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Deficiency of heme-regulated eIF2 kinase decreases hepcidin expression and splenic iron in HFE^–/– mice

¹ Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA
² Division of Hematology/Oncology, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA

Correspondence: Jane-Jane Chen, E25-406A, MIT, 77 Massachusetts Avenue, Cambridge, MA 02139, USA. E-mail: j-jchen{at}mit.edu

Heme-regulated eIF2 kinase (HRI) is essential for regulating globin translation in iron deficiency and in β-thalassemia. We investigated the role of heme-regulated eIF2 kinase in hemoglobin and red blood cell production as well as in iron homeostasis in a mouse model of iron overload. We show that HRI deficiency does not significantly affect red cell parameters of hemochromatosis (HFE^–/–) mice. Importantly, heme-regulated eIF2 kinase deficiency exacerbates decreases in hepcidin expression and splenic macrophage iron in HFE^–/– mice. Furthermore, the serum level of bone morphogenic protein 2, which positively regulates hepcidin, is reduced in heme-regulated eIF2 kinase deficiency, but not in HFE deficiency.

Key words: heme-regulated eIF2 kinase, hepcidin, iron deficiency.