| First Author | Wang Z | Year | 2013 |
| Journal | Physiol Rep | Volume | 1 |
| Issue | 2 | Pages | e00018 |
| PubMed ID | 24303107 | Mgi Jnum | J:227960 |
| Mgi Id | MGI:5704049 | Doi | 10.1002/phy2.18 |
| Citation | Wang Z, et al. (2013) Decreased stability of erythroblastic islands in integrin beta3-deficient mice. Physiol Rep 1(2):e00018 |
| abstractText | 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 alphav integrin. Because integrins are biologically active as alpha/beta heterodimers, we asked whether beta3 could be a heterodimerization partner of alphav integrin in EIs. To this end we compared stress erythropoiesis driven by two different mechanisms, namely that of integrin beta3-deficient (beta3(-/-)) 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 beta3(-/-) mice had much less erythropoietic stimulation than tg6 mice beta3(-/-) blood contained more erythrocytes of a lower maturity stage. Unexpectedly, membranes of peripheral erythrocytes from beta3(-/-) 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 beta3(-/-) bone marrow. In conclusion, absence of integrin beta3 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. |
