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Lookup NU author(s): Dr Seva TelezhkinORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Calcium signaling is essential to support erythroid proliferation and differentiation. Precise control of the intracellular Ca2+ levels in erythroid precursor cells (EPCs) is afforded by coordinated expression and function of several cation channels, including the recently identified N-methyl-d-aspartate receptor (NMDAR). Here, we characterized the changes in Ca2+ uptake and electric currents mediated by the NMDARs occurring during EPC differentiation using flow cytometry and patch clamp. During erythropoietic maturation, subunit composition and properties of the receptor changed; in proerythroblasts and basophilic erythroblasts, fast deactivating currents with high amplitudes were mediated by the GluN2A subunit-dominated receptors, while at the polychromatic and orthochromatic erythroblast stages, the GluN2C subunit was getting more abundant, overriding the expression of GluN2A. At these stages, the currents mediated by the NMDARs carried the features characteristic of the GluN2C-containing receptors, such as prolonged decay time and lower conductance. Kinetics of this switch in NMDAR properties and abundance varied markedly from donor to donor. Despite this variability, NMDARs were essential for survival of EPCs in any subject tested. Our findings indicate that NMDARs have a dual role during erythropoiesis, supporting survival of polychromatic erythroblasts and contributing to the Ca2+ homeostasis from the orthochromatic erythroblast stage to circulating red blood cells.
Author(s): Hänggi P, Telezhkin V, Kemp PJ, Schmugge M, Gassmann M, Goede JS, Speer O, Bogdanova A
Publication type: Article
Publication status: Published
Journal: American Journal of Physiology: Cell Physiology
Year: 2015
Volume: 308
Issue: 12
Pages: C993–C1007
Print publication date: 15/06/2015
Acceptance date: 17/03/2015
Date deposited: 09/03/2017
ISSN (print): 0363-6143
ISSN (electronic): 1522-1563
Publisher: American Physiological Society
URL: https://doi.org/10.1152/ajpcell.00395.2014
DOI: 10.1152/ajpcell.00395.2014
PubMed id: 25788577
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