ArticlePloS one2016
Epigallocatechin-3-Gallate Upregulates miR-221 to Inhibit Osteopontin-Dependent Hepatic Fibrosis.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
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- Phenolic compounds and epigenetic mechanisms regulating gene expression: effects on human health.Journal of physiology and biochemistry · 2025Review
- Regulatory Effects of Coffee/Chlorogenic Acid and Tea/Epigallocatechin-3-Current issues in molecular biology · 2025Review
- The Potential Protective Effects of EGCG Against Epilepsy-Induced Damage in Rats by Mitigating Oxidative Stress, Inflammation, and Apoptosis.Scientifica · 2025Article
- Advancements in Plant-Based Therapeutics for Hepatic Fibrosis: Molecular Mechanisms and Nanoparticulate Drug Delivery Systems.International journal of molecular sciences · 2024Review
- The roles of epigallocatechin gallate in the tumor microenvironment, metabolic reprogramming, and immunotherapy.Frontiers in immunology · 2024Review
- Review
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- The relationship between polyphenols and miRNAs: A novel therapeutic strategy for metabolic associated fatty liver disease.Hepatology forum · 2021Review
- Arsenic-induced uterine apoptotic damage is protected by ethyl acetate fraction of Camellia sinensis (green tea) via Bcl-2-BAX through NF-κB regulations in Wistar rats.Environmental science and pollution research international · 2021Article
- Osteopontin as a Regulator of Colorectal Cancer Progression and Its Clinical Applications.Cancers · 2021Review
- Targeting myosin 1c inhibits murine hepatic fibrogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- A Comprehensive Review of Natural Products against Liver Fibrosis: Flavonoids, Quinones, Lignans, Phenols, and Acids.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Green Tea Polyphenol-Sensitive Calcium Signaling in Immune T Cell Function.Frontiers in nutrition · 2020Review
- Quercetin, Epigallocatechin Gallate, Curcumin, and Resveratrol: From Dietary Sources to Human MicroRNA Modulation.Molecules (Basel, Switzerland) · 2019Review
- Epigallocatechin-3-Gallate Reduces Hepatic Oxidative Stress and Lowers CYP-Mediated Bioactivation and Toxicity of Acetaminophen in Rats.Nutrients · 2019Article
- Green Tea Prevents NAFLD by Modulation of miR-34a and miR-194 Expression in a High-Fat Diet Mouse Model.Oxidative medicine and cellular longevity · 2019Article
- The Potential and Action Mechanism of Polyphenols in the Treatment of Liver Diseases.Oxidative medicine and cellular longevity · 2018Review
- Molecular Pathogenesis of Chlamydia Disease Complications: Epithelial-Mesenchymal Transition and Fibrosis.Infection and immunity · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteopontin (OPN) promotes hepatic fibrosis, and developing therapies targeting OPN expression in settings of hepatic injury holds promise. The polyphenol epigallocatechin-3-gallate (EGCG), found in high concentrations in green tea, downregulates OPN expression through OPN mRNA degradation, but the mechanism is unknown. Previous work has shown that microRNAs can decrease OPN mRNA levels, and other studies have shown that EGCG modulates the expression of multiple microRNAs. In our study, we first demonstrated that OPN induces hepatic stellate cells to transform into an activated state. We then identified three microRNAs which target OPN mRNA: miR-181a, miR-10b, and miR-221. In vitro results show that EGCG upregulates all three microRNAs, and all three microRNAs are capable of down regulating OPN mRNA when administered alone. Interestingly, only miR-221 is necessary for EGCG-mediated OPN mRNA degradation and miR-221 inhibition reduces the effects of EGCG on cell function. In vivo experiments show that thioacetamide (TAA)-induced cell cytotoxicity upregulates OPN expression; treatment with EGCG blocks the effects of TAA. Furthermore, chronic treatment of EGCG in vivo upregulates all three microRNAs equally, suggesting that in more chronic treatment all three microRNAs are involved in modulating OPN expression. We conclude that in in vitro and in vivo models of TAA-induced hepatic fibrosis, EGCG inhibits OPN-dependent injury and fibrosis. EGCG works primarily by upregulating miR-221 to accelerate OPN degradation. EGCG may therefore have utility as a protective agent in settings of liver injury.
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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.