Extrahepatic deficiency of transferrin receptor 2 is associated with increased erythropoiesis independent of iron overload.

ABSTRACT: Transferrin receptor 2 (TFR2) is a transmembrane protein expressed mainly in hepatocytes and in developing erythroid cells and is an important focal point in systemic iron regulation. Loss of TFR2 function results in a rare form of the iron-overload disease hereditary hemochromatosis. Although TFR2 in the liver has been shown to be important for regulating iron homeostasis in the body, TFR2's function in erythroid progenitors remains controversial. In this report, we analyzed TFR2-deficient mice in the presence or absence of iron overload to distinguish between the effects caused by a high iron load and those caused by loss of TFR2 function. Analysis of bone marrow from TFR2-deficient mice revealed a reduction in the early burst-forming unit-erythroid and an expansion of late-stage erythro

SUBMITTER: Wortham AM 

PROVIDER: S-EPMC7086028 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature