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首页> 外文期刊>Cell metabolism >Interaction of the hereditary hemochromatosis protein HFE with transferrin receptor 2 is required for transferrin-induced hepcidin expression.
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Interaction of the hereditary hemochromatosis protein HFE with transferrin receptor 2 is required for transferrin-induced hepcidin expression.

机译：遗传性血色素沉着病蛋白HFE与运铁蛋白受体2相互作用是运铁蛋白诱导的铁调素表达所必需的。

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摘要

The mechanisms that allow the body to sense iron levels in order to maintain iron homeostasis are unknown. Patients with the most common form of hereditary iron overload have mutations in the hereditary hemochromatosis protein HFE. They have lower levels of hepcidin than unaffected individuals. Hepcidin, a hepatic peptide hormone, negatively regulates iron efflux from the intestines into the blood. We report two hepatic cell lines, WIF-B cells and HepG2 cells transfected with HFE, where hepcidin expression responded to iron-loaded transferrin. The response was abolished when endogenous transferrin receptor 2 (TfR2) was suppressed or in primary hepatocytes lacking either functional TfR2 or HFE. Furthermore, transferrin-treated HepG2 cells transfected with HFE chimeras containing only the alpha3 and cytoplasmic domains could upregulate hepcidin expression. Since the HFE alpha3 domain interacts with TfR2, these results supported our finding that TfR2/HFE complex is required for transcriptional regulation of hepcidin by holo-Tf.
机译：允许人体感应铁水平以维持铁稳态的机制尚不清楚。具有最常见形式的遗传性铁超负荷的患者，遗传性血色素沉着蛋白HFE发生突变。与未受影响的人相比，他们的铁调素水平较低。 Hepcidin是一种肝肽激素，对铁从肠道到血液的流出负调节作用。我们报告了两个肝细胞系，WIF-B细胞和转染了HFE的HepG2细胞，其中铁调素对铁载铁蛋白的表达有反应。当内源性转铁蛋白受体2（TfR2）被抑制或在缺乏功能性TfR2或HFE的原代肝细胞中，反应消失。此外，转铁蛋白处理过的仅包含alpha3和胞质结构域的HFE嵌合体转染的HepG2细胞可以上调hepcidin的表达。由于HFE alpha3结构域与TfR2相互作用，因此这些结果支持了我们的发现，即完整的Tf对Hepcidin的转录调控需要TfR2 / HFE复合体。

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