Maea expressed by macrophages, but not erythroblasts, maintains postnatal murine bone marrow erythroblastic islands.

Autor:	Wei Q; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research.; Department of Cell Biology, and., Boulais PE; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research.; Department of Cell Biology, and., Zhang D; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research.; Department of Cell Biology, and., Pinho S; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research.; Department of Cell Biology, and.; Department of Medicine, Albert Einstein College of Medicine, Bronx, NY; and., Tanaka M; Laboratory of Immune Regulation, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan., Frenette PS; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research.; Department of Cell Biology, and.; Department of Medicine, Albert Einstein College of Medicine, Bronx, NY; and.
Jazyk:	angličtina
Zdroj:	Blood [Blood] 2019 Mar 14; Vol. 133 (11), pp. 1222-1232. Date of Electronic Publication: 2019 Jan 23.
DOI:	10.1182/blood-2018-11-888180
Abstrakt:	The erythroblastic island (EI), formed by a central macrophage and developing erythroblasts (EBs), was first described decades ago and was recently shown to play an in vivo role in homeostatic and pathological erythropoiesis. The exact molecular mechanisms, however, mediating the interactions between macrophages and EBs remain unclear. Macrophage-EB attacher (Maea) has previously been suggested to mediate homophilic adhesion bounds bridging macrophages and EBs. Maea -deficient mice die perinatally with anemia and defective erythrocyte enucleation, suggesting a critical role in fetal erythropoiesis. Here, we generated conditional knockout mouse models of Maea to assess its cellular and postnatal contributions. Deletion of Maea in macrophages using Csf1r -Cre or CD169 -Cre caused severe reductions of bone marrow (BM) macrophages, EBs, and in vivo island formation, whereas its deletion in the erythroid lineage using Epor -Cre had no such phenotype, suggesting a dominant role of Maea in the macrophage for BM erythropoiesis. Interestingly, Maea deletion in spleen macrophages did not alter their numbers or functions. Postnatal Maea deletion using Mx1 -Cre or function inhibition using a novel monoclonal antibody also impaired BM erythropoiesis. These results indicate that Maea contributes to adult BM erythropoiesis by regulating the maintenance of macrophages and their interaction with EBs via an as-yet-unidentified EB receptor. (© 2019 by The American Society of Hematology.)
Databáze:	MEDLINE
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