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Wang Z, Vogel O, Kuhn G, et al. Decreased stability of erythroblastic islands in integrin β3-deficient mice. Physiol Rep. 2013;1(2):e00018doi: 10.1002/phy2.18.
Wang, Z., Vogel, O., Kuhn, G., Gassmann, M., & Vogel, J. (2013). Decreased stability of erythroblastic islands in integrin β3-deficient mice. Physiological reports, 1(2), e00018. https://doi.org/10.1002/phy2.18
Wang, Zhenghui, et al. "Decreased stability of erythroblastic islands in integrin β3-deficient mice." Physiological reports vol. 1,2 (2013): e00018. doi: https://doi.org/10.1002/phy2.18
Wang Z, Vogel O, Kuhn G, Gassmann M, Vogel J. Decreased stability of erythroblastic islands in integrin β3-deficient mice. Physiol Rep. 2013 Jul;1(2):e00018. doi: 10.1002/phy2.18. Epub 2013 Jun 28. PMID: 24303107; PMCID: PMC3831914.
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Physiol Rep. 2013 Jul;1(2):e00018. doi: 10.1002/phy2.18. Epub 2013 Jun 28.

Decreased stability of erythroblastic islands in integrin β3-deficient mice.

Physiological reports

Zhenghui Wang, Olga Vogel, Gisela Kuhn, Max Gassmann, Johannes Vogel

Affiliations

  1. Institute of Veterinary Physiology, Vetsuisse Faculty University of Zürich and Zürich Center for Integrative Human Physiology (ZIHP) Zürich, Switzerland.

PMID: 24303107 PMCID: PMC3831914 DOI: 10.1002/phy2.18

Abstract

Erythroblasts proliferate and differentiate in hematopoietic organs within erythroblastic islands (EI) composed of erythropoietic progenitor cells attached to a central macrophage. This cellular interaction crucially involves the erythroid intercellular adhesion molecule-4 (ICAM-4) and αv integrin. Because integrins are biologically active as α/β heterodimers, we asked whether β3 could be a heterodimerization partner of αv integrin in EIs. To this end we compared stress erythropoiesis driven by two different mechanisms, namely that of integrin β3-deficient (β3(-/-)) mice that exhibit impaired hemostasis due to platelet dysfunction with that of systemically erythropoietin-overexpressing (tg6) mice. While compared to the respective wild type (wt) controls β3(-/-) mice had much less erythropoietic stimulation than tg6 mice β3(-/-) blood contained more erythrocytes of a lower maturity stage. Unexpectedly, membranes of peripheral erythrocytes from β3(-/-) mice (but not those from either wt control or from tg6 mice) contained calnexin, a chaperone that is normally completely lost during terminal differentiation of reticulocytes prior to their release into the circulation. In contrast to erythropoietin-overexpressing mice, the erythropoietic subpopulations representing orthochromatic erythroblasts and premature reticulocytes as well as the number of cells per EI were reduced in β3(-/-) bone marrow. In conclusion, absence of integrin β3 impairs adhesion of the latest erythroid developmental stage to the central macrophage of EIs resulting in preterm release of abnormally immature erythrocytes into the circulation.

Keywords: Bone marrow niche; calnexin; chaperone; erythroblast differentiation; erythroblastic island; integrins; stress erythropoiesis

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