Maternal‐fetal transfer of selenium in the mouse
| Autor: | Kristina E. Hill, Suguru Kurokawa, Gary E. Olson, Virginia P. Winfrey, Raymond F. Burk, Amy K. Motley |
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| Rok vydání: | 2013 |
| Předmět: |
Male
inorganic chemicals medicine.medical_specialty Time Factors Low-density lipoprotein receptor-related protein 8 Placenta SEPP1 chemistry.chemical_element Biology Biochemistry Research Communications Mice Selenium Pregnancy Selenoprotein P Internal medicine Genetics medicine Animals Maternal-Fetal Exchange Molecular Biology LDL-Receptor Related Proteins Yolk Sac Mice Knockout chemistry.chemical_classification Glutathione Peroxidase Fetus Glutathione peroxidase food and beverages Biological Transport Immunohistochemistry Mice Inbred C57BL Low Density Lipoprotein Receptor-Related Protein-2 Endocrinology medicine.anatomical_structure Microscopy Fluorescence chemistry embryonic structures Female Selenoprotein Biotechnology |
| Zdroj: | The FASEB Journal. 27:3249-3256 |
| ISSN: | 1530-6860 0892-6638 |
| DOI: | 10.1096/fj.13-231852 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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