Figure 3. Ablation of Slc39a14 in the Hfe2^−/− Mouse Model of Juvenile Hemochromatosis Prevents Hepatic Iron Overload.

(A) Tissue non-heme iron concentrations in WT, Slc39a14^−/−, Hfe2^−/−, and Hfe2^−/−;Slc39a14^−/− mice at 6 wk of age (n = 4–11 per group). (B) Iron absorption (% of dose) was measured after intragastric gavage of ⁵⁹Fe (n = 4–10 per group). (C–E) Hepatic, pancreatic, and splenic ⁵⁹Fe accumulation (% of absorbed ⁵⁹Fe) was measured after intragastric gavage of ⁵⁹Fe (n = 4–11 per group). (F–H) Representative images of Perls’ iron stain in paraffin-embedded liver sections of mice at 6 wk of age (n = 3 per group). (F, G) Liver sections processed by using standard Perls’ iron stain (blue stain) and hematoxylin counterstain. Scale bars, 200 and 100 μm, respectively. (H) Serial liver sections processed by using DAB-enhanced Perls’ stain (black stain) and neutral red counterstain. Arrows indicate iron deposits in non-parenchymal cells. Scale bars, 100 μm. (I–L) Plasma iron indices. (I) Plasma iron concentrations (n = 4–6 per group). (J) Total iron-binding capacity, TIBC (n = 4–6 per group). (K) Transferrin saturation (n = 4–6 per group). (L) Plasma NTBI concentrations (n = 5–9 per group). (M) Body weights of mice at 6 wk of age (n = 7–11 per group). All data are shown as the mean ± SEM. Means without a common superscript differ significantly (p < 0.05). See also Figure S1, Figure S2, Figure S3, Figure S5, and Table S1.