Figure 1.
Hepcidin deficiency protects neutrophils from intracellular iron overload. Liver hepcidin (Hamp1) expression evaluated by real-time quantitative polymerase chain reaction, plasma iron, and transferrin saturation in mice fed an iron-rich diet for 6 weeks (EIO model) vs controls (A) or Hamp1Δlivervs Hamp1lox/lox mice (B) (n ≥ 3 mice per group). (C) Blood neutrophil cell count in the EIO model vs control and Hamp1Δliver vs Hamp1lox/lox mice (n = 3 mice per group). (D) Western blot detection of FTH, TfR1, FPN and β-actin on neutrophils isolated from the different mouse models as indicated (n = 3 mice per condition). Data are representative of 2 independent experiments. (E) Quantification of the band intensity expressed in arbitrary units (a.u.). All results are shown as mean ± standard error of the mean (SEM). **P < .01; ***P < .001; ****P < .0001.

Hepcidin deficiency protects neutrophils from intracellular iron overload. Liver hepcidin (Hamp1) expression evaluated by real-time quantitative polymerase chain reaction, plasma iron, and transferrin saturation in mice fed an iron-rich diet for 6 weeks (EIO model) vs controls (A) or Hamp1Δlivervs Hamp1lox/lox mice (B) (n ≥ 3 mice per group). (C) Blood neutrophil cell count in the EIO model vs control and Hamp1Δliver vs Hamp1lox/lox mice (n = 3 mice per group). (D) Western blot detection of FTH, TfR1, FPN and β-actin on neutrophils isolated from the different mouse models as indicated (n = 3 mice per condition). Data are representative of 2 independent experiments. (E) Quantification of the band intensity expressed in arbitrary units (a.u.). All results are shown as mean ± standard error of the mean (SEM). **P < .01; ***P < .001; ****P < .0001.

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