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Regulation of K562 cell transferrin receptors by exogenous iron
Author(s) -
Rudolph Natalie S.,
OhlssonWilhelm Betsy M.,
Leary James F.,
Rowley Peter T.
Publication year - 1985
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041220315
Subject(s) - transferrin receptor , transferrin , receptor , flow cytometry , chemistry , cell , intracellular , cell growth , biochemistry , cell surface receptor , k562 cells , microbiology and biotechnology , cell culture , biology , genetics
Single‐cell analysis of K562 human erythroleukemia cells by flow cytometry was used to demonstrate the specific role of iron in regulating transferrin receptors (TfRs) and to establish that TfR expression does not necessarily correlate with growth rate. Exogenous iron concentration in culture was manipulated by supplementing the medium with sera having different iron concentrations over the range 0.6 to 5.4 μg/ml/ by the addition of iron in the form of FeCl 3 , iron‐saturated serum, or diferric transferrin, and by the addition of the iron chelator Desferal (desferrioxamine). TfR expression was negatively correlated with exogenous iron content: any treatment that reduced exogenous iron supply by at least 15% resulted in as much as a 1.8‐fold increase in external receptors, detected as binding by both transferrin and monoclonal anti‐TfR antibodies, and a 1.5‐fold increase in the pool of internal receptors, as detected by anti‐TfR antibody binding. None of these treatments altered growth rate, total cellular protein content, protein synthetic rate, cell cycle distribution or cell size. The rapid (12 hr) and reversible induction of internal and external receptors by Desferal was inhibited by cyclohexionide and therefore may have resulted from de novo synthesis and not just mobilization of internal receptor pool to the cell surface. The correlation between growth rate and TfR expression previously observed in these and other cells must be secondary to cellular mechanisms that maintain intracellular iron pools by regulating synthesis, recycling, and cell surface expression of TfRs.