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首页> 外文期刊>American Journal of Physiology >Vesicular transport and apotransferrin in intestinal iron absorption, as shown in the Caco-2 cell model.
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Vesicular transport and apotransferrin in intestinal iron absorption, as shown in the Caco-2 cell model.

机译：如Caco-2细胞模型所示，小肠铁吸收中的囊泡转运和载脂蛋白转铁蛋白。

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摘要

The potential roles of vesicular transport and apotransferrin (entering from the blood) in intestinal Fe absorption were investigated using Caco-2 cell monolayers with tight junctions in bicameral chambers as a model. As shown previously, addition of 39 microM apotransferrin (apoTf) to the basolateral fluid during absorption studies markedly stimulated overall transport of 1 microM (59)Fe from the apical to the basal chamber and stimulated its basolateral release from prelabeled cells, implicating endo- and exocytosis. Rates of transport more than doubled. Uptake was also stimulated, but only 20%. Specific inhibitors of aspects of vesicular trafficking were applied to determine their potential effects on uptake, retention, and basolateral (overall) transport of (59)Fe. Nocodazole and 5'-(4-fluorosulfonylbenzoyl)-adenosine each reduced uptake and basolateral transport up to 50%. Brefeldin A inhibited about 10%. Tyrphostin A8 (AG10) reduced uptake 35% but markedly stimulated basolateral efflux, particularly that dependent on apoTf. Cooling of cells to 4 degrees C (which causes depolymerization of microtubules and lowers energy availability) profoundly inhibited uptake and basolateral transfer of Fe (7- to 12-fold). Apical efflux (which was substantial) was not temperature affected. Our results support the involvement of apoTf cycling in intestinal Fe absorption and indicate that as much as half of the iron uses apoTf and non-apoTf-dependent vesicular pathways to cross the basolateral membrane and brush border of enterocytes.
机译：使用在双房室紧密连接的Caco-2细胞单层模型研究了囊泡运输和载脂蛋白（从血液中进入）在肠道铁吸收中的潜在作用。如前所示，在吸收研究期间向基底外侧液中添加39 microM载脂蛋白ApoTf显着刺激了1 microM（59）Fe从根尖到基底腔的整体转运，并刺激了基底层从预先标记的细胞中释放，这牵涉到内膜和内膜。胞吐作用。运输速度增加了一倍以上。摄取也受到刺激，但只有20％。应用了水泡运输方面的特定抑制剂来确定其对（59）Fe的摄取，保留和基底外侧（整体）运输的潜在影响。诺考达唑和5'-（4-氟磺酰基苯甲酰基）-腺苷分别将摄取和基底外侧转运降低了50％。布雷菲德菌素A抑制约10％。 Tyrphostin A8（AG10）减少了35％的摄取，但明显刺激了基底外侧外排，尤其是依赖apoTf的基底外排。将细胞冷却至4摄氏度（这会导致微管解聚并降低能量利用率）会大大抑制铁的摄取和基底外侧转移（7至12倍）。顶端外排（很大）不受温度影响。我们的结果支持apoTf循环参与肠道铁的吸收，并表明多达一半的铁利用apoTf和非apoTf依赖性囊泡途径穿过基底外侧膜和肠上皮细胞的刷缘。

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