Hepcidin antimicrobial peptide transgenic mice exhibit features of the anemia of inflammation

Cindy N. Roy, Howard H. Mak, Imo Akpan, Grigoriy Losyev, David Zurakowski, Nancy C. Andrews

Research output: Contribution to journalArticle

Abstract

The anemia of inflammation is an acquired disorder affecting patients with a variety of medical conditions, and it is characterized by changes in iron homeostasis and erythropoiesis. Mounting evidence suggests that hepcidin antimicrobial peptide plays a primary role in the pathogenesis of the anemia of inflammation. To evaluate which features of this anemia can be attributed to hepcidin, we have generated mice carrying a tetracycline-regulated hepcidin transgene. Expression of the hepcidin transgene resulted in down-regulation of endogenous hepcidin mRNA. The transgenic mice developed a mild-to-moderate anemia associated with iron deficiency and ironrestricted erythropoiesis. Similar to the anemia of inflammation, iron accumulated in tissue macrophages, whereas a relative paucity of iron was found in the liver. Circulating erythrocytes in transgenic animals had normal survival rates, but transgenic animals had an impaired response to erythropoietin. Thus, hepcidin transgenic mice recapitulate each of the key features of anemia of inflammation in human patients and serve as a useful model of this prevalent disorder.

Original languageEnglish (US)
Pages (from-to)4038-4044
Number of pages7
JournalBlood
Volume109
Issue number9
DOIs
StatePublished - May 1 2007

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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    Roy, C. N., Mak, H. H., Akpan, I., Losyev, G., Zurakowski, D., & Andrews, N. C. (2007). Hepcidin antimicrobial peptide transgenic mice exhibit features of the anemia of inflammation. Blood, 109(9), 4038-4044. https://doi.org/10.1182/blood-2006-10-051755