ArticlePloS one2015
Treatment with 4-methylpyrazole modulated stellate cells and natural killer cells and ameliorated liver fibrosis in mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- The Important Roles of Natural Killer Cells in Liver Fibrosis.Biomedicines · 2023Review
- Safety assessment of compliant, highly invasive, lipid A-altered, O-antigen-defected Salmonella strains as prospective vaccine delivery systems.Veterinary research · 2022Article
- The antifibrotic role of natural killer cells in liver fibrosis.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- The Role of Carnitine Orotate Complex in Fatty Liver.Diabetes & metabolism journal · 2021Article
- Targeting myosin 1c inhibits murine hepatic fibrogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Comparing distress of mouse models for liver damage.Scientific reports · 2020Article
- XRP44X Enhances the Cytotoxic Activity of Natural Killer Cells by Activating the c-JUN N-Terminal Kinase Signaling Pathway.Development & reproduction · 2020Article
- CD4World journal of hepatology · 2017Article
- Hepatic immunophenotyping for streptozotocin-induced hyperglycemia in mice.Scientific reports · 2016Article
- Single cell analysis in native tissue: Quantification of the retinoid content of hepatic stellate cells.Scientific reports · 2016Article
- MicroRNA-378 limits activation of hepatic stellate cells and liver fibrosis by suppressing Gli3 expression.Nature communications · 2016Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsAccumulating evidence suggests that retinol and its metabolites are closely associated with liver fibrogenesis. Recently, we demonstrated that genetic ablation of alcohol dehydrogenase 3 (ADH3), a retinol metabolizing gene that is expressed in hepatic stellate cells (HSCs) and natural killer (NK) cells, attenuated liver fibrosis in mice. In the current study, we investigated whether pharmacological ablation of ADH3 has therapeutic effects on experimentally induced liver fibrosis in mice.
methodsLiver fibrosis was induced by intraperitoneal injections of carbon tetrachloride (CCl4) or bile duct ligation (BDL) for two weeks. To inhibit ADH3-mediated retinol metabolism, 10 μg 4-methylpyrazole (4-MP)/g of body weight was administered to mice treated with CCl4 or subjected to BDL. The mice were sacrificed at week 2 to evaluate the regression of liver fibrosis. Liver sections were stained for collagen and α-smooth muscle actin (α-SMA). In addition, HSCs and NK cells were isolated from control and treated mice livers for molecular and immunological studies.
resultsTreatment with 4-MP attenuated CCl4- and BDL-induced liver fibrosis in mice, without any adverse effects. HSCs from 4-MP treated mice depicted decreased levels of retinoic acids and increased retinol content than HSCs from control mice. In addition, the expression of α-SMA, transforming growth factor-β1 (TGF-β1), and type I collagen α1 was significantly reduced in the HSCs of 4-MP treated mice compared to the HSCs from control mice. Furthermore, inhibition of retinol metabolism by 4-MP increased interferon-γ production in NK cells, resulting in increased apoptosis of activated HSCs.
conclusionsBased on our data, we conclude that inhibition of retinol metabolism by 4-MP ameliorates liver fibrosis in mice through activation of NK cells and suppression of HSCs. Therefore, retinol and its metabolizing enzyme, ADH3, might be potential targets for therapeutic intervention of liver fibrosis.
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