Mouse Model Yields Possible Alternative Treatment for Chronic Anemia

Researchers working with a mouse model of chronic anemia have identified a protein that can enhance or replace erythropoietin therapy.

Erythropoietin (Epo) is a therapeutic agent that is commonly produced by recombinant DNA technology in mammalian cell culture. It is used in treating anemia resulting from chronic kidney disease, from the treatment of cancer (chemotherapy and radiation), and from other critical illnesses (heart failure).

Investigators at the University of Lausanne (Switzerland) found that treatment of mouse erythroblasts with Epo stimulated the release of Gas6 (growth arrest–specific gene 6) protein, and that Gas6 enhanced Epo receptor signaling by activating the serine-threonine kinase Akt in these cells. In the absence of Gas6, red blood cell progenitors and erythroblasts were resistant to the survival activity of Epo and failed to restore hematocrit levels in response to anemia.

Additional data reported in the January 10, 2008, issue of the Journal of Clinical Investigation showed that when mice with acute anemia were treated with Gas6, the protein normalized hematocrit levels without causing undesired erythrocytosis. In a transgenic mouse model of chronic anemia caused by insufficient Epo production, Gas6 worked in tandem with Epo in restoring hematocrit levels.

The investigators concluded by suggesting, "These findings may have implications for the treatment of patients with anemia who fail to adequately respond to Epo.”


Related Links:
University of Lausanne