ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Tissue factor-dependent coagulation contributes to alpha-naphthylisothiocyanate-induced cholestatic liver injury in mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice.BMC gastroenterology · 2025Article
- Neutrophil extracellular traps induce intrahepatic thrombotic tendency and liver damage in cholestatic liver disease.Hepatology communications · 2024Article
- Von Willebrand factor exerts hepatoprotective effects in acute but not chronic cholestatic liver injury in mice.Toxicology · 2021Article
- Article
- Chitinase 3-like-1 promotes intrahepatic activation of coagulation through induction of tissue factor in mice.Hepatology (Baltimore, Md.) · 2018Article
- Plasminogen Activator Inhibitor-1 Reduces Tissue-Type Plasminogen Activator-Dependent Fibrinolysis and Intrahepatic Hemorrhage in Experimental Acetaminophen Overdose.The American journal of pathology · 2018Article
- Fibrin(ogen) drives repair after acetaminophen-induced liver injury via leukocyte αJournal of hepatology · 2017Article
- Validation of precision-cut liver slices to study drug-induced cholestasis: a transcriptomics approach.Archives of toxicology · 2017Article
- Dose-dependent effects of alpha-naphthylisothiocyanate disconnect biliary fibrosis from hepatocellular necrosis.Journal of biochemical and molecular toxicology · 2017Article
- Role of hemostatic factors in hepatic injury and disease: animal models de-liver.Journal of thrombosis and haemostasis : JTH · 2016Review
- Role of Fibrin(ogen) in Progression of Liver Disease: Guilt by Association?Seminars in thrombosis and hemostasis · 2016Review
- Hepatocyte tissue factor contributes to the hypercoagulable state in a mouse model of chronic liver injury.Journal of hepatology · 2016Article
- Coagulation in liver toxicity and disease: role of hepatocyte tissue factor.Thrombosis research · 2014Review
- Article
- Fibrin(ogen)-independent role of plasminogen activators in acetaminophen-induced liver injury.The American journal of pathology · 2012Article
- Early growth response factor-1 limits biliary fibrosis in a model of xenobiotic-induced cholestasis in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Fibrinogen deficiency increases liver injury and early growth response-1 (Egr-1) expression in a model of chronic xenobiotic-induced cholestasis.The American journal of pathology · 2011Article
- Tissue factor contributes to neutrophil CD11b expression in alpha-naphthylisothiocyanate-treated mice.Toxicology and applied pharmacology · 2011Article
- Role of fibrinogen and protease-activated receptors in acute xenobiotic-induced cholestatic liver injury.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Protective effects of Moutan Cortex Radicis against acute hepatotoxicity.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Separation of concentrated bile acids from hepatic parenchymal cells is a key function of the bile duct epithelial cells (BDECs) that form intrahepatic bile ducts. Using coimmunostaining, we found that tissue factor (TF), the principal activator of coagulation, colocalized with cytokeratin 19, a marker of BDECs in the adult mouse liver. BDEC injury induced by xenobiotics such as alpha-naphthylisothiocyanate (ANIT) causes cholestasis, inflammation, and hepatocellular injury. We tested the hypothesis that acute ANIT-induced cholestatic hepatitis is associated with TF-dependent activation of coagulation and determined the role of TF in ANIT hepatotoxicity. Treatment of mice with ANIT (60 mg/kg) caused multifocal hepatic necrosis and significantly increased serum biomarkers of cholestasis and hepatic parenchymal cell injury. ANIT treatment also significantly increased liver TF expression and activity. ANIT-induced activation of the coagulation cascade was shown by increased plasma thrombin-antithrombin levels and significant deposition of fibrin within the necrotic foci. ANIT-induced coagulation and liver injury were reduced in low-TF mice, which express 1% of normal TF levels. The results indicate that ANIT-induced liver injury is accompanied by TF-dependent activation of the coagulation cascade and that TF contributes to the progression of injury during acute cholestatic hepatitis.
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