期刊
NATURE MEDICINE
卷 19, 期 4, 页码 437-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3126
关键词
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资金
- US National Institutes of Health [NIDDK-1R01DK090554, NIDDK-1R01DK095112]
- European Community
- Rofar (The Roche Foundation for Anemia Research)
- Children's Cancer and Blood Foundation
- American Portuguese biomedical research fund (APBRF, USA)/Inova grant
- Fundacao para a Ciencia e Tecnologia, Portugal [SFRH/BD/24813/2005]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/24813/2005] Funding Source: FCT
Regulation of erythropoiesis is achieved by the integration of distinct signals. Among them, macrophages are emerging as erythropoietin-complementary regulators of erythroid development, particularly under stress conditions. We investigated the contribution of macrophages to physiological and pathological conditions of enhanced erythropoiesis. We used mouse models of induced anemia, polycythemia vera and beta-thalassemia in which macrophages were chemically depleted. Our data indicate that macrophages contribute decisively to recovery from induced anemia, as well as the pathological progression of polycythemia vera and b-thalassemia, by modulating erythroid proliferation and differentiation. We validated these observations in primary human cultures, showing a direct impact of macrophages on the proliferation and enucleation of erythroblasts from healthy individuals and patients with polycythemia vera or b-thalassemia. The contribution of macrophages to stress and pathological erythropoiesis, which we have termed stress erythropoiesis macrophage-supporting activity, may have therapeutic implications.
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