ArticleLeukemia2019
Inflammation-induced glycolytic switch controls suppressivity of mesenchymal stem cells via STAT1 glycosylation.
Article in Leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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
54 citing papers in PubMed, 112 citations in OpenAlex.
- Glycolytic flux sustains human Th1 identity and effector function via STAT1 glycosylation.Life science alliance · 2026Article
- Article
- PARP inhibition augments immunomodulatory function of mesenchymal stem/stromal cells by promoting STAT1 phosphorylation.Stem cell research & therapy · 2025Article
- Palmitate enhances MSC immunomodulation of human macrophages via the ceramide/CCL2 axis in vitro.Stem cell research & therapy · 2025Article
- Indoleamine-2,3-dioxygenase: An important controller in maintaining mesenchymal stem cell-mediated immunomodulatory homeostasis.Acta pharmaceutica Sinica. B · 2025Review
- Advantages of cell proliferation and immune regulation in CD146+NESTIN+ HUMSCs: insights from single-cell RNA sequencing.Stem cells (Dayton, Ohio) · 2025Article
- Sugar symphony: glycosylation in cancer metabolism and stemness.Trends in cell biology · 2025Review
- The role of PKM2-mediated metabolic reprogramming in the osteogenic differentiation of BMSCs under diabetic periodontitis conditions.Stem cell research & therapy · 2025Article
- Article
- Mechanical sensing protein PIEZO1 controls osteoarthritis via glycolysis mediated mesenchymal stem cells-Th17 cells crosstalk.Cell death & disease · 2025Article
- Translational potential of mesenchymal stem cells in regenerative therapies for human diseases: challenges and opportunities.Stem cell research & therapy · 2024Review
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Article
- Article
- SOD2 promotes the immunosuppressive function of mesenchymal stem cells at the expense of adipocyte differentiation.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Factors Defining Human Adipose Stem/Stromal Cell Immunomodulation in Vitro.Stem cell reviews and reports · 2024Review
- Mesenchymal stem cell application in pulmonary disease treatment with emphasis on their interaction with lung-resident immune cells.Frontiers in immunology · 2024Review
- The role of O-GlcNAcylation in bone metabolic diseases.Frontiers in physiology · 2024Review
- Molecular mechanisms of cellular metabolic homeostasis in stem cells.International journal of oral science · 2023Review
- Lactate: an alternative pathway for the immunosuppressive properties of mesenchymal stem/stromal cells.Stem cell research & therapy · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesenchymal stem cells (MSCs) represent key contributors to tissue homeostasis and promising therapeutics for hyperinflammatory conditions including graft-versus-host disease. Their immunomodulatory effects are controlled by microenvironmental signals. The MSCs' functional response towards inflammatory cues is known as MSC-"licensing" and includes indoleamine 2,3-dioxygenase (IDO) upregulation. MSCs use tryptophan-depleting IDO to suppress T-cells. Increasing evidence suggests that several functions are (co-)determined by the cells' metabolic commitment. MSCs are capable of both, high levels of glycolysis and of oxidative phosphorylation. Although several studies have addressed alterations of the immune regulatory phenotype elicited by inflammatory priming metabolic mechanisms controlling this process remain unknown. We demonstrate that inflammatory MSC-licensing causes metabolic shifts including enhanced glycolysis and increased fatty acid oxidation. Yet, only interfering with glycolysis impacts IDO upregulation and impedes T-cell-suppressivity. We identified the Janus kinase (JAK)/signal transducer and activator of transcription (STAT)1 pathway as a regulator of both glycolysis and IDO, and show that enhanced glucose turnover is linked to abundant STAT1 glycosylation. Inhibiting the responsible O-acetylglucosamine (O-GlcNAc) transferase abolishes STAT1 activity together with IDO upregulation. Our data suggest that STAT1-O-GlcNAcylation increases its stability towards degradation thus sustaining downstream effects. This pathway could represent a target for interventions aiming to enhance the MSCs' immunoregulatory potency.
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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.