARP was determined by Westernblot or Immunofluorescence (IF). Apoptosis was determined byDNA ladder assay in placental explants. All procedures wereapproved by ethical review committee at the Alejandro PosadasNational Hospital. We observed that HIF-1 alpha stabilizationincreased DNA fragmentation in placental explants (*p