Liver expression of hepcidin and other iron genes in two mouse models of beta-thalassemia

th3/+ , which have the greater, age-dependent, iron overload. Hepcidin RNA was not increased despite iron overload in both strains. Fpn RNA was increased and Tfr2 was decreased in older ani- mals. Inflammatory cytokine levels were striking variable and unrelated to hepcidin lev- els. Interpretation and Conclusions. Although anemia is reported to inhibit hepcidin expres- sion, normal hepcidin synthesis was maintained in both thalassemic models studied. However, hepcidin levels were inappropriate for the body iron, especially in Hbb th3/+ 10- month-old animals. As we previously reported in wild type mice after parenteral iron overload, Tfr2 is reduced and Fpn RNA increased in thalassemic mice. Inflammatory cytokines did not play a major role in increasing hepcidin levels or in modifying iron homeostasis in this study.