Washington: Scientists have identified a hormone which regulates the iron supply needed for red blood-cell production.
The finding, by researchers from the University of California - Los Angeles, can lead to treatments for blood disorders associated with both iron deficiencies and overloads.
Iron is an essential functional component of hemoglobin, the molecule that transports oxygen throughout the body.
Using a mouse model, researchers found that a hormone called erythroferrone is made by red blood-cell progenitors in the bone marrow in order to match iron supply with the demands of red blood-cell production.
Erythroferrone is greatly increased when red blood-cell production is stimulated, such as after bleeding or in response to anemia.
The erythroferrone hormone acts by regulating the main iron hormone, hepcidin, which controls the absorption of iron from food and the distribution of iron in the body.
Increased erythroferrone suppresses hepcidin and allows more iron to be made available for red blood-cell production.
"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.
"Modulating the activity of erythroferrone could be a viable strategy for the treatment of iron disorders of both overabundance and scarcity," Ganz said.
Researchers first focused on what happens in the bone marrow after hemorrhage. Then they focused on a specific protein that was secreted into the blood.
This protein attracted their attention because it belonged to a family of proteins involved in cell-to-cell communication.
Using recombinant DNA technology, they showed that the hormone suppressed the production of hepcidin and demonstrated the effect it had on iron metabolism.
The team foresees that the discovery could help people with a common congenital blood disorder called Cooley's anemia, also known as thalassemia, which causes excessive destruction of red blood cells and of their progenitors in the bone marrow.
The study was published in the journal Nature Genetics.