ArticleCellular and molecular gastroenterology and hepatology2022
Regulation of Liver Regeneration by Hepatocyte O-GlcNAcylation in Mice.
Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- <p>Collagen III regulates the termination of liver regeneration by suppressing hepatocyte proliferation and promoting functional recovery</p>.Molecular medicine reports · 2026Article
- HCF-1 as a key modulator of OGT function and O-GlcNAcylation in the liver.Scientific reports · 2025Article
- Identifying novel mechanisms of per- and polyfluoroalkyl substance-induced hepatotoxicity using FRG humanized mice.Archives of toxicology · 2024Article
- Regulation of hepatic xenosensor function by HNF4alpha.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Review
- Diet-inducing hypercholesterolemia show decreased O-GlcNAcylation of liver proteins through modulation of AMPK.Journal of physiology and biochemistry · 2024Article
- Article
- Article
- HNF4α in Hepatocyte Health and Disease.Seminars in liver disease · 2023Review
- O-GlycNacylation Remission Retards the Progression of Non-Alcoholic Fatty Liver Disease.Cells · 2022Review
- Effect of PdInternational journal of molecular sciences · 2022Article
- Protein O-GlcNAcylation and the regulation of energy homeostasis: lessons from knock-out mouse models.Journal of biomedical science · 2022Review
- Article
- Biomarker discovery in acetaminophen hepatotoxicity: leveraging single-cell transcriptomics and mechanistic insight.Expert review of clinical pharmacologyReview
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsThe liver has a unique capacity to regenerate after injury in a highly orchestrated and regulated manner. Here, we report that O-GlcNAcylation, an intracellular post-translational modification regulated by 2 enzymes, O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), is a critical termination signal for liver regeneration following partial hepatectomy (PHX).
methodsWe studied liver regeneration after PHX on hepatocyte specific OGT and OGA knockout mice (OGT-KO and OGA-KO), which caused a significant decrease (OGT-KO) and increase (OGA-KO) in hepatic O-GlcNAcylation, respectively.
resultsOGA-KO mice had normal regeneration, but the OGT-KO mice exhibited substantial defects in termination of liver regeneration with increased liver injury, sustained cell proliferation resulting in significant hepatomegaly, hepatic dysplasia, and appearance of small nodules at 28 days after PHX. This was accompanied by a sustained increase in expression of cyclins along with significant induction in pro-inflammatory and pro-fibrotic gene expression in the OGT-KO livers. RNA-sequencing studies revealed inactivation of hepatocyte nuclear 4 alpha (HNF4α), the master regulator of hepatic differentiation and a known termination signal, in OGT-KO mice at 28 days after PHX, which was confirmed by both Western blot and immunohistochemistry analysis. Furthermore, a significant decrease in HNFα target genes was observed in OGT-KO mice, indicating a lack of hepatocyte differentiation following decreased hepatic O-GlcNAcylation. Immunoprecipitation experiments revealed HNF4α is O-GlcNAcylated in normal differentiated hepatocytes.
conclusionsThese studies show that O-GlcNAcylation plays a critical role in the termination of liver regeneration via regulation of HNF4α in hepatocytes.
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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.