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首页> 外文期刊>Cell metabolism >The transferrin receptor modulates Hfe-dependent regulation of hepcidin expression.
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The transferrin receptor modulates Hfe-dependent regulation of hepcidin expression.

机译：转铁蛋白受体调节铁调素表达的Hfe依赖性调节。

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摘要

Hemochromatosis is caused by mutations in HFE, a protein that competes with transferrin (TF) for binding to transferrin receptor 1 (TFR1). We developed mutant mouse strains to gain insight into the role of the Hfe/Tfr1 complex in regulating iron homeostasis. We introduced mutations into a ubiquitously expressed Tfr1 transgene or the endogenous Tfr1 locus to promote or prevent the Hfe/Tfr1 interaction. Under conditions favoring a constitutive Hfe/Tfr1 interaction, mice developed iron overload attributable to inappropriately low expression of the hormone hepcidin. In contrast, mice carrying a mutation that interferes with the Hfe/Tfr1 interaction developed iron deficiency associated with inappropriately high hepcidin expression. High-level expression of a liver-specific Hfe transgene in Hfe-/- mice was also associated with increased hepcidin production and iron deficiency. Together, these models suggest that Hfe induces hepcidin expression when it is not in complex with Tfr1.
机译：血色素沉着症是由HFE突变引起的，HFE是一种与运铁蛋白（TF）竞争与运铁蛋白受体1（TFR1）结合的蛋白质。我们开发了突变小鼠品系，以了解Hfe / Tfr1复合物在调节铁稳态中的作用。我们将突变引入到普遍表达的Tfr1转基因或内源性Tfr1基因座中，以促进或阻止Hfe / Tfr1相互作用。在有利于组成型Hfe / Tfr1相互作用的条件下，小鼠出现铁过载，这归因于激素hepcidin的不适当的低表达。相反，携带突变干扰Hfe / Tfr1相互作用的小鼠会出现铁缺乏症，而铁缺乏症与铁调素过高表达有关。在Hfe-/-小鼠中肝脏特异性Hfe转基因的高水平表达还与铁调素产量增加和铁缺乏相关。总之，这些模型表明，当Hfe与Tfr1不复合时，它会诱导hepcidin表达。

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