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Strain specific modulation of tissue iron content and HFE gene expression in mice
Author(s) -
Lee SeungMin,
Lim Vanessa,
Vulpe Christopher D
Publication year - 2006
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.20.4.a194-a
Subject(s) - hemochromatosis , basal (medicine) , hereditary hemochromatosis , gene , biology , gene expression , mutant , phenotype , missense mutation , hepcidin , genetics , endocrinology , medicine , immunology , inflammation , insulin
The effect of genetic background on the development of hereditary hemochromatosis (HH) has been recognized widely. Animal models for the disease display different levels of iron accumulation in their liver tissues depending on the strain. Knowing the origin of difference to account for various phenotypic outcomes is important to understand how HH develops and what key playing factors are. Taking advantage of the homogeneous genetic background of mice strains, 18 strains of mice were investigated for their iron levels in the liver. Liver is one of the major organs to store body iron and a place to control iron uptake via the intestine by controlling the expression of an iron hormone like peptide. We found that AKR/J strains showed the highest iron basal levels and B10.D2‐H2/oSNJ showed the lowest iron basal levels compared to those of other strains chosen for our study. These two strains were compared in the terms of the expression of genes in iron metabolism. Among eight iron‐related genes examined HFE, which is known for its missense mutation causing hereditary hemochromatosis was significantly different in the transcript levels between AKR/J and B10.D2‐H2/oSNJ as evidenced by the results from real time PCR. The differential basal expression levels of HFE transcripts between these two strains along with the difference in their basal iron tissue levels may indicate that regulatory molecules to control the expression of HFE gene affect the decision of basal iron levels in the liver.