which secrete erythroferrone
Credit: Leon Kautz/UCLA
Researchers have discovered a new hormone, called erythroferrone, which regulates hepcidin, the main iron hormone that controls iron absorption and distribution in the body.
Using a mouse model, reseachers determined that erythroferrone is made by red blood-cell progenitors in the bone marrow, and its levels vary according to the demand for red blood cells.
“Modulating the activity of erythroferrone,” said study author Tomas Ganz, MD, PhD, of the David Geffen School of Medicine at UCLA, “could be a viable strategy for the treatment of iron disorders of both overabundance and scarcity.”
Higher levels of erythroferrone suppress hepcidin, thereby allowing more iron to be made available for red blood-cell production. Erythroferrone, or drugs acting like it, could suppress hepcidin and make more iron available for red blood-cell production.
The team began their inquiry by studying the impact of hemorrhage on the bone marrow. That led them to focus on a specific protein that was secreted in the blood. The protein belonged to a family of proteins involved in cell-to-cell communication.
They used recombinant DNA technology and found that the hormone suppressed the production of hepcidin, which affected iron metabolism.
Erythroferrone-deficient mice do not suppress hepcidin quickly after hemorrhage and consequently have delayed recovery from blood loss.
The investigators also found that erythroferrone expression is greatly increased in Hbbth3/+ mice with thalassemia intermedia, indicating that the hormone contributes to the suppression of hepcidin and iron overload characteristic of the disease.
“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, PhD, also of the David Geffen School of Medicine at UCLA.
“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,” she said.
The investigators reported their findings recently in Nature Genetics.
They noted that further research is needed to understand the role of the new hormone in various blood diseases and to study the mechanisms through which erythroferrone regulates hepcidin.
