ArticleThe Journal of biological chemistry2017
Lipopolysaccharide (LPS)-stimulated iNOS Induction Is Increased by Glucosamine under Normal Glucose Conditions but Is Inhibited by Glucosamine under High Glucose Conditions in Macrophage Cells.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 82 citations in OpenAlex.
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Anti-inflammatory activity and antioxidant capacity of Clerodendrum japonicum (Thunb.) sweet extract in LPS-stimulated macrophages.Genes & genomics · 2026Article
- The microbiota-mitochondria axis: linking metabolic dysfunction to neurodegeneration.Metabolic brain disease · 2026Review
- Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Alloxan attenuates glucosamine-induced NF-κB activation and proinflammatory gene expression under normoglycemic conditions.BMB reports · 2025Article
- The gut-adipose/pancreas axis: a novel perspective on glycolipid metabolism dysregulation in MAFLD and T2DM pathogenesis.Frontiers in endocrinology · 2025Review
- Real-time monitoring of cellular superoxide anion release in THP-1 cells using a catalytically amplified superoxide dismutase-based microbiosensor.Analytical and bioanalytical chemistry · 2024Article
- Transient receptor potential vanilloid 1 interacts with Toll-like receptor 4 (TLR4)/cluster of differentiation 14 (CD14) signaling pathway in lipopolysaccharide-mediated inflammation in macrophages.Experimental animals · 2024Article
- O-GlcNAcylation: a pro-survival response to acute stress in the cardiovascular and central nervous systems.European journal of medical research · 2024Review
- Purine Metabolism and Hexosamine Biosynthetic Pathway Abnormalities in Diarrheal Weaned Piglets Identified Using Metabolomics.Animals : an open access journal from MDPI · 2024Article
- O-GlcNAcylation in ischemic diseases.Frontiers in pharmacology · 2024Review
- Carfilzomib Mitigates Lipopolysaccharide/D-Galactosamine/Dimethylsulfoxide-Induced Acute Liver Failure in Mice.Biomedicines · 2023Article
- Crosstalk of TNF-α, IFN-γ, NF-kB, STAT1 and redox signaling in lipopolysaccharide/d-galactosamine/dimethylsulfoxide-induced fulminant hepatic failure in mice.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Extract ofPharmaceutical biology · 2022Article
- Hexokinase 1 cellular localization regulates the metabolic fate of glucose.Molecular cell · 2022Article
- Targeting ProteinCells · 2022Review
- O-GlcNAcylation regulation of cellular signaling in cancer.Cellular signalling · 2022Review
- In vitro and in vivo anti-inflammatory activity of Tetrastigma sulcatum leaf extract, pure compound and its derivatives.Inflammopharmacology · 2022Article
- Inhibition of O-GlcNAcylation protects from Shiga toxin-mediated cell injury and lethality in host.EMBO molecular medicine · 2022Article
- ProteinFrontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the regulatory effect of glucosamine (GlcN) for the production of nitric oxide (NO) and expression of inducible NO synthase (iNOS) under various glucose conditions in macrophage cells. At normal glucose concentrations, GlcN dose dependently increased LPS-stimulated production of NO/iNOS. However, GlcN suppressed NO/iNOS production under high glucose culture conditions. Moreover, GlcN suppressed LPS-induced up-regulation of COX-2, IL-6, and TNF-α mRNAs under 25 mm glucose conditions yet did not inhibit up-regulation under 5 mm glucose conditions. Glucose itself dose dependently increased LPS-induced iNOS expression. LPS-induced MAPK and IκB-α phosphorylation did not significantly differ at normal and high glucose conditions. The activity of LPS-induced nuclear factor-κB (NF-κB) and DNA binding of c-Rel to the iNOS promoter were inhibited under high glucose conditions in comparison with no significant changes under normal glucose conditions. In addition, we found that the LPS-induced increase in O-GlcNAcylation as well as DNA binding of c-Rel to the iNOS promoter were further increased by GlcN under normal glucose conditions. However, both O-GlcNAcylation and DNA binding of c-Rel decreased under high glucose conditions. The NF-κB inhibitor, pyrrolidine dithiocarbamate, inhibited LPS-induced iNOS expression under high glucose conditions but it did not influence iNOS induction under normal glucose conditions. In addition, pyrrolidine dithiocarbamate inhibited NF-κB DNA binding and c-Rel O-GlcNAcylation only under high glucose conditions. By blocking transcription with actinomycin D, we found that stability of LPS-induced iNOS mRNA was increased by GlcN under normal glucose conditions. These results suggest that GlcN regulates inflammation by sensing energy states of normal and fuel excess.
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