ArticleBritish journal of pharmacology2013
O-GlcNAcylation and p50/p105 binding of c-Rel are dynamically regulated by LPS and glucosamine in BV2 microglia cells.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Alloxan attenuates glucosamine-induced NF-κB activation and proinflammatory gene expression under normoglycemic conditions.BMB reports · 2025Article
- Glutamine alleviates immunosuppression in polymicrobial sepsis by augmenting bacterial phagocytosis through sustaining the GFAT-DRP1 dependent mitochondrial calcium dynamics.Clinical science (London, England : 1979) · 2025Article
- O‑GlcNAcylation: The crosstalk between infection immunity and autophagy in sepsis (Review).Molecular medicine reports · 2025Review
- Brain O-GlcNAcylation: Bridging physiological functions, disease mechanisms, and therapeutic applications.Molecular psychiatry · 2025Review
- Pharmacologically increasing O-GlcNAcylation increases complexity of astrocytes in the dentate gyrus of TgF344-AD rats.Frontiers in aging neuroscience · 2025Article
- Glut3 promotes cellular O-GlcNAcylation as a distinctive tumor-supportive feature in Treg cells.Cellular & molecular immunology · 2024Article
- Chronic rapid eye movement sleep deprivation aggravates the pathogenesis of Alzheimer's disease by decreasing brain O-GlcNAc cycling in mice.Journal of neuroinflammation · 2024Article
- Glucosamine increases macrophage lipid accumulation by regulating the mammalian target of rapamycin signaling pathway.BMB reports · 2024Article
- The role of O-GlcNAcylation in bone metabolic diseases.Frontiers in physiology · 2024Review
- Metabolism-driven glycosylation represents therapeutic opportunities in interstitial lung diseases.Frontiers in immunology · 2024Review
- The interaction of O-GlcNAc-modified NLRX1 and IKK-α modulates IL-1β expression in M1 macrophages.In vitro cellular & developmental biology. Animal · 2022Article
- Glucosamine regulates macrophage function in heart failure.Clinical and translational medicine · 2022Article
- Targeting ProteinCells · 2022Review
- O-Linked β-Frontiers in immunology · 2022Review
- Large Screening Identifies ACE2 Positively Correlates With NF-κB Signaling Activity and Targeting NF-κB Signaling Drugs Suppress ACE2 Levels.Frontiers in pharmacology · 2021Article
- Regulation of Nuclear Factor-kappaB Function byFrontiers in cell and developmental biology · 2021Review
- The role of O-GlcNAcylation in immunity against infections.Immunology · 2020Review
- O-GlcNAcylation and its role in the immune system.Journal of biomedical science · 2020Review
- O-GlcNAcylation in immunity and inflammation: An intricate system (Review).International journal of molecular medicine · 2019Review
- Modulation of the NOD-like receptors NOD1 and NOD2: A chemist's perspective.Bioorganic & medicinal chemistry letters · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposePreviously, we demonstrated that glucosamine (GlcN) exerts a suppressive effect on LPS-induced inducible NOS (iNOS) through the inhibition of NF-κB activation in BV2 mouse microglial cells. The purpose of the present study was to examine the mechanisms by which GlcN inhibits NF-κB activation. EXPERIMENTAL APPROACH: BV2 cells were stimulated with LPS with or without GlcN. NF-κB/c-Rel activities were studied by EMSA, nuclear translocation, reporter assay or chromatin immunoprecipitation. Wheat germ agglutinin precipitation or galactosyltransferase assay were used to measure O-linked N-acetylglucosamine (O-GlcNAc) modification (O-GlcNAcylation) of c-Rel. Protein-protein interactions were examined by co-immunoprecipitation. KEY
resultsLPS stimulated the activation of c-Rel, increased the O-GlcNAcylation of c-Rel and enhanced the binding of c-Rel to the NF-κB site in the iNOS promoter; GlcN attenuated these effects of LPS. O-GlcNAcylation of both nuclear and cytosolic forms of c-Rel was increased by LPS and reduced by GlcN. LPS increased the interaction of c-Rel with O-GlcNAc transferase (OGT) and p50/p105, and GlcN suppressed these interactions. Knockdown of OGT reduced the c-Rel O-GlcNAcylation and c-Rel-p50 interaction in response to LPS, but did not affect either the binding of c-Rel to the iNOS promoter or the transcriptional activity of c-Rel. CONCLUSIONS AND IMPLICATIONS: In BV2 microglial cells, the anti-inflammatory effect of GlcN is mediated by prevention of the prolonged activation of transcription factors, c-Rel and NF-κB. Further clarification of the mechanism by which GlcN exerts this effect will facilitate the development of pharmacological strategies for preventing excessive NO formation when targeting inflammatory diseases of the periphery or CNS.
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