University of California Los Angeles researchers claim to have discovered a new hormone that controls the iron supply required for red blood-cell production.
The researchers used a mouse model and discovered that the hormone, erythroferrone, is made by red blood-cell progenitors in the bone marrow to match iron supply with the demand of red blood-cell production. The hormone supply increases when red blood-cell production is activated due to injuries or when a person is anemic.
"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, a professor of medicine and pathology at the David Geffen School of Medicine at UCLA, in a press release. "Modulating the activity of erythroferrone could be a viable strategy for the treatment of iron disorders of both overabundance and scarcity."
"Our previous work anticipated that a regulator of hepcidin could be secreted by the bone marrow," said the study's first author, Leon Kautz, a postdoctoral fellow at UCLA. "In this research, we searched for new substances that were made in bone marrow that could fill that role."
Researchers concentrated on the happenings in the bone marrow after hemorrhage. Then they focused on a particular protein that was secreted into the blood. The protein was important because it belonged to a family of proteins involved in cell-to-cell communication.
Researchers said that the discovery might be helpful for new treatments for blood disorders associated with both iron deficiencies and overloads.
"Overproduction of erythroferrone may be a major cause of iron overload in untransfused patients and may contribute to iron overload in transfused patients," said study author Elizabeta Nemeth, a professor of medicine at the David Geffen School of Medicine at UCLA and co-director of the UCLA Center for Iron Disorders. "The identification of erythroferrone can potentially allow researchers and drug developers to target the hormone for specific treatment to prevent iron overload in Cooley's anemia."
The findings of the study have been published in the journal 'Nature Genetics.'
