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Transferrin receptor and ferritin levels during murine mammary gland development

Authors :
Gopalan Shyamala
Prem Ponka
Ania Wilczynska
Herbert M. Schulman
Yves Gauthier
Source :
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1010:1-6
Publication Year :
1989
Publisher :
Elsevier BV, 1989.

Abstract

Various types of proliferating cell are known to express transferrin receptors which are necessary for transferrin-mediated cellular iron uptake. Neither the mechanism nor the physiological role of transferrin receptor induction has been established with certainty; although it may reflect an increased cellular requirement for iron which is essential for ribonucleotide reductase, a key enzyme of DNA synthesis. The aim of this study was to examine murine mammary gland transferrin-receptor levels during gland development. As compared to virgin controls, total mammary gland transferrin receptors expressed on the basis of DNA, increase during pregnancy and lactation by 29- and 45-fold, respectively. However, on the basis of DNA, mammary gland ferritin, measured by radioimmunoassay, decreased by about 75% and 85% during pregnancy and lactation, respectively, indicating that the increased transferrin receptor levels probably do not lead to intracellular iron accumulation. When epithelial cells from mammary glands of pregnant mice were cultured in vitro transferrin receptor expression correlated with cell proliferation. These results suggest that normal mammary growth which occurs mainly in mammary epithelial cells is associated with a significant increase in transferrin receptor. Since transferrin receptor levels remain high during lactation they are not associated solely with tissue growth, but may also function in transporting iron during milk production.

Details

ISSN :
01674889
Volume :
1010
Database :
OpenAIRE
Journal :
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
Accession number :
edsair.doi.dedup.....bef14646ef933a7aba3222a054eb1845
Full Text :
https://doi.org/10.1016/0167-4889(89)90176-6