Journal
BLOOD
Volume 105, Issue 7, Pages 2741-2748Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2004-02-0703
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Funding
- NHLBI NIH HHS [R01 HL70720, R01 HL070720] Funding Source: Medline
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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. (c) 2005 by The American Society of Hematology.
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