EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Dokumenter

  • Daniel Hidalgo
  • Bejder, Jacob
  • Ramona Pop
  • Kyle Gellatly
  • Yung Hwang
  • S Maxwell Scalf
  • Anna E Eastman
  • Jane-Jane Chen
  • Lihua Julie Zhu
  • Jules A A C Heuberger
  • Shangqin Guo
  • Mark J Koury
  • Nordsborg, Nikolai Baastrup
  • Merav Socolovsky

The erythroid terminal differentiation program couples sequential cell divisions with progressive reductions in cell size. The erythropoietin receptor (EpoR) is essential for erythroblast survival, but its other functions are not well characterized. Here we use Epor-/- mouse erythroblasts endowed with survival signaling to identify novel non-redundant EpoR functions. We find that, paradoxically, EpoR signaling increases red cell size while also increasing the number and speed of erythroblast cell cycles. EpoR-regulation of cell size is independent of established red cell size regulation by iron. High erythropoietin (Epo) increases red cell size in wild-type mice and in human volunteers. The increase in mean corpuscular volume (MCV) outlasts the duration of Epo treatment and is not the result of increased reticulocyte number. Our work shows that EpoR signaling alters the relationship between cycling and cell size. Further, diagnostic interpretations of increased MCV should now include high Epo levels and hypoxic stress.

OriginalsprogEngelsk
Artikelnummer7334
TidsskriftNature Communications
Vol/bind12
Antal sider17
ISSN2041-1723
DOI
StatusUdgivet - 2021

Bibliografisk note

CURIS 2021 NEXS 380
© 2021. The Author(s).

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