The loss-of-function of PKCα mitigates iron overload in hereditary hemochromatosis. (A) Serum iron level was measured in female and male Hfe^−/− and Hfe^−/−; PKCα^−/− mice (4 weeks old). Liver nonheme iron content was measured in female and male Hfe^−/− and Hfe^−/−; PKCα^−/− mice at (B) 4 and (C) 12 weeks of age. (D) Perls iron staining shows iron deposition in the liver of female and male Hfe^−/− and Hfe^−/−; PKCα^−/− mice. (E) Duodenal Fpn expression in female and male Hfe^−/− and Hfe^−/−; PKCα^−/− mice by immunoblotting with anti-mouse Fpn antibody. (F-H) Female and male Hfe^−/− mice were fed an iron-deficient diet from when they were born until 3 weeks of age. Mice were then transferred onto chow diet and receive PKC412 (50 mg/kg body weight) or vehicle for 2 weeks. (F) Duodenal Fpn expression and (G) serum and (H) liver iron content were determined. Data are expressed as mean ± SEM (n = 3-7). ∗P < .01; and ∗∗P < .05 compared with Hfe^−/− mice or the corresponding controls. Bar, 100 μm.