Macrophages support pathological erythropoiesis in polycythemia vera and β-thalassemia
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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 β-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 β-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 β-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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Erythroid island macrophages are a population of bone marrow-resident macrophages that support erythropoiesis as nurse cells.
“Erythroid island macrophages (EIM) are a population of BM-resident macrophages that support erythropoiesis as “nurse cells” [17, 192].”
From “Pumping iron”—how macrophages handle iron at the systemic, microenvironmental, and cellular levels (2017) · cites this paper as [192]
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- Authors
- Ramos, P., Casu, C., Gardenghi, S., Breda, L., Crielaard, B. J., Guy, E., Marongiu, M. F., Gupta, R., Levine, R. L., Abdel-Wahab, O., Ebert, B. L., Van Rooijen, N., Ghaffari, S., Grady, R. W., Giardina, P. J., & Rivella, S.
- Affiliations
- Weill Cornell Medicine (US)
- Memorial Sloan Kettering Cancer Center (US)
- Brigham and Women's Hospital (US)
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Rivella, Stefano
- ORCID
- Venue
- Nature Medicine
- Published
- 2013-03-17
- Volume
- 19
- Issue
- 4
- Pages
- 437-445
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3618568
- OpenAlex
- W2023747882
- Cited by
- 227
- References
- 66
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 7 · 2023: 20 · 2022: 14 · 2021: 15 · 2020: 19 · 2019: 13 · 2018: 13 · 2017: 26 · 2016: 18 · 2015: 27 · 2014: 31 · 2013: 10
- FWCI
- 14.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Pure Amsterdam UMC (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK090554, R01DK095112)
- Topics
- Health Sciences › Medicine › Genetics › Myeloproliferative Neoplasms: Diagnosis and Treatment
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Keywords
- macrophages, erythropoiesis, polycythemia vera, beta-thalassemia, erythroblasts, erythroblast enucleation, erythroid proliferation, erythropoietin, macrophage depletion, stress erythropoiesis, red blood cell recovery
- MeSH terms
- Animals, Clodronic Acid, Disease Models, Animal, Erythrocyte Count, Erythropoiesis, Female, Hematocrit, Hemoglobins, Humans, Macrophages, Male, Mice, Inbred C57BL, Polycythemia Vera, Reticulocytes, Stress, Physiological, beta-Thalassemia, Mice
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