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首页> 外文期刊>Cell metabolism >SLC39A14 Is Required for the Development of Hepatocellular Iron Overload in Murine Models of Hereditary Hemochromatosis
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SLC39A14 Is Required for the Development of Hepatocellular Iron Overload in Murine Models of Hereditary Hemochromatosis

机译：SLC39A14是遗传性血色素沉着症小鼠模型中肝细胞铁超负荷发展所必需的

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摘要

Nearly all forms of hereditary hemochromatosis are characterized by pathological iron accumulation in the liver, pancreas, and heart. These tissues preferentially load iron because they take up non-transferrin-bound iron (NTBI), which appears in the plasma during iron overload. Yet, how tissues take up NTBI is largely unknown. We report that ablation of Slc39a14, the gene coding for solute carrier SLC39A14 (also called ZIP14), in mice markedly reduced the uptake of plasma NTBI by the liver and pancreas. To test the role of SLC39A14 in tissue iron loading, we crossed Slc39a14(-/-) mice with Hfe(-/-) and Hfe2(-/-) mice, animal models of type 1 and type 2 (juvenile) hemochromatosis, respectively. Slc39a14 deficiency in hemochromatotic mice greatly diminished iron loading of the liver and prevented iron deposition in hepatocytes and pancreatic acinar cells. The data suggest that inhibition of SLC39A14 may mitigate hepatic and pancreatic iron loading and associated pathologies in iron overload disorders.
机译：几乎所有形式的遗传性血色素沉着病都以肝脏，胰腺和心脏中的病理性铁蓄积为特征。这些组织优先加载铁，因为它们吸收了非铁传递蛋白结合的铁（NTBI），铁在铁超负荷时会出现在血浆中。但是，组织如何吸收NTBI仍然是未知的。我们报告的消融Slc39a14，编码溶质载体SLC39A14（也称为ZIP14）的基因，在小鼠中明显减少了肝脏和胰腺对血浆NTBI的吸收。为了测试SLC39A14在组织铁负荷中的作用，我们分别将Slc39a14（-/-）小鼠与Hfe（-/-）和Hfe2（-/-）小鼠，1型和2型（青少年）血色素沉着症动物模型进行了杂交。血色素沉着症小鼠中Slc39a14的缺乏大大减少了肝脏的铁负荷，并阻止了铁在肝细胞和胰腺腺泡细胞中的沉积。数据表明，SLC39A14的抑制作用可减轻铁超负荷性疾病中肝脏和胰腺的铁负荷和相关病理。

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