ArticleWorld journal of gastroenterology2013
Role of activin A in carbon tetrachloride-induced acute liver injury.
Article in World journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026Review
- Activin A plays an essential role in migration and proliferation of hepatic stellate cells via Smad3 and calcium signaling.Scientific reports · 2024Article
- FGF21 alleviates acute liver injury by inducing the SIRT1-autophagy signalling pathway.Journal of cellular and molecular medicine · 2022Article
- Hepatoprotective effects of blue honeysuckle on CClFood science & nutrition · 2019Article
- Adenovirus‑mediated knockdown of activin A receptor type 2A attenuates immune‑induced hepatic fibrosis in mice and inhibits interleukin‑17‑induced activation of primary hepatic stellate cells.International journal of molecular medicine · 2018Article
- Endothelial transcription factor KLF2 negatively regulates liver regeneration via induction of activin A.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Urinary and Serum Metabolomics Analyses Uncover That Total Glucosides of Paeony Protect Liver against Acute Injury Potentially via Reprogramming of Multiple Metabolic Pathways.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Involvement of TGF-β1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice.PloS one · 2016Article
- Activins and Follistatin in Chronic Hepatitis C and Its Treatment with Pegylated-Interferon-α Based Therapy.Mediators of inflammation · 2015Review
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the expression and role of activin A in a mouse model of acute chemical liver injury.
methodsAcute liver injury in C57BL/6 male mice was induced by intraperitoneal injection with carbon tetrachloride (CCl4) (0.5 mL/kg, body weight) dissolved in olive oil (1:19 v/v). Mice were sacrificed 1, 3, 5 and 7 d after the treatment. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were examined and pathological changes of liver observed by hematoxylin and eosin staining to evaluate the liver injury. Activin A protein levels in serum and hepatic tissue homogenate of mice were detected by enzyme-linked immunosorbent assay, and the expression pattern of activin A protein in livers of mice was examined by immunohistochemistry. Activin type IIA receptor (ActRIIA) and Smad3 expressions in the liver were analyzed by real-time quantitative reverse transcription-polymerase chain reaction. In order to further investigate the role of activin A, we also utilized activin A blocking experiment by anti-activin A antibody (500 μg/kg, body weight) injection into mouse tail vein.
resultsIn CCl4-treated mice, serum ALT and AST levels were significantly increased, compared with that in control mice (P < 0.01). Furthermore, the serious necrosis was observed around hepatic portal areas in CCl4-treated mice. Simultaneously, activin A levels in serum and hepatic tissue homogenate of mice treated with CCl4 for 1, 3 and 5 d increased significantly, compared with that in control mice (P < 0.01). Activin A protein expression in hepatocytes not within the necrotic area was also upregulated in mice following CCl4 treatment. Not only activin A, but also ActRIIA and activin signaling molecule Smad3 mRNA expressions in injury liver induced by CCl4 were significantly higher than that in control liver. In addition, levels of serum ALT and AST in CCl4-treated mice were significantly decreased by injection of anti-activin A antibody to block endogenous activin A action, compared with that in CCl4-treated mice by injection of immunoglobulin G instead of anti-activin A antibody (P < 0.01), and the severity of liver injury was also reduced remarkably.
conclusionThese data show that activin A is involved in CCl4-induced acute liver injury. Blocking activin A actions may be a therapeutic approach for acute liver injury.
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