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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Characterization of iron uptake from transferrin by murine endothelial cells.
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Characterization of iron uptake from transferrin by murine endothelial cells.

机译：鼠内皮细胞从转铁蛋白摄取铁的特征。

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Iron is required by the brain for normal function, however, the mechanisms by which it crosses the blood-brain barrier (BBB) are poorly understood. The uptake and efflux of transferrin (Tf) and Fe by murine brain-derived (bEND3) and lymph node-derived (m1END1) endothelial cell lines was compared. The effects of iron chelators, metabolic inhibitors and the cellular activators, lipopolysaccharide (LPS) and tumour necrosis factor-alpha (TNF-alpha), on Tf and Fe uptake were investigated. Cells were incubated with 59Fe-125I-Tf; Fe uptake was shown to increase linearly over time for both cell lines, while Tf uptake reached a plateau within 2 h. Both Tf and Fe uptake were saturable. bEND3 cells were shown to have half as many Tf receptors as m1END1 cells, but the mean cycling times of a Tf molecule were the same. Tf and Fe efflux from the cells were measured over time, revealing that after 2 h only 25% of the Tf but 80% of the Fe remained associated with the cells. Of 7 iron chelators, only deferriprone (L1) markedly decreased Tf uptake. However, Fe uptake was reduced by more than 50% by L1, pyridoxal isonicotinoyl hydrazone (PIH) and desferrithiocin (DFT). The cellular activators TNF-alpha or LPS had little effect on Tf turnover, but they accelerated Fe uptake in both endothelial cell types. Phenylarsenoxide (PhAsO) and N-ethyl maleimide (NEM), inhibitors of Tf endocytosis, reduced both Tf and Fe uptake in both cell lines, while bafilomycin A1, an inhibitor of endosomal acidification, reduced Fe uptake but did not affect Tf uptake. The results suggest that Tf and Fe uptake by both bEND3 and m1END1 is via receptor-mediated endocytosis with release of Fe from Tf within the cell and recycling of apo-Tf. On the basis of Tf- and Fe-metabolism both cell lines are similar and therefore well suited for use in in vitro models for Fe transport across the BBB.
机译：铁是大脑正常功能所必需的，但是，铁穿过血脑屏障（BBB）的机制了解甚少。比较了小鼠脑源性（bEND3）和淋巴结源性（m1END1）内皮细胞系对转铁蛋白（Tf）和铁的吸收和流出。研究了铁螯合剂，代谢抑制剂和细胞活化剂脂多糖（LPS）和肿瘤坏死因子-α（TNF-α）对Tf和Fe吸收的影响。细胞与59Fe-125I-Tf一起温育。对于两种细胞系，Fe的吸收均显示随时间线性增加，而Tf的吸收在2 h内达到平稳。 Tf和Fe的吸收均达到饱和。已显示bEND3细胞的Tf受体数量是m1END1细胞的一半，但是Tf分子的平均循环时间是相同的。随时间测量细胞的Tf和Fe外排，发现2小时后，只有25％的Tf和80％的Fe仍与细胞结合。在7种铁螯合剂中，只有去铁酮（L1）显着降低了Tf吸收。但是，L1，吡ido醛异烟酰yl（PIH）和去铁硫霉素（DFT）将铁的吸收量降低了50％以上。细胞激活剂TNF-α或LPS对Tf周转率影响不大，但它们在两种内皮细胞类型中均加速了Fe的吸收。 Tf内吞的抑制剂苯砷氧化物（PhAsO）和N-乙基马来酰亚胺（NEM）减少了两种细胞系的Tf和Fe摄取，而内体酸化抑制剂Bafilomycin A1减少了Fe的摄取，但不影响Tf的摄取。结果表明，bEND3和m1END1都通过受体介导的内吞作用吸收Tf和Fe，其中Fe从Tf释放到细胞内，并回收apo-Tf。基于Tf和Fe的代谢，两种细胞系相似，因此非常适合用于跨BBB转运Fe的体外模型。

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