ArticleThe EMBO journal2024
Chromatin modifier Hmga2 promotes adult hematopoietic stem cell function and blood regeneration in stress conditions.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Hmga2-dependent cAMP signaling drives UVB-induced melanocyte stem cell activation.The Journal of investigative dermatology · 2026Article
- Nitric oxide induces p53-mediated cell death in human nasal epithelial cells.Scientific reports · 2026Article
- High Mobility Group A1 Chromatin Keys: Unlocking the Genome During MPN Progression.International journal of molecular sciences · 2025Review
- Inhibition of HMGA2 binding to AT-rich DNA by its negatively charged C-terminus.Nucleic acids research · 2025Article
- 3' UTR-truncated HMGA2 promotes erythroblasts production from human embryonic stem cells.Stem cells translational medicine · 2025Article
- Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025Review
- Epigenetic Regulation of CXC Chemokine Expression by Environmental Electrophiles Through DNA Methyltransferase Inhibition.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
The molecular mechanisms governing the response of hematopoietic stem cells (HSCs) to stress insults remain poorly defined. Here, we investigated effects of conditional knock-out or overexpression of Hmga2 (High mobility group AT-hook 2), a transcriptional activator of stem cell genes in fetal HSCs. While Hmga2 overexpression did not affect adult hematopoiesis under homeostasis, it accelerated HSC expansion in response to injection with 5-fluorouracil (5-FU) or in vitro treatment with TNF-α. In contrast, HSC and megakaryocyte progenitor cell numbers were decreased in Hmga2 KO animals. Transcription of inflammatory genes was repressed in Hmga2-overexpressing mice injected with 5-FU, and Hmga2 bound to distinct regions and chromatin accessibility was decreased in HSCs upon stress. Mechanistically, we found that casein kinase 2 (CK2) phosphorylates the Hmga2 acidic domain, promoting its access and binding to chromatin, transcription of anti-inflammatory target genes, and the expansion of HSCs under stress conditions. Notably, the identified stress-regulated Hmga2 gene signature is activated in hematopoietic stem progenitor cells of human myelodysplastic syndrome patients. In sum, these results reveal a TNF-α/CK2/phospho-Hmga2 axis controlling adult stress hematopoiesis.
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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 OpenQuestion graph.