ArticleMolecular and cellular biochemistry1991
Transferrin receptor expression and the regulation of placental iron uptake.
Article in Molecular and cellular biochemistry, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 25 citations in OpenAlex.
- Chelators as Antineuroblastomas Agents.Physiological research · 2023Article
- ZIP8 is an iron and zinc transporter whose cell-surface expression is up-regulated by cellular iron loading.The Journal of biological chemistry · 2012Article
- Association of the transferrin receptor in human placenta with HFE, the protein defective in hereditary hemochromatosis.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Developmental patterns of aluminum and five essential mineral elements in the central nervous system of the fetal and infant guinea pig.Biological trace element research · 1996Article
- Expression of haemopexin receptors by cultured human cytotrophoblast.The Biochemical journal · 1995Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Placental transferrin receptors, located at the apical side of syncytiotrophoblast, mediate placental iron uptake. Regulation of transferrin receptors on the fetal-maternal exchange area could be a major determinant in the regulation of trans-placental iron transport. Transferrin receptor expression in cultured human term cytotrophoblasts is on a much lower level than in choriocarcinoma cells, with a higher proportion of receptors located on the cell surface. Differentiation of cells, either due to longer culture periods or to 8-bromo-cAMP treatment does not lead to an increase of transferrin receptor expression. In vitro, the level of expression is largely regulated by the cellular density in the culture dishes. Low cellular occupancy of the dish leads to a high level of transferrin receptors. Treatment with iron-sources results in a down regulation of transferrin receptors. Thus, though the level of transferrin receptors in cultured normal trophoblast is at a constant level, unaffected by differentiation, high levels of maternal transferrin-iron availability can lead to a decrease in placental iron uptake. This feed-back mechanism makes placental iron uptake independent of maternal iron stores.
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