Dōngwùxué yánjiū, 2024-01, Vol.45 (1), p.79-94
2024
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- Autor(en) / Beteiligte
- Titel
- Loss of LBP triggers lipid metabolic disorder through H3K27 acetylation-mediated C/EBPβ- SCD activation in non-alcoholic fatty liver disease
- Ist Teil von
- Dōngwùxué yánjiū, 2024-01, Vol.45 (1), p.79-94
- Ort / Verlag
- China: Kunming Institute of Zoology, The Chinese Academy of Sciences
- Erscheinungsjahr
- 2024
- Quelle
- Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
- Beschreibungen/Notizen
- Non-alcoholic fatty liver disease (NAFLD) is associated with mutations in lipopolysaccharide-binding protein ( ), but the underlying epigenetic mechanisms remain understudied. Herein, rats with NAFLD were established and used to conduct integrative targeting-active enhancer histone H3 lysine 27 acetylation (H3K27ac) chromatin immunoprecipitation coupled with high-throughput and transcriptomic sequencing analysis to explore the potential epigenetic pathomechanisms of active enhancers of NAFLD exacerbation upon deficiency. Notably, reduced the inflammatory response but markedly aggravated high-fat diet (HFD)-induced NAFLD in rats, with pronounced alterations in the histone acetylome and regulatory transcriptome. In total, 1 128 differential enhancer-target genes significantly enriched in cholesterol and fatty acid metabolism were identified between wild-type (WT) and NAFLD rats. Based on integrative analysis, CCAAT/enhancer-binding protein β (C/EBPβ) was identified as a pivotal transcription factor (TF) and contributor to dysregulated histone acetylome H3K27ac, and the lipid metabolism gene was identified as a downstream effector exacerbating NAFLD. This study not only broadens our understanding of the essential role of in the pathogenesis of NAFLD from an epigenetics perspective but also identifies key TF C/EBPβ and functional gene as potential regulators and therapeutic targets.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 2095-8137, 0254-5853DOI: 10.24272/j.issn.2095-8137.2023.022Titel-ID: cdi_proquest_journals_2973211967
- Format
- –
- Schlagworte
- Acetylation, Animals, Carbohydrates, CCAAT/enhancer-binding protein, Cholesterol, Chromatin, Enhancers, Epigenetics, Fatty acids, Fatty liver, Genes, Genomes, High fat diet, Histone H3, Histones, Histones - metabolism, Immunoprecipitation, Inflammation, Inflammatory response, Lipid metabolism, Lipids, Lipopolysaccharide-binding protein, Lipopolysaccharides, Liver, Liver diseases, Localization, Lysine, Metabolic disorders, Mutation, Non-alcoholic Fatty Liver Disease - etiology, Non-alcoholic Fatty Liver Disease - veterinary, Pathogenesis, Proteins, Rats, Sequence analysis, Stearoyl-CoA Desaturase - metabolism, Therapeutic targets, Transcription, Transcription factors, Transcriptomes, Transcriptomics