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Endocrinology. 2014 Mar;155(3):1099-106. doi: 10.1210/en.2013-1425. Epub 2013 Jan 1.

NDRG1 deficiency attenuates fetal growth and the intrauterine response to hypoxic injury.

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Magee-Womens Research Institute (J.L., X.H.S., T.M., Y.B., Y.S.), Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15213; Department of Obstetrics and Gynecology (B.C.), Washington University, St Louis, Missouri 63110; Department of Molecular Pathogenesis (K.K.), National Cerebral and Cardiovascular Center, Osaka, Japan 565-8565; and Department of Microbiology and Molecular Genetics (Y.B., Y.S.), University of Pittsburgh, Pittsburgh, Pennsylvania 15213.


Intrauterine mammalian development depends on the preservation of placental function. The expression of the protein N-myc downstream-regulated gene 1 (NDRG1) is increased in placentas of human pregnancies affected by fetal growth restriction and in hypoxic primary human trophoblasts, where NDRG1 attenuates cell injury. We sought to assess the function of placental NDRG1 in vivo and tested the hypothesis that NDRG1 deficiency in the mouse embryo impairs placental function and consequently intrauterine growth. We found that Ndrg1 knock-out embryos were growth restricted in comparison to wild-type or heterozygous counterparts. Furthermore, hypoxia reduced the survival of female, but not male, knock-out embryos. Ndrg1 deletion caused significant alterations in placental gene expression, with a marked reduction in transcription of several lipoproteins in the placental labyrinth. These transcriptional changes were associated with reduced fetal:maternal serum cholesterol ratio exclusively in hypoxic female embryos. Collectively, our findings indicate that NDRG1 promotes fetal growth and regulates the metabolic response to intrauterine hypoxic injury in a sexually dichotomous manner.

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