Blood:转铁蛋白受体1通过微调铁调素反应控制系统铁稳态

2019-01-03 MedSci MedSci原创

中心点:TfrcAlb-Cre小鼠表现为低肝细胞铁、轻度血铁过少和小红细胞血症,主要是由于血调素表达异常。Tfr1对根据肝细胞铁负荷微调铁调素至关重要,但对肝细胞的基础铁供应可有可无。摘要:转铁蛋白受体1(Tfr1)介导发育中的红系细胞和其他类型的细胞对循环中的转铁蛋白结合铁的摄取。其至关重要的生理功能通过Tfr1敲除(Tfr1-/-)小鼠胚胎致死表型和几种组织特异性敲除的病理得到强调。Carin

中心点:

TfrcAlb-Cre小鼠表现为低肝细胞铁、轻度血铁过少和小红细胞血症,主要是由于血调素表达异常。

Tfr1对根据肝细胞铁负荷微调铁调素至关重要,但对肝细胞的基础铁供应可有可无。

摘要:

转铁蛋白受体1(Tfr1)介导发育中的红系细胞和其他类型的细胞对循环中的转铁蛋白结合铁的摄取。其至关重要的生理功能通过Tfr1敲除(Tfr1-/-)小鼠胚胎致死表型和几种组织特异性敲除的病理得到强调。

Carine Fillebeen等人建立Tfrcalb-Cre小鼠,肝细胞特异性的敲除Tfr1,来研究Tfr1对肝细胞和全身铁稳态的影响。TfrcAlb-Cre小鼠可存活,无任何明显的肝脏病理。但由于Tfr1缺陷的肝细胞内化转铁蛋白铁的能力减弱,其肝铁含量(LIC)要低于同窝对照的(Tfrcfl/fl)。即使肝Hamp mRNA和铁调素/LIC比例在前者中要明显升高。重要的是,还伴随中度的血铁过少和小红细胞血症,使得Tfrcalb-Cre小鼠容易发生铁缺陷性贫血。

Tfrcalb-Cre小鼠在膳食铁处理或全转铁蛋白注射后会适当调节Hamp表达。全转铁蛋白还可触发原代TfrcAlb-Cre肝细胞的Hamp mRNA、铁蛋白和Tfr2适度诱导。研究人员进一步发现这些细胞可从59Fe-转铁蛋白中获得59Fe,可能是通过Tfr2。

总而言之,本研究表明Tfr1对于基础肝细胞铁供应是多余的,但对于根据肝细胞铁负荷微调铁调素反应至关重要。本研究结果与Tfr1通过与Hfe的相互作用抑制铁信号传递给铁调素的功能一致。此外,他们还强调了肝细胞Tfr1是细胞和系统铁调节通路之间的桥梁。

原始出处:

Carine Fillebeen, et al.Transferrin receptor 1 controls systemic iron homeostasis by fine-tuning hepcidin expression to hepatocellular iron load.Blood 2018 :blood-2018-05-850404; doi: https://doi.org/10.1182/blood-2018-05-850404 

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    2019-10-20 changfy
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    2019-07-18 Boyinsh
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