Abstract

[This corrects the article on p. e55095 in vol. 8.].

Highlights

  • Erythropoiesis is a multistep process that involves the differentiation of early pluripotent hematopoietic stem cells through a series of lineage-committed cells including erythroid burst-forming unit (BFU-E) and erythroid colony-forming unit (CFU-E) progenitor cells

  • The initiation of this stress response was independent of erythropoietin and bone morphogenetic protein 4 (BMP4), and was observed in endothelial myrAkt1 mice reconstituted with wild-type bone marrow

  • We have shown that over-expression of constitutively active Akt1 in the endothelium results in increased splenic erythropoiesis, which mimics a stress-like phenotype

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Summary

Introduction

Erythropoiesis is a multistep process that involves the differentiation of early pluripotent hematopoietic stem cells through a series of lineage-committed cells including erythroid burst-forming unit (BFU-E) and erythroid colony-forming unit (CFU-E) progenitor cells. In mice, stress or tissue hypoxia results in increased erythropoiesis in the spleen. This response, termed stress erythropoiesis, involves the rapid proliferative response of a population of erythropoietic progenitor cells. Recent studies on stress erythropoiesis have defined it as a qualitatively different process from steady-state erythropoiesis, and have identified a subset of progenitors that are specific to the stress response [1,2]. The differentiation of progenitors in both pathways is dependent upon erythropoietin, but stress erythropoietic progenitors appear to require bone morphogenetic protein 4 (BMP4) for expansion in the spleen [3,4,5,6]

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