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Copper (Cu) is an essential trace element that requires tight homeostatic regulation to ensure appropriate supply while not causing cytotoxicity due to its strong redox potential. Our previous in vivo study has shown that iron deficiency (FeD) increases Cu levels in brain tissues, particularly in the choroid plexus, where the blood-cerebrospinal fluid (CSF) barrier resides. This study was designed to elucidate the mechanism by which FeD results in excess Cu accumulation at the blood-CSF barrier. The effect of FeD on cellular Cu retention and transporters Cu transporter-1 (Ctr1), divalent metal transporter 1 (DMT1), antioxidant protein-1 (ATOX1) and ATP7A was examined in choroidal epithelial Z310 cells. The results revealed that deferoximine treatment (FeD) resulted in 70% increase in cellular Cu retention (P &lt; 0.05). A significant increase in the mRNA levels of DMT1, but not Ctr1, was also observed after FeD treatment, suggesting a critical role of DMT1 in cellular Cu regulation during FeD. Knocking down Ctr1 or DMT1 resulted in significantly lower Cu uptake by Z310 cells, whereas the knocking down of ATOX1 or ATP7A led to substantial increases of cellular retention of Cu. Taken together, these results suggest that Ctr1, DMT1, ATOX1 and ATP7A contribute to Cu transport at the blood-CSF barrier, and that the accumulation of intracellular Cu found in the Z310 cells during FeD appears to be mediated, at least in part, via the upregulation of DMT1 after FeD treatment.

Mechanism of copper transport at the blood–cerebrospinal fluid barrier: influence of iron deficiency in an in vitro model