Figure 5
Figure 5. Cellular distribution of iron after 2 weeks of PR65 injections for the prevention of iron overload. Representative images are shown. Horizontal bars indicate 400 μm (10 ×) and 100 μm (40 ×). Iron accumulation was seen in the splenic red pulp of PR65–treated mice but not solvent-treated mice. Similarly, iron accumulation in duodenal enterocytes was seen only in PR65-treated mice. Compared with heart iron staining of solvent-injected mice, there was less iron accumulation in the heart of animals injected with 50 and 100 nmol of PR65, consistent with the quantitative method in Figure 4. Liver iron loading in mice treated with 20 and 50 nmol of PR65 was similar to that of the baseline group and much less than the iron loading in the solvent-treated group. At the highest PR65 dose, liver iron was lower than at baseline indicating that mice were able to mobilize liver iron despite high minihepcidin activity.

Cellular distribution of iron after 2 weeks of PR65 injections for the prevention of iron overload. Representative images are shown. Horizontal bars indicate 400 μm (10 ×) and 100 μm (40 ×). Iron accumulation was seen in the splenic red pulp of PR65–treated mice but not solvent-treated mice. Similarly, iron accumulation in duodenal enterocytes was seen only in PR65-treated mice. Compared with heart iron staining of solvent-injected mice, there was less iron accumulation in the heart of animals injected with 50 and 100 nmol of PR65, consistent with the quantitative method in Figure 4. Liver iron loading in mice treated with 20 and 50 nmol of PR65 was similar to that of the baseline group and much less than the iron loading in the solvent-treated group. At the highest PR65 dose, liver iron was lower than at baseline indicating that mice were able to mobilize liver iron despite high minihepcidin activity.

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