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Iron deficiency increases Zip14 expression in hepatocytes
Author(s) -
Nam Hyeyoung,
Liuzzi Juan P,
Knutson Mitchell D
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1118-a
Subject(s) - gene isoform , messenger rna , transferrin receptor , hepatocyte , chemistry , transferrin , microbiology and biotechnology , iron deficiency , dmt1 , transporter , biology , medicine , gene , biochemistry , in vitro , anemia
Zip14, a member of the ZIP family of metal ion transporters, has recently been shown to transport both zinc and iron (Liuzzi et al., PNAS, 2006). Studies using mouse liver reveal that Zip14 mRNA levels correlate strongly and positively with transferrin receptor (TfR) mRNA levels, suggesting that Zip14 transcript levels increase as cellular iron levels decrease. The aim of this study was to examine the effect of iron deficiency on Zip14 mRNA levels in AML12 cells, a mouse hepatocyte cell line. AML12 cells were incubated for 24 h in medium lacking or containing an iron chelator (50 μM of either desferrioxamine, DFO, or salicyladehyde isonicotinoyl hydrazone, SIH). Levels of Zip14 and TfR mRNA were assessed by quantitative RT‐PCR. DFO and SIH treatments depleted cellular iron, as indicated by 3‐ to 4‐fold increases, respectively, in TfR mRNA abundance. Levels of Zip14 short isoform mRNA increased by 60% (P<0.01) in DFO and SIH‐treated cells, whereas levels of Zip14 long isoform mRNA increased by nearly 200% (P<0.01). These observations suggest that Zip14‐mediated iron/zinc transport into hepatocytes increases in response to iron deficiency. Supported by NIH grant DK065064.