In the July 2 issue of the Journal of Clinical Investigation, Jodie Babitt and colleagues from Harvard Medical School show that administration of a recombinant form of the protein hemojuvelin (HJV) to mice was able to mobilize iron stored in the spleen to the blood, thereby increasing serum iron levels. This protein or other compounds that modulate this signaling pathway may be useful in treating anemia.
Iron plays an important role in the function of molecules such as hemoglobin that transport oxygen throughout the body. The concentration of iron is tightly regulated by hepcidin, a peptide hormone secreted by the liver. High hepcidin levels result in anemia while decreased hepcidin levels cause iron overload diseases.
In this issue of the JCI, Babitt et al. show that injection into mice over a period of weeks of a recombinant form of HJV binds bone morphogenetic proteins (BMPs), acts as an antagonist of BMP, thereby decreasing hepcidin expression and raising liver and serum iron levels.
In an accompanying commentary, Jerry Kaplan from the University of Utah School of Medicine discusses several reasons why these results are important. ?First, they suggest the possibility of pharmacological intervention for disorders resulting from excessive hepcidin production, as seen in?anemia. Second, they provide a mechanistic explanation for the role of HJV in iron overload disease.?
TITLE: Modulation of bone morphogenetic protein signaling in vivo regulates systemic iron balance