ArticleThe Journal of experimental medicine2021
PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 92 citations in OpenAlex.
- P-selectin delineates conserved functional heterogeneity in early hematopoietic stem cell aging in humans and mice.The EMBO journal · 2026Article
- Inflammageing and clonal haematopoiesis interplay and their impact on human disease.Nature reviews. Molecular cell biology · 2026Review
- Metabolic and epigenetic interplay in HSPC specification: A balance between extrinsic and intrinsic cues.iScience · 2026Review
- Epigenetic profiling of hematopoietic stem cells from male mice identifies KDR and PU.1 as regulators of aging transcriptome and caloric restriction response.Nature communications · 2026Article
- An inflammatory and quiescent HSC subpopulation expands with age in humans.Genome biology · 2026Article
- Scaffolding-dependent CASP1 constrains excessive cell-intrinsic inflammatory signaling in leukemia.Cell chemical biology · 2026Article
- USP7 sustains hematopoietic stem cell homeostasis partially via PU.1 stabilization.International journal of biological sciences · 2026Article
- Bone marrow cellular profile in patients with diabetes: association of statin therapy with CD34+ cells.Frontiers in endocrinology · 2026Observational
- Bone marrow-derived emergency monopoiesis drives brain-lung axis injury after traumatic brain injury via IL-1.Journal of neuroinflammation · 2025Article
- Ageing, immune fitness and cancer.Nature reviews. Cancer · 2025Review
- An Inflammatory and Quiescent HSC Subpopulation Expands with Age in Humans.bioRxiv : the preprint server for biology · 2025Article
- An Isoform-Specific RUNX1C-BTG2 Axis Governs AML Quiescence and Chemoresistance.Blood cancer discovery · 2025Article
- Spi1 aggravates neuropathic pain by modulating Clec7a-mediated neuroinflammation and microglial phagocytosis.The journal of headache and pain · 2025Article
- PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression.Journal of pharmaceutical analysis · 2025Article
- Function of hematopoiesis and bone marrow niche in inflammation and non-hematopoietic diseases.Life medicine · 2025Review
- Article
- Transcriptional activation of regenerative hematopoiesis via microenvironmental sensing.Nature immunology · 2025Article
- Article
- Transcription factor networks in cellular quiescence.Nature cell biology · 2025Review
- Kmt2c restricts G-CSF-driven HSC mobilization and granulocyte production in a methyltransferase-independent manner.Cell reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
Abstract
Hematopoietic stem cells (HSCs) are capable of entering the cell cycle to replenish the blood system in response to inflammatory cues; however, excessive proliferation in response to chronic inflammation can lead to either HSC attrition or expansion. The mechanism(s) that limit HSC proliferation and expansion triggered by inflammatory signals are poorly defined. Here, we show that long-term HSCs (HSCLT) rapidly repress protein synthesis and cell cycle genes following treatment with the proinflammatory cytokine interleukin (IL)-1. This gene program is associated with activation of the transcription factor PU.1 and direct PU.1 binding at repressed target genes. Notably, PU.1 is required to repress cell cycle and protein synthesis genes, and IL-1 exposure triggers aberrant protein synthesis and cell cycle activity in PU.1-deficient HSCs. These features are associated with expansion of phenotypic PU.1-deficient HSCs. Thus, we identify a PU.1-dependent mechanism triggered by innate immune stimulation that limits HSC proliferation and pool size. These findings provide insight into how HSCs maintain homeostasis during inflammatory stress.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.