Cited by 98Hematopoietic Stem Cell TransplantationMesenchymal stem cell researchBlood disorders and treatments
Self-Renewal of Multipotent Long-Term Repopulating Hematopoietic Stem Cells Is Negatively Regulated by FAS and Tumor Necrosis Factor Receptor Activation
Open accessBryder, David, Ramsfjell, Veslemøy, Dybedal, Ingunn, Theilgaard-Mönch, Kim, Högerkorp, Carl-Magnus, Adolfsson, Jörgen, Borge, Ole Johan, Jacobsen, Sten Eirik W.·2001·The Journal of Experimental Medicine
DOI 10.1084/jem.194.7.941PMC PMC2193477
Abstract
Multipotent self-renewing hematopoietic stem cells (HSCs) are responsible for reconstitution of all blood cell lineages. Whereas growth stimulatory cytokines have been demonstrated to promote HSC self-renewal, the potential role of negative regulators remains elusive. Receptors for tumor necrosis factor (TNF) and Fas ligand have been implicated as regulators of steady-state hematopoiesis, and if overexpressed mediate bone marrow failure. However, it has been proposed that hematopoietic progenitors rather than stem cells might be targeted by Fas activation. Here, murine Lin−Sca1+c-kit+ stem cells revealed little or no constitutive expression of Fas and failed to respond to an agonistic anti-Fas antibody. However, if induced to undergo self-renewal in the presence of TNF-α, the entire short and long-term repopulating HSC pool acquired Fas expression at high levels and concomitant activation of Fas suppressed in vitro growth of Lin−Sca1+c-kit+ cells cultured at the single cell level. Moreover, Lin−Sca1+c-kit+ stem cells undergoing self-renewal divisions in vitro were severely and irreversibly compromised in their short- and long-term multilineage reconstituting ability if activated by TNF-α or through Fas, providing the first evidence for negative regulators of HSC self-renewal.
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TP53-heterozygous HSPC from pre-TP53-sAML patients showed downregulation of TNFα- and TGFβ-associated gene signatures, with upregulated expression of oxidative phosphorylation, DNA repair and interferon (IFN) response genes, without changes in IFN receptor expression levels or concurrent IFN treatment.
“TP53-heterozygous HSPC from pre-TP53-sAML patients showed downregulation of TNFα- and TGFβ-associated gene signatures, both of which are known to be associated with HSC attrition32,33, with upregulated expression of oxidative phosphorylation, DNA repair and interferon (IFN) response genes (Supplementary Table 5 and Fig. 4c–e), without changes in IFN receptor expression levels or concurrent IFN”
From Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution (2023) · cites this paper as [32]
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Self-citation
- Authors
- Bryder, D., Ramsfjell, V., Dybedal, I., Theilgaard-Mönch, K., Högerkorp, C.-M., Adolfsson, J., Borge, O. J., & Jacobsen, S. E. W.
- Affiliations
- Skåne University Hospital (SE)
- bThe Granulocyte Research Laboratory, Rigshospitalet, University of Copenhagen, Copenhagen 2100, Denmark
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2001-10-01
- Volume
- 194
- Issue
- 7
- Pages
- 941-952
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2193477
- OpenAlex
- W2137350608
- Cited by
- 98
- References
- 1
- Citations by year
- 2024: 1 · 2023: 2 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 4 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 2 · 2014: 7 · 2013: 2 · 2012: 5
- FWCI
- 3.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Keywords
- hematopoietic stem cells, self-renewal, Fas, TNF receptor, TNF-α, negative regulation, multilineage reconstitution, bone marrow failure, Fas ligand
- MeSH terms
- Animals, Antigens, Ly, Cell Division, Cell Separation, Cells, Cultured, Hematopoiesis, Hematopoietic Stem Cells, Membrane Proteins, Mice, Inbred C57BL, Tumor Necrosis Factor-alpha, Bone Marrow Transplantation, Receptors, Tumor Necrosis Factor, Antigens, CD34, Proto-Oncogene Proteins c-kit, fas Receptor, Mice
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