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EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis
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EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis
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Journal Article
EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis
2021
Overview
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.
Maturing erythroblasts become smaller with every cell division. Here, the authors show that Epo stimulation promotes cell division and also generates larger red cells, and that this occurs in mouse and human cells, suggesting that red cell size could be a diagnostic marker for hypoxic stress.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14/1
/ 96
/ 96/21
/ 96/31
/ 96/35
/ 96/95
/ Adult
/ Animals
/ Cycles
/ Cyclin-Dependent Kinase Inhibitor p27 - metabolism
/ Embryo, Mammalian - metabolism
/ Erythroblasts - drug effects
/ Erythropoietin - administration & dosage
/ Erythropoietin - pharmacology
/ Female
/ Humanities and Social Sciences
/ Humans
/ Hypoxia
/ Male
/ Mice
/ Protein Serine-Threonine Kinases - metabolism
/ Receptors, Erythropoietin - metabolism
/ Receptors, Transferrin - metabolism
/ Reticulocytes - drug effects
/ Science
/ Survival
