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Erythroferrone Frees Up Iron for Red Blood Cell Production by Inhibiting Hepcidin

By BiotechDaily International staff writers
Posted on 11 Jun 2014
Image: A microscopic image of erythroblasts which are the bone marrow cells that secrete erythroferrone (Photo courtesy of UCLA - University of California, Los Angeles).
Image: A microscopic image of erythroblasts which are the bone marrow cells that secrete erythroferrone (Photo courtesy of UCLA - University of California, Los Angeles).
A recent paper outlined a novel biochemical pathway in the bone marrow that regulates the increase production of red blood cells that are required following blood loss due to hemorrhage or anemia.

Investigators at the University of California, Los Angeles (UCLA; USA) have been studying the newly discovered hormone erythroferrone (ERFE) and its affect on another hormone, hepcidin.

Hepcidin is a peptide hormone encoded by the HAMP gene and produced primarily by the liver. This hormone appears to be the master regulator of iron homeostasis in humans and other mammals. Hepcidin functions to inhibit iron transport across the gut mucosa, thereby preventing excess iron absorption and maintaining normal iron levels within the body. Hepcidin also inhibits transport of iron out of macrophages (where iron is stored). Therefore, anemia can develop in states of high hepcidin levels, where serum iron levels drop because iron is trapped inside macrophages. The question being asked in the current study was how hepcidin was regulated to release iron when a sudden increase in red blood cell synthesis was called for.

For this study the investigators genetically engineered a line of mice that produced exceptionally low levels of ERFE. They found that these mice failed to suppress hepcidin rapidly after hemorrhage and exhibited a delay in recovery from blood loss. Results from a different set of experiments revealed that ERFE expression was greatly increased in Hbbth3/+ mice with thalassemia intermedia, where it contributed to the suppression of hepcidin and the systemic iron overload characteristic of this disease.

"If there is too little iron, it causes anemia. If there is too much iron, the iron overload accumulates in the liver and organs, where it is toxic and causes damage," said senior author Dr. Tomas Ganz, professor of medicine and pathology at the UCLA. "Modulating the activity of erythroferrone could be a viable strategy for the treatment of iron disorders of both overabundance and scarcity."

The description of ERFE activity was published in the June 1, 2014, online edition of the journal Nature Genetics.

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University of California, Los Angeles



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