[38-OR]: Sexual dimorphism in the effect of @entity32 on trophoblast function with XXXX .

@entity1 @entity32 @entity7738 @entity9135 @entity2125 @entity2451 @entity28 @entity310 @entity519 @entity1468 @entity60441 @entity5985 @entity10018
OBJECTIVES: @entity28 and @entity1468 are associated with increased @entity32 and oxidative stress in the placenta. With @entity1468 greater @entity32 , @entity519 and apoptosis were found in placentas of male vs female placentas. We find increased @entity10018 expression, and associated decreased placental mitochondrial function with severe @entity1468 . We investigated if the inflammatory transcription factors @entity7738 and NFkB regulate placental @entity10018 expression in a sexually dimorphic manner. METHODS: Placentas were collected at term (C section, no labor) from healthy lean @entity1 (n=6 each sex) and trophoblast cultures prepared. Trophoblasts were treated with @entity310 (10ng/ml, 2h) and expression of @entity10018 , @entity7738 , NFkB and mitochondrial function measured. RESULTS: @entity310 treatment significantly increased placental NFkB @entity9135 expression in both sexes but @entity2451 ( @entity2451 ) only in female placentas. This was accompanied by significantly increased binding of @entity2451 to the @entity60441 promoter and increased @entity10018 expression only in female placentas. Correspondingly significantly decreased expression of the @entity10018 mitochondrial target proteins @entity5985 cluster assembly proteins and @entity2125 dehydrogenase 1a subcomplex 4 was found in the female placentas treated with @entity310 together with a significant reduction in mitochondrial respiration. Inhibition of @entity2451 by siRNA abolished the effect of @entity310 on @entity10018 expression and mitochondrial respiration in the female placenta. CONCLUSIONS: We find sexual dimorphism in the effect of @entity32 on placental @entity10018 expression perhaps mediated by the @entity2451 pathway. This may link placental @entity32 in @entity1468 to decreased mitochondrial function in pregnancies with a female fetus. DISCLOSURES: L. Myatt: None. C. Guo: None. S. Muralimanoharan: None. A. Maloyan: None.
