ArticleJournal of cellular biochemistry2017
RAR-Related Orphan Receptor Gamma (ROR-γ) Mediates Epithelial-Mesenchymal Transition Of Hepatocytes During Hepatic Fibrosis.
Article in Journal of cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Exploring Cirrhosis: Insights into Advances in Therapeutic Strategies.International journal of molecular sciences · 2025Review
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- Hydrodynamic Delivery: Characteristics, Applications, and Technological Advances.Pharmaceutics · 2023Review
- Bile Acids and Biliary Fibrosis.Cells · 2023Review
- Targeted Assessment of Mucosal Immune Gene Expression Predicts Clinical Outcomes in Children with Ulcerative Colitis.Journal of Crohn's & colitis · 2022Article
- Establishment of a reference single-cell RNA sequencing dataset for human pancreatic adenocarcinoma.iScience · 2022Article
- Implications of Heterogeneity of Epithelial-Mesenchymal States in Acromegaly Therapeutic Pharmacologic Response.Biomedicines · 2022Article
- Death-Associated Protein 6 (Daxx) Alleviates Liver Fibrosis by Modulating Smad2 Acetylation.Cells · 2021Article
- Article
- Article
- Pterostilbene prevents hepatocyte epithelial-mesenchymal transition in fructose-induced liver fibrosis through suppressing miR-34a/Sirt1/p53 and TGF-β1/Smads signalling.British journal of pharmacology · 2019Article
- Long-chain fatty acid activates hepatocytes through CD36 mediated oxidative stress.Lipids in health and disease · 2018Article
- Reversal effect of Jagged1 signaling inhibition on CCl4-induced hepatic fibrosis in rats.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-mesenchymal transition (EMT) is involved in many different types of cellular behavior, including liver fibrosis. In this report, we studied a novel function of RAR-related orphan receptor gamma (ROR-γ) in hepatocyte EMT during liver fibrosis. To induce EMT in vitro, primary hepatocytes and FL83B cells were treated with TGF-β1. Expression of ROR-γ was analyzed by Western blot in the fibrotic mouse livers and human livers with cirrhosis. To verify the role of ROR-γ in hepatocyte EMT, we silenced ROR-γ in FL83B cells using a lentiviral short hairpin RNA (shRNA) vector. The therapeutic effect of ROR-γ silencing was investigated in a mouse model of TAA-induced fibrosis by hydrodynamic injection of plasmids. ROR-γ expression was elevated in hepatocyte cells treated with TGF-β1, and ROR-γ protein levels were elevated in the fibrotic mouse livers and human livers with cirrhosis. Knockdown of ROR-γ resulted in the attenuation of TGF-β1-induced EMT in hepatocytes. Strikingly, ROR-γ bound to ROR-specific DNA response elements (ROREs) in the promoter region of TGF-β type I receptor (Tgfbr1) and Smad2, resulting in the downregulation of Tgfbr1 and Smad2 after silencing of ROR-γ. Therapeutic delivery of shRNA against ROR-γ attenuated hepatocyte EMT and ameliorated liver fibrosis in a mouse model of TAA-induced liver fibrosis. Overall, our results suggest that ROR-γ regulates TGF-β-induced EMT in hepatocytes during liver fibrosis. We suggest that ROR-γ may become a potential therapeutic target in treating liver fibrosis. J. Cell. Biochem. 118: 2026-2036, 2017. © 2016 The Authors. Journal of Cellular Biochemistry Published by Wiley Periodicals Inc.
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