CIQUIBIC   05472
CENTRO DE INVESTIGACIONES EN QUIMICA BIOLOGICA DE CORDOBA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
HYPOXIA INCREASES THE EXPRESSION OF KRÜPPEL LIKE FACTOR 6 (KLF6) IN THE PLACENTA
Autor/es:
RACCA, ANA C.; RIDANO, MAGALÍ EVELIN; BEVILACQUA, ESTELA; GENTI-RAIMONDI, SUSANA; GRAHAM, CHARLES H.; PANZETTA-DUTARI, GRACIELA
Lugar:
Rosario
Reunión:
Congreso; 50 Reuniòn Anual de la Sociedad Argentina de Investifación en Bioquímica y Biología Molecular; 2014
Institución organizadora:
SAIB
Resumen:
HYPOXIA INCREASES THE EXPRESSION OF KRÜPPEL LIKE FACTOR 6 (KLF6) IN THE PLACENTA Racca AC1, Ridano ME1, Bevilacqua E2, Genti-Raimondi S1, Graham CH3*, and Panzetta-Dutari G1* 1CIBICI-CONICET. Univ Nac Córdoba, Arg.2University of Sao Paulo, Brazil. 3Queen?s University, Canada aracca@fcq.unc.edu.ar Preeclampsia (PE) is a pregnancy-specific disorder related to abnormal placental blood perfusion and poor trophoblast invasion. It is an important cause of maternal and fetal mortality and morbidity. While its pathophysiology has not been fully elucidated, placental oxidative stress injury appears as one important mechanism. In addition, normal early placentation occurs in a relatively hypoxic environment and throughout this period, HIF-1α mediates low oxygen tension effects. KLF6 is a transcription factor highly expressed in placenta, involved in carcinogenesis and cell differentiation in various systems. Interestingly, in mouse kidney KLF6 expression is up-regulated following ischemia/reperfusion. Our aim was to elucidate whether placental KLF6 expression depends on oxygen level. We found that hypoxia increases KLF6 expression early and transiently in placental cells and tissue. KLF6 up-regulation was partially dependent on HIF-1α as revealed by siRNA knockdown and western-blot assays. Furthermore, immunohistochemical analysis showed a decrease in the nucleo/cytoplasmic KLF6 expression ratio in PE placentas compared to control. According to these data, KLF6 is a potential mediator of hypoxic effects participating in normal and/or pathological placental development. Supported by CONICET, FONCyT, SECyT-UNC, and IUBMB and JCS fellowships. (*equal contribution).