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首页> 外文期刊>The Journal of Reproduction and Development >Fetal Loss and Hyposulfataemia in Pregnant NaS1 Transporter Null Mice
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Fetal Loss and Hyposulfataemia in Pregnant NaS1 Transporter Null Mice

机译：NaS1转运蛋白空小鼠的胎儿丢失和低硫酸血症

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摘要

Sulfate is important for growth and development, and is supplied from mother to fetus throughout pregnancy. We used NaS1 sulfate transporter null ( Nas1 -/-) mice to investigate the role of NaS1 in maintaining sulfate homeostasis during pregnancy and to determine the physiological consequences of maternal hyposulfataemia on fetal, placental and postnatal growth. We show that maternal serum (≤0.5 mM), fetal serum (-/- mice when compared with maternal serum (≈2.0 mM), fetal serum (≈1.5 mM) and amniotic fluid (≈1.7 mM) sulfate levels in pregnant Nas1+/+ mice. After 12 days of pregnancy, fetal reabsorptions led to markedly reduced (by ≥50%) fetal numbers in Nas1-/- mice. Placental labyrinth and spongiotrophoblast layers were increased (by ≈140%) in pregnant Nas1-/- mice when compared to pregnant Nas1+/+ mice. Birth weights of progeny from female Nas1-/- mice were increased (by ≈7%) when compared to progeny of Nas1+/+ mice. These findings show that NaS1 is essential to maintain high maternal and fetal sulfate levels, which is important for maintaining pregnancy, placental development and normal birth weight.
机译：硫酸盐对于生长和发育很重要，并且在整个怀孕期间都会从母亲供应给胎儿。我们使用NaS1硫酸盐转运蛋白无效（Nas1 -/-）小鼠研究了NaS1在怀孕期间维持硫酸盐稳态的作用，并确定了母体低硫酸盐血症对胎儿，胎盘和产后生长的生理影响。我们显示母体血清（≤0.5mM），胎儿血清（-/-小鼠）与母体血清（≈2.0mM），胎儿血清（≈1.5mM）和羊水（≈1.7mM）相比在怀孕的Nas1 + / + 小鼠中，胎儿的重吸收导致Nas1 -/-小鼠中的胎儿重吸收明显减少（≥50％）。与怀孕的Nas1 + / + 小鼠相比，怀孕的Nas1 -//-小鼠的迷宫和海绵滋养层增加了（约140％）。与Nas1 + / + 小鼠的后代相比，-/-小鼠增加了（约7％），这些发现表明NaS1对维持高母婴水平至关重要硫酸盐水平，对于维持妊娠，胎盘发育和正常出生体重很重要。

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