Maternal-fetal transfer of selenium in the mouse
Maternal-fetal transfer of selenium in the mouse
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DOI：
10.1096/fj.13-231852
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发表时间：
2013-08-01
期刊：
影响因子：
4.8
通讯作者：
Kurokawa, Suguru
中科院分区：
文献类型：
--
作者：
Burk, Raymond F.;Olson, Gary E.;Kurokawa, Suguru
硒蛋白P（Sepp 1）通过受体介导的内吞作用摄取其硒。其他细胞外硒蛋白，谷胱甘肽过氧化物酶-3（Gpx 3），尚未显示出运输硒。用Sepp 1、Sepp 1受体载脂蛋白E受体2（apoER 2）和megalin以及Gpx 3基因改变的小鼠研究母胎硒转移。免疫细胞化学（ICC）显示受体非依赖性摄取Sepp 1和Gpx 3在相同的囊泡的d-13内脏卵黄囊细胞，这表明摄取的胞饮。ICC也显示apoER 2介导的摄取母体Sepp 1在d-18胎盘。因此，两个硒蛋白依赖的母胎硒转移机制被确定。硒在d-18胎仔中定量，机制被破坏。母亲Sepp 1缺失，降低母亲全身硒，减少胎儿硒充足的条件下，但胎儿的apoER 2的删除没有。在缺硒条件下，胎儿apoER 2缺失确实使胎儿硒减少了51%，验证了胎盘Sepp 1-apoER 2机制的功能。母体Gpx 3缺失使胎儿硒减少13%，但仅在缺硒条件下。这些结果表明，硒蛋白的摄取机制，确保硒转移到胎儿在缺硒条件下。在硒充足的条件下，它们的破坏（apoER 2缺失、Gpx 3缺失）对胎儿硒的影响失败，表明存在另外的母-胎硒转移机制。F.、Olson，G. E、Hill，K. E、副总裁温弗瑞，Motley，A. K.，和Kurokawa，S.硒在小鼠体内的母胎传递。
Selenoprotein P (Sepp1) is taken up by receptor-mediated endocytosis for its selenium. The other extracellular selenoprotein, glutathione peroxidase-3 (Gpx3), has not been shown to transport selenium. Mice with genetic alterations of Sepp1, the Sepp1 receptors apolipoprotein E receptor-2 (apoER2) and megalin, and Gpx3 were used to investigate maternal-fetal selenium transfer. Immunocytochemistry (ICC) showed receptor-independent uptake of Sepp1 and Gpx3 in the same vesicles of d-13 visceral yolk sac cells, suggesting uptake by pinocytosis. ICC also showed apoER2-mediated uptake of maternal Sepp1 in the d-18 placenta. Thus, two selenoprotein-dependent maternal-fetal selenium transfer mechanisms were identified. Selenium was quantified in d-18 fetuses with the mechanisms disrupted. Maternal Sepp1 deletion, which lowers maternal whole-body selenium, decreased fetal selenium under selenium-adequate conditions but deletion of fetal apoER2 did not. Fetal apoER2 deletion did decrease fetal selenium, by 51%, under selenium-deficient conditions, verifying function of the placental Sepp1-apoER2 mechanism. Maternal Gpx3 deletion decreased fetal selenium, by 13%, but only under selenium-deficient conditions. These findings indicate that the selenoprotein uptake mechanisms ensure selenium transfer to the fetus under selenium-deficient conditions. The failure of their disruptions (apoER2 deletion, Gpx3 deletion) to affect fetal selenium under selenium-adequate conditions indicates the existence of an additional maternal-fetal selenium transfer mechanism.Burk, R. F., Olson, G. E., Hill, K. E., Winfrey, V. P., Motley, A. K., and Kurokawa, S. Maternal-fetal transfer of selenium in the mouse.