EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis
Daniel Hidalgo,
Jacob Bejder,
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,
Nikolai Baastrup Nordsborg () and
Merav Socolovsky ()
Additional contact information
Daniel Hidalgo: University of Massachusetts Chan Medical School
Jacob Bejder: University of Copenhagen
Ramona Pop: University of Massachusetts Chan Medical School
Kyle Gellatly: University of Massachusetts Chan Medical School
Yung Hwang: University of Massachusetts Chan Medical School
S. Maxwell Scalf: Yale University
Anna E. Eastman: Yale University
Jane-Jane Chen: Institute for Medical Engineering & Science, MIT
Lihua Julie Zhu: University of Massachusetts Chan Medical School
Jules A. A. C. Heuberger: Centre for Human Drug Research
Shangqin Guo: Yale University
Mark J. Koury: Vanderbilt University Medical Center
Nikolai Baastrup Nordsborg: University of Copenhagen
Merav Socolovsky: University of Massachusetts Chan Medical School
Nature Communications, 2021, vol. 12, issue 1, 1-17
Abstract:
Abstract 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.
Date: 2021
References: Add references at CitEc
Citations:
Downloads: (external link)
https://www.nature.com/articles/s41467-021-27562-4 Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-27562-4
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/s41467-021-27562-4
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().