Molecular insights into stress erythropoiesis.

Abstract:

PURPOSE OF REVIEW:In addition to its essential role in baseline erythropoiesis, the hormone erythropoietin drives the erythropoietic response to hypoxic stress. A mechanistic understanding of stress erythropoiesis would benefit multiple clinical settings, and may aid in understanding leukemogenesis. RECENT FINDINGS:The spectrum of progenitors targeted by the erythropoietin receptor is broader during stress than during baseline erythropoiesis. Further, the requirement for erythropoietin receptor signaling is more stringent during stress. However, erythropoietin receptor signaling has been mostly studied in vitro, where it is difficult to relate signaling events to stress-dependent changes in erythroid homeostasis. Here we review advances in flow cytometry that allow the identification and study of murine erythroid precursors in hematopoietic tissue as they are responding to stress in vivo. The death receptor Fas and its ligand, FasL, are coexpressed by early splenic erythroblasts, suppressing erythroblast survival and erythropoietic rate. During stress, erythropoietin receptor signaling downregulates erythroblast Fas and FasL, consequently increasing erythropoietic rate. SUMMARY:Erythropoietic rate is regulated at least in part through the erythropoietin receptor-mediated survival of splenic early erythroblasts. Future research will delineate how multiple antiapoptotic pathways, potentially activated by the erythropoietin receptor, interact to produce the remarkable dynamic range of erythropoiesis.

journal_name

Curr Opin Hematol

authors

Socolovsky M

doi

10.1097/MOH.0b013e3280de2bf1

subject

Has Abstract

pub_date

2007-05-01 00:00:00

pages

215-24

issue

3

eissn

1065-6251

issn

1531-7048

pii

00062752-200705000-00007

journal_volume

14

pub_type

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