ArticleMetabolic brain disease2014
O-GlcNAcylation as a novel ammonia-induced posttranslational protein modification in cultured rat astrocytes.
Article in Metabolic brain disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Resveratrol in Patients with Minimal Hepatic Encephalopathy.Nutrients · 2018Trial
- The role of ammonia in chronic liver disease.Hepatology communications · 2026Review
- Effect of Ammonia onAntioxidants (Basel, Switzerland) · 2026Article
- O-GlcNAc as ammonia-induced glycosylation during the development of hyperammonemia.Journal of molecular histology · 2025Article
- O-GlcNAc modulation of nuclear pore complexes orchestrates mRNA export efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cellular Pathogenesis of Hepatic Encephalopathy: An Update.Biomolecules · 2023Review
- Review
- O-GlcNAcylation enhances CPS1 catalytic efficiency for ammonia and promotes ureagenesis.Nature communications · 2022Article
- Role of ammonia for brain abnormal protein glycosylation during the development of hepatitis B virus-related liver diseases.Cell & bioscience · 2022Article
- InAntioxidants (Basel, Switzerland) · 2020Article
- Analysis of Risk Factors for Postoperative Delirium After Liver Transplantation.Neuropsychiatric disease and treatment · 2020Article
- Hepatic encephalopathy is linked to alterations of autophagic flux in astrocytes.EBioMedicine · 2019Article
- Hepatic encephalopathy: Lessons from preclinical studies.World journal of hepatology · 2019Review
- Hyperammonemia in Hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018Review
- O-GlcNAc cycling in the developing, adult and geriatric brain.Journal of bioenergetics and biomembranes · 2018Review
- Ammonia promotes endothelial cell survival via the heme oxygenase-1-mediated release of carbon monoxide.Free radical biology & medicine · 2017Article
- Recent advances in hepatic encephalopathy.F1000Research · 2017Review
- Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress.Brain research · 2016Review
- Ammonium ions improve the survival of glutamine-starved hybridoma cells.Cell & bioscience · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic encephalopathy (HE) is a clinical manifestation of a low grade cerebral edema with a mutual interrelationship between osmotic- and oxidative stress. This leads to RNA oxidation and posttranslational protein modifications such as protein tyrosine nitration with pathophysiological relevance. Here, we report on O-GlcNAcylation as another ammonia-induced posttranslational protein modification in cultured rat astrocytes. NH4Cl induced O-GlcNAcylation of distinct proteins (25-250 kDa) in astrocytes in a dose- and time-dependent manner. Exposure of astrocytes to NH4Cl (5 mmol/l) for 48 h and 72 h significantly increased protein O-GlcNAcylation by about 2-fold and 4-fold, respectively. NH4Cl at a concentration of 1 mmol/l was sufficient to double protein O-GlcNAcylation in astrocytes after 72 h as compared to untreated controls. Ammonia-induced protein O-GlcNAcylation was sensitive towards glutamine-synthetase inhibition by methionine sulfoximine (MSO), but was not induced by hypoosmolarity (205 mosmol/l) or CH3NH3Cl (5 mmol/l). Increased protein O-GlcNAcylation in NH4Cl (5 mmol/l, 48 h)-treated astrocytes was fully reversible within 24 h after withdrawal of NH4Cl from culture medium. Amongst the proteins which are O-GlcNAcylated in response to ammonia, GAPDH was identified. It is concluded that ammonia induces reversible protein O-GlcNAcylation in astrocytes that depends on glutamine synthesis but not on astrocyte swelling per se or ammonia-induced pH-changes. In view of the complex involvement of O-GlcNAcylation in cell regulation, such as energy metabolism, apoptosis and circadian rhythmicity and in pathologies, such as neurodegenerative diseases, O-GlcNAcylation might contribute to the pathophysiology of hepatic encephalopathy.
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