BMP4 and Madh5 regulate the erythroid response to acute anemia

Laurie E. Lenox, John M. Perry, Robert F. Paulson

Research output: Contribution to journalArticle

119 Scopus citations

Abstract

Acute anemia initiates a systemic response that results in the rapid mobilization and differentiation of erythroid progenitors in the adult spleen. The flexed-tail (f) mutant mice exhibit normal steady-state erythropoiesis but are unable to rapidly respond to acute erythropoietic stress. Here, we show that f/f mutant mice have a mutation in Madh5. Our analysis shows that BMP4/Madh5-dependent signaling, regulated by hypoxia, initiates the differentiation and expansion of erythroid progenitors in the spleen. These findings suggest a new model where stress erythroid progenitors, resident in the spleen, are poised to respond to changes in the microenvironment induced by acute anemia.

Original languageEnglish (US)
Pages (from-to)2741-2748
Number of pages8
JournalBlood
Volume105
Issue number7
DOIs
StatePublished - Apr 1 2005

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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