ArticleJournal of translational medicine2022
GM-CSF impairs erythropoiesis by disrupting erythroblastic island formation via macrophages.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Immune regulation by erythroid cells: how erythroid progenitor cells and mature red blood cells shape immunity.Nature reviews. Immunology · 2026Review
- CD163Biomarker research · 2026Article
- Evolutionary transfer learning enables organism-wide inference of mammalian enhancer landscapes.bioRxiv : the preprint server for biology · 2026Article
- Redox Modulation of Erythropoiesis by Selenoproteins.Biological trace element research · 2026Review
- Macrophages in Hematopoiesis and Related Blood Diseases.Genomics, proteomics & bioinformatics · 2025Review
- Synovium-On-A-Chip: Simulating the Microenvironment of the Rheumatoid Arthritis Synovium via Multicell Interactions to Target Fibroblast-Like Synoviocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Decoding the immune microenvironment of secondary chronic myelomonocytic leukemia due to diffuse large B-cell lymphoma with CD19 CAR-T failure by single-cell RNA-sequencing.Chinese medical journal · 2025Article
- LMNB1/CDKN1A Signaling Regulates the Cell Cycle and Promotes Hepatocellular Carcinoma Progression.Current cancer drug targets · 2025Article
- Pro- and anti-inflammatory cytokines mediate the progression of severe anemia in malaria-infected children: A prospective study.Immunity, inflammation and disease · 2024Article
- Pivotal functions and impact of long con-coding RNAs on cellular processes and genome integrity.Journal of biomedical science · 2024Review
- Identification and prognostic analysis of ferroptosis‑related gene HSPA5 to predict the progression of lung squamous cell carcinoma.Oncology letters · 2024Article
- Dysfunction of CD169Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- CD169-CD43 interaction is involved in erythroblastic island formation and erythroid differentiation.Haematologica · 2023Article
- Contributions of bone marrow monocytes/macrophages in myeloproliferative neoplasms with JAK2Annals of hematology · 2023Article
- Targeting macrophages: a novel treatment strategy in solid tumors.Journal of translational medicine · 2022Review
- Identification and prognostic analysis of biomarkers to predict the progression of pancreatic cancer patients.Molecular medicine (Cambridge, Mass.) · 2022Article
- SIRPα and PD1 expression on tumor-associated macrophage predict prognosis of intrahepatic cholangiocarcinoma.Journal of translational medicine · 2022Article
- Identification of macrophage correlated biomarkers to predict the prognosis in patients with intrahepatic cholangiocarcinoma.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Anemia is a significant complication of chronic inflammation and may be related to dysregulated activities among erythroblastic island (EBI) macrophages. GM-CSF was reported to be upregulated and attracted as a therapeutic target in many inflammatory diseases. Among EBIs, we found that the GM-CSF receptor is preferentially and highly expressed among EBI macrophages but not among erythroblasts. GM-CSF treatment significantly decreases human EBI formation in vitro by decreasing the adhesion molecule expression of CD163. RNA-sequence analysis suggests that GM-CSF treatment impairs the supporting function of human EBI macrophages during erythropoiesis. GM-CSF treatment also polarizes human EBI macrophages from M2-like type to M1-like type. In addition, GM-CSF decreases mouse bone marrow (BM) erythroblasts as well as EBI macrophages, leading to a reduction in EBI numbers. In defining the molecular mechanism at work, we found that GM-CSF treatment significantly decreases the adhesion molecule expression of CD163 and Vcam1 in vivo. Importantly, GM-CSF treatment also decreases the phagocytosis rate of EBI macrophages in mouse BM as well as decreases the expression of the engulfment-related molecules Mertk, Axl, and Timd4. In addition, GM-CSF treatment polarizes mouse BM EBI macrophages from M2-like type to M1-like type. Thus, we document that GM-CSF impairs EBI formation in mice and humans. Our findings support that targeting GM-CSF or reprogramming EBI macrophages might be a novel strategy to treat anemia resulting from inflammatory diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.