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首页> 外文期刊>Journal of Cellular Physiology >Mouse HFE inhibits Tf-uptake and iron accumulation but induces non-transferrin bound iron (NTBI)-uptake in transformed mouse fibroblasts.
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Mouse HFE inhibits Tf-uptake and iron accumulation but induces non-transferrin bound iron (NTBI)-uptake in transformed mouse fibroblasts.

机译：鼠标HFE抑制Tf-uptake积累和铁但引发non-transferrin绑定铁(NTBI)在小鼠成纤维细胞转化吸收。

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摘要

Iron-uptake and storage are tightly regulated to guarantee sufficient iron for essential cellular processes and to prevent the production of damaging free radicals. A non-classical class I MHC molecule, the hemochromatosis factor (HFE), has been shown to regulate iron metabolism, potentially via its interaction with the transferrin receptor. Whereas, the effect of human HFE (hHFE) on transferrin/transferrin receptor association, as well as on transferrin receptor recycling and the level of cellular iron pools in various cell lines was analyzed, very little is known about the mouse HFE (mHFE) protein. In the following study, our aim was to analyze in more detail the function of mHFE. Surprisingly, we observed that over-expression of mHFE, but not of hHFE, in a mouse transformed cell line, results in a most significant inhibition of transferrin-uptake which correlated with apoptotic cell death. mHFE inhibited transferrin-uptake immediately following transfection and this inhibition persisted in the surviving stable transfectants. Concomitantly, cellular iron derived from transferrin-iron uptake was dramatically limited. The activation of a non-transferrin bound iron-uptake pathway that functions in the stable mHFE-transfected clones could explain their normal growth curves and survival. The hypothesis that iron starvation can induce iron-uptake by a novel transferrin-independent pathway is discussed.
机译：铁摄入和存储有严格的规定保证足够的铁细胞至关重要过程和防止生产有害的自由基。MHC分子,血色沉着病的因素(HFE),可以调节铁代谢,可能通过交互转铁蛋白受体。人类HFE (hHFE)转铁蛋白和转铁蛋白转铁蛋白受体协会,以及回收和受体细胞铁的水平分析了池在不同细胞系,非常对鼠标HFE (mHFE)蛋白质。详细分析mHFE的功能。令人惊讶的是,我们观察到的表达mHFE,但不是hHFE,鼠标了细胞系,结果最重要抑制transferrin-uptake相关与凋亡细胞死亡。transferrin-uptake后立即转染这抑制坚持幸存的稳定转染子。细胞铁来自transferrin-iron急剧吸收是有限的。non-transferrin绑定铁摄入途径mHFE-transfected功能的稳定克隆可以解释他们的正常生长曲线和生存。可以诱导铁摄入的小说transferrin-independent途径进行了探讨。

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