Fig. 3.

Proposed model of the cell-to-cell modulation of iron trafficking within the adult neurovascular unit. a Homeostatic levels of intracellular iron in BMVEC, astrocytes, and neurons. b Astrocytes supply iron to neurons deficient in iron. c Neuronal iron levels are restored. Intracellular levels of iron within astrocytes drop after sufficiently supplying neurons. This drop in astrocyte iron causes the binding of endogenous IRP to the IRE of Fpn inhibiting translation. Depression in iron efflux through astrocyte Fpn catalyzes turnover of the permease. d Depletion of Fpn from the plasma membrane of astrocytes allows for GPI-Cp to catalyze iron efflux from BMVEC Fpn which can then be sequestered by astrocytes. This sequestration of iron from BMVEC will restore the intracellular iron levels of astrocytes allowing the cycle to continue. Iron is depicted entering cells through a divalent cation transporter represented here with DMT1