ArticleBlood advances2022
Deleterious effect of bone marrow-resident macrophages on hematopoietic stem cells in response to total body irradiation.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Macrophages in post-chemoradiotherapy hematopoietic injury: a double-edged sword.Cell communication and signaling : CCS · 2026Review
- Post-irradiation dietary restriction impairs hematopoiesis via inhibition of the pentose phosphate pathway in hematopoietic stem and progenitor cells.Cell death & disease · 2026Article
- EMP1 safeguards hematopoietic stem cells by suppressing sphingolipid metabolism and alleviating endoplasmic reticulum stress.Nature communications · 2025Article
- Second bone marrow transplantation into regenerating hematopoiesis enhances reconstitution of immune system.Frontiers in immunology · 2024Article
- Hematopoietic and stromal DMP1-Cre labeled cells form a unique niche in the bone marrow.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone marrow (BM) resident macrophages interact with a population of long-term hematopoietic stem cells (LT-HSCs) but their role on LT-HSC properties after stress is not well defined. Here, we show that a 2 Gy-total body irradiation (TBI)-mediated death of LT-HSCs is associated with increased percentages of LT-HSCs with reactive oxygen species (ROS) and of BM resident macrophages producing nitric oxide (NO), resulting in an increased percentage of LT-HSCs with endogenous cytotoxic peroxynitrites. Pharmacological or genetic depletion of BM resident macrophages impairs the radio-induced increases in the percentage of both ROS+ LT-HSCs and peroxynitrite+ LT-HSCs and results in a complete recovery of a functional pool of LT-HSCs. Finally, we show that after a 2 Gy-TBI, a specific decrease of NO production by BM resident macrophages improves the LT-HSC recovery, whereas an exogenous NO delivery decreases the LT-HSC compartment. Altogether, these results show that BM resident macrophages are involved in the response of LT-HSCs to a 2 Gy-TBI and suggest that regulation of NO production can be used to modulate some deleterious effects of a TBI on LT-HSCs.
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