Abstract
SFT (stimulator of Fe transport) is a novel transport protein that has been found to facilitate uptake of iron presented to cells as either Fe(II) or Fe(III). When HeLa cells are exposed to the iron chelator desferrioxamine, levels of SFT mRNA increase in an actinomycin D-sensitive manner. In contrast, cells exposed to high levels of iron down-regulate SFT expression in a time-dependent and reversible fashion. Thus, homeostatic regulation of SFT expression not only ensures that sufficient levels of iron are maintained but also limits excessive assimilation to prevent potentially harmful effects of this toxic metal. The unexpected observation that SFT transcript levels are up-regulated in hemochromatosis patients therefore suggests that enhanced SFT expression contributes to the etiology of this iron overload disorder.
Highlights
Transport of iron by microbes, plants, and animals is a tightly regulated process that is limited to prevent harmful effects due to overload of this toxic metal
This profile appears to overlap with the appearance of SFT transcripts, which have been found in human intestine, spleen, thymus, prostate, testis, ovaries, and peripheral blood lymphocytes, with low levels observed for colon [9]
The recent elucidation of the gene for this disease led to the discovery that defects in a nonclassical major histocompatibility complex (MHC) class I protein, HFE, are responsible for the iron overload exhibited by patients [11]
Summary
Transport of iron by microbes, plants, and animals is a tightly regulated process that is limited to prevent harmful effects due to overload of this toxic metal (for a comprehensive review of this field, please see Ref. 1). While DCT1/Nramp2 transcripts are known to be increased in the intestine of iron-deficient animals [6], regulation of SFT expression in response to iron levels has yet to be characterized.
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