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首頁> 美國衛(wèi)生研究院文獻>The Journal of Nutrition >Silencing the Menkes Copper-Transporting ATPase (Atp7a) Gene in Rat Intestinal Epithelial (IEC-6) Cells Increases Iron Flux via Transcriptional Induction of Ferroportin 1 (Fpn1)
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Silencing the Menkes Copper-Transporting ATPase (Atp7a) Gene in Rat Intestinal Epithelial (IEC-6) Cells Increases Iron Flux via Transcriptional Induction of Ferroportin 1 (Fpn1)

機譯：沉默大鼠腸道上皮細胞（IEC-6）中的Menkes銅運輸ATPase（Atp7a）基因通過鐵轉(zhuǎn)運蛋白1（Fpn1）的轉(zhuǎn)錄誘導(dǎo)增加鐵通量。

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The Menkes copper-transporting ATPase (Atp7a) gene is induced in rat duodenum during iron deficiency, consistent with copper accumulation in the intestinal mucosa and liver. To test the hypothesis that ATP7A influences intestinal iron metabolism, the Atp7a gene was silenced in rat intestinal epithelial (IEC-6) cells using short hairpin RNA (shRNA) technology. Perturbations in intracellular copper homeostasis were noted in knockdown cells, consistent with the dual roles of ATP7A in pumping copper into the trans-Golgi (for cuproenzyme synthesis) and exporting copper from cells. Intracellular iron concentrations were unaffected by Atp7a knockdown. Unexpectedly, however, vectorial iron (59Fe) transport increased (∼33%) in knockdown cells grown in bicameral inserts and increased further (∼70%) by iron deprivation (compared with negative control shRNA-transfected cells). Additional experiments were designed to elucidate the molecular mechanism of increased transepithelial iron flux. Enhanced iron uptake by knockdown cells was associated with increased expression of a ferrireductase (duodenal cytochrome b) and activity of a cell-surface ferrireductase. Increased iron efflux from knockdown cells was likely mediated via transcriptional activation of the ferroportin 1 gene (by an unknown mechanism). Moreover, Atp7a knockdown significantly attenuated expression of an iron oxidase [hephaestin (HEPH); by ∼80%] and membrane ferroxidase activity (by ∼50%). Cytosolic ferroxidase activity, however, was retained in knockdown cells (75% of control cells), perhaps compensating for diminished HEPH activity. This investigation has thus documented alterations in iron homeostasis associated with Atp7a knockdown in enterocyte-like cells. Alterations in copper transport, trafficking, or distribution may underlie the increase in transepithelial iron flux noted when ATP7A activity is diminished.
機譯：缺鐵期間在大鼠十二指腸中誘導(dǎo)了Menkes銅運輸ATPase（Atp7a）基因，這與腸粘膜和肝臟中的銅積累一致。為了檢驗ATP7A影響腸道鐵代謝的假設(shè)，使用短發(fā)夾RNA（shRNA）技術(shù)在大鼠腸上皮（IEC-6）細胞中沉默了Atp7a基因。在敲低的細胞中注意到細胞內(nèi)銅穩(wěn)態(tài)的擾動，這與ATP7A在將銅泵入反式高爾基體（用于銅酶合成）和從細胞輸出銅的雙重作用中一致。細胞內(nèi)鐵濃度不受Atp7a敲低的影響。然而，出乎意料的是，在雙前體插入物中生長的敲低細胞中，矢量鐵（ 59 Fe）轉(zhuǎn)運增加（?33％），并且由于鐵的剝奪（與陰性對照shRNA轉(zhuǎn)染相比）進一步增加（?70％）細胞）。設(shè)計了其他實驗來闡明經(jīng)上皮鐵通量增加的分子機制。敲低細胞對鐵的吸收增加與亞鐵還原酶（十二指腸細胞色素b）的表達增加和細胞表面亞鐵還原酶的活性有關(guān)。來自敲低細胞的鐵外排增加可能是通過鐵轉(zhuǎn)運蛋白1基因的轉(zhuǎn)錄激活介導(dǎo)的（通過未知機制）。此外，Atp7a敲低顯著減弱了鐵氧化酶[hephaestin（HEPH）；約80％]和膜鐵氧化酶活性（約50％）。但是，胞質(zhì)亞鐵氧化酶的活性保留在擊倒細胞中（占對照細胞的75％），也許可以彌補HEPH活性的降低。這項研究因此證明了與腸細胞樣細胞中Atp7a敲低相關(guān)的鐵穩(wěn)態(tài)的改變。當(dāng)ATP7A活性降低時，銅轉(zhuǎn)運，運輸或分布的變化可能是跨上皮鐵通量增加的原因。

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