HFE-related hereditary hemochromatosis results in hepatic iron overload. Hepatocytes acquire transferrin-bound iron via transferrin receptor (Tfr) 1 and Tfr1-independent pathways (possibly Tfr2-mediated). In this study, the role of Hfe in the regulation of hepatic transferrin-bound iron uptake by th
Transferrin receptors and the uptake and release of iron by isolated hepatocytes
โ Scribed by Stephen P. Young; Philip Aisen
- Publisher
- John Wiley and Sons
- Year
- 1981
- Tongue
- English
- Weight
- 683 KB
- Volume
- 1
- Category
- Article
- ISSN
- 0270-9139
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โฆ Synopsis
Isolated rat hepatocytes accumulate iron from iron-transferrin by a process which is dependent on the temperature and on the transferrin concentration, and which is diminished by treatment of the cells with a proteolytic enzyme. These observations are consistent with a mechanism for iron uptake into hepatocytes involving the binding of iron-transferrin to a specific cell-surface receptor.
Apotransferrin is also able to bind to the hepatocyte but the apparent binding constant is about 35 times lower than that observed fvr the binding of iron-transferrin. The binding of apotransferrin to the cells is completely abolished by a low concentration of iron-transferrin. This suggests that the apotransferrin is binding weakly to the same receptor to which iron-transferrin binds and that there are no receptors on the surface of the hepatocyte specific for apotransferrin. In the absence of such specific-binding sites, apotransferrin may act as a passive acceptor of iron released from the hepatocyte.
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