ArticleAlcoholism, clinical and experimental research2016
Processing of miR17-92 Cluster in Hepatic Stellate Cells Promotes Hepatic Fibrogenesis During Alcohol-Induced Injury.
Article in Alcoholism, clinical and experimental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Noncoding RNA and Alcohol Use Disorder: A Scoping Review of Current Research and Knowledge Gaps.Alcohol research : current reviews · 2025Article
- Molecular regulators of alcoholic liver disease: a comprehensive analysis of microRNAs and long non-coding RNAs.Frontiers in medicine · 2025Review
- Extracellular Vesicles in Viral Liver Diseases.Viruses · 2024Review
- Unearthing the Potential Therapeutic Effects of Oxyresveratrol Based on Intrinsic Links between Pharmacological Effects: Implications for the Gut-Liver-Brain Axis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The potential role of extracellular vesicles as hepatic diagnostic and therapeutic tools: Can the dream come true?iLIVER · 2024Review
- Extracellular Vesicles as Delivery Vehicles for Non-Coding RNAs: Potential Biomarkers for Chronic Liver Diseases.Biomolecules · 2024Review
- MiRNAs in Alcohol-Related Liver Diseases and Hepatocellular Carcinoma: A Step toward New Therapeutic Approaches?Cancers · 2023Review
- MicroRNAs and Nonalcoholic Steatohepatitis: A Review.International journal of molecular sciences · 2023Review
- Unraveling the Emerging Niche Role of Hepatic Stellate Cell-derived Exosomes in Liver Diseases.Journal of clinical and translational hepatology · 2023Review
- Extracellular Vesicles as Biomarkers in Liver Disease.International journal of molecular sciences · 2022Review
- Small extracellular vesicles and liver diseases: From diagnosis to therapy.World journal of hepatology · 2022Review
- Pathological Contribution of Extracellular Vesicles and Their MicroRNAs to Progression of Chronic Liver Disease.Biology · 2022Review
- Ethanol Induces Secretion of Proinflammatory Extracellular Vesicles That Inhibit Adult Hippocampal Neurogenesis Through G9a/GLP-Epigenetic Signaling.Frontiers in immunology · 2022Article
- Extracellular vesicles in inflammation: Focus on the microRNA cargo of EVs in modulation of liver diseases.Journal of leukocyte biology · 2022Review
- Pathogenic and Potential Therapeutic Roles of Exosomes Derived From Immune Cells in Liver Diseases.Frontiers in immunology · 2022Review
- MicroRNA 200a inhibits liver fibrosis ofBioengineered · 2021Article
- Hepatic stellate cell-derived exosomes modulate macrophage inflammatory response.Experimental cell research · 2021Article
- Diagnosis and Therapeutic Management of Liver Fibrosis by MicroRNA.International journal of molecular sciences · 2021Review
- Bile extracellular vesicles from end-stage liver disease patients show altered microRNA content.Hepatology international · 2021Article
- Exosomal microRNAs as diagnostic and therapeutic biomarkers in non-malignant liver diseases.Archives of pharmacal research · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundExposure to alcohol and its metabolites can initiate hepatic injury and fibrogenesis. Fibrosis is mediated through hepatic stellate cell (HSC) activation, leading to global changes in mRNA and microRNA (miR) expression. miRs are expressed in cells or shuttled to exosomes which can be detected in tissue culture media (TCM) and biological fluids. The mechanisms and function underlying the differential expression and processing of miRs and their downstream effects during hepatic injury remain poorly understood.
methodsExpression of primary (pri)-miR17-92. and individual members of this cluster, miR17a, 18a, 19a, 20a, 19b, and 92, were examined in primary HSCs and human LX2 cells exposed to alcohol-conditioned media (CM), liver tissue from a rodent model of alcoholic injury, and in exosomes from TCM and plasma of rodent models and patients with alcoholic liver disease (ALD). miR expression was examined in HSCs transduced with an AAV2 vector carrying GFP-miR19b or GFP-control transgene under the collagen promoter.
resultsProfibrotic markers were enhanced in primary HSCs and LX2 cells exposed to alcohol-CM, concomitant with decreased miR19b expression and a significant increase in pri-miR17-92. Increased pri-miR17-92 was confirmed in a rodent model of alcohol-induced liver injury. Individual members of the cluster were inversely proportionate in cells and exosomes. AAV2-mediated miR19b overexpression inhibited miR17-92 and altered expression of individual cluster members in cells and exosomes. Expression of individual miR17-92 cluster members in plasma exosomes isolated from patients with ALD was similar to that seen in a rodent model of alcoholic injury and in vitro.
conclusionsReintroduction of miR19b inhibits HSC activation and modulates expression of pri-miR17-92 and the inverse expression of individual cluster members in cells and exosomes. Better understanding of miR17-92 processing may provide mechanistic insights into the role of individual miRs and exosomes during hepatic injury, revealing new therapeutic targets.
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