ArticleInflammation2017
A20 Attenuates Liver Fibrosis in NAFLD and Inhibits Inflammation Responses.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Impaired flux of bile acids from the liver to the gut reveals microbiome-immune interactions associated with liver damage.NPJ biofilms and microbiomes · 2023Article
- Modeling drug-induced liver injury and screening for anti-hepatofibrotic compounds using human PSC-derived organoids.Cell regeneration (London, England) · 2023Article
- miR-200a-3p facilitates bladder cancer cell proliferation by targeting theTranslational andrology and urology · 2021Article
- Knockout of the Cannabinoid Receptor 2 Gene Promotes Inflammation and Hepatic Stellate Cell Activation by Promoting A20/Nuclear Factor-κB (NF-κB) Expression in Mice with Carbon Tetrachloride-Induced Liver Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Genetic risk factors for autoimmune hepatitis: implications for phenotypic heterogeneity and biomarkers for drug response.Human genomics · 2021Review
- A20 Orchestrates Inflammatory Response in the Oral Mucosa through Restraining NF-κB Activity.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported A20 was able to inhibit lipid accumulation in nonalcoholic steatohepatitis. We want to investigate whether A20 influences liver fibrosis in this study. Liver tissues from patients with hepatic fibrosis (n = 9) and healthy individuals (n = 7) were studied for A20 protein level by immunohistochemistry. A20 messenger RNA (mRNA) and protein level were also analyzed in two murine hepatic fibrosis models: methionine- and choline-deficient (MCD) diet and extrahepatic bile duct ligation (BDL) operation by real-time PCR and western blot. In vitro, the LX-2 human hepatic stellate cell line was treated by LPS at 0, 0.001, 0.01, 0.1, and 1 μg/mL for 6 h or at the concentration of 0.1 μg/mL for 0, 6, 12, and 24 h, then A20 expression levels were detected by western blot and PCR. The mRNA level of α-SMA, collagen I, collagen III, TGF-β, IL-6, MCP-1, and TLR4 was also examined by PCR. We then overexpressed A20 in LX-2 cells using adenovirus technique. Levels of α-SMA, collagen I, collagen III, TGF-β, IL-6, MCP-1, and TLR4 were examined in A20-overexpression LX-2 cells. Patients with hepatic fibrosis showed significantly higher A20 protein level compared with healthy controls. A20 mRNA and protein levels were also increased in livers from MCD feeding or BDL operation mice in comparison to normal controls. In LX-2 cells, LPS induced A20 protein in a concentration-dependent manner. The mRNA levels of α-SMA, collagen I, collagen III, TGF-β, IL-6, MCP-1, and TLR4 were increased after LPS treatment. Overexpression of A20 in LX-2 cells inhibited α-SMA deposition and collagen I, collagen III secretion. TGF-β, IL-6, MCP-1, and TLR4 mRNA levels were also reduced in A20-overexpression LX-2 cells in response to LPS stimulation. A20 overexpression inhibits hepatic stellate cell activation, which could be the mechanism for high A20 expression protected livers from fibrosis. Enhancement of A20 expression seems to be rational therapeutic strategies for liver fibrosis.
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