Figure 1
Figure 1. Results of hyperhepcidinemia in the livers of E17.5 Tmprss6−/− fetuses and during postnatal development on iron homeostasis and hematological parameters. The phenotype analyzed in E17.5 fetuses include liver Hamp1 mRNA levels relative to Cyclophilin expression assessed by quantitative polymerase chain reaction (A); placenta ferroportin (FPN), membrane protein expression assessed by western blot analysis with β-actin as a loading control (B) (quantification of the membrane was performed using ImageJ and is presented in supplemental Figure 7); total nonheme body iron (C); and MCV (D). The phenotype analyzed during postnatal development included liver Hamp1 mRNA (E), Hb (F), and MCV (G). Data are presented as mean ± standard deviation. *P < .05; **P < .005; ***P < .0005

Results of hyperhepcidinemia in the livers of E17.5 Tmprss6−/− fetuses and during postnatal development on iron homeostasis and hematological parameters. The phenotype analyzed in E17.5 fetuses include liver Hamp1 mRNA levels relative to Cyclophilin expression assessed by quantitative polymerase chain reaction (A); placenta ferroportin (FPN), membrane protein expression assessed by western blot analysis with β-actin as a loading control (B) (quantification of the membrane was performed using ImageJ and is presented in supplemental Figure 7); total nonheme body iron (C); and MCV (D). The phenotype analyzed during postnatal development included liver Hamp1 mRNA (E), Hb (F), and MCV (G). Data are presented as mean ± standard deviation. *P < .05; **P < .005; ***P < .0005

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