ArticleGastroenterology2008
Keratin mutation predisposes to mouse liver fibrosis and unmasks differential effects of the carbon tetrachloride and thioacetamide models.
Article in Gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 60 citations in OpenAlex.
- Pathogenic role of serpin B3-positive neutrophils in reinforcing thrombus stiffening during ischemic stroke.Blood · 2026Article
- N-n-Butyl haloperidol iodide ameliorates liver fibrosis and hepatic stellate cell activation in mice.Acta pharmacologica Sinica · 2022Article
- SNS-032 attenuates liver fibrosis by anti-active hepatic stellate cellsFrontiers in pharmacology · 2022Article
- Role of Vitamin D as Protective Agent against Induced Liver Damage in Male Rats.Archives of Razi Institute · 2021Article
- Revealing the Roles of Keratin 8/18-Associated Signaling Proteins Involved in the Development of Hepatocellular Carcinoma.International journal of molecular sciences · 2021Review
- The role of keratins in the digestive system: lessons from transgenic mouse models.Histochemistry and cell biology · 2018Review
- Granulocyte colony stimulating factor treatment in non-alcoholic fatty liver disease: beyond marrow cell mobilization.Oncotarget · 2017Article
- Hepatocyte-Specific Deletion of Mouse Lamin A/C Leads to Male-Selective Steatohepatitis.Cellular and molecular gastroenterology and hepatology · 2017Article
- High-Throughput Screening for Drugs that Modulate Intermediate Filament Proteins.Methods in enzymology · 2016Article
- Absence of keratin 8 or 18 promotes antimitochondrial autoantibody formation in aging male mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Human keratin 8 variants promote mouse acetaminophen hepatotoxicity coupled with c-jun amino-terminal kinase activation and protein adduct formation.Hepatology (Baltimore, Md.) · 2015Article
- Prevalence of genetic variants of keratins 8 and 18 in patients with drug-induced liver injury.BMC medicine · 2015Article
- Keratin 8 variants are infrequent in patients with alcohol-related liver cirrhosis and do not associate with development of hepatocellular carcinoma.BMC gastroenterology · 2012Article
- Costaining for keratins 8/18 plus ubiquitin improves detection of hepatocyte injury in nonalcoholic fatty liver disease.Human pathology · 2012Article
- Non-coding keratin variants associate with liver fibrosis progression in patients with hemochromatosis.PloS one · 2012Article
- A mouse model of cholestasis-associated cholangiocarcinoma and transcription factors involved in progression.Gastroenterology · 2011Article
- Identification of cytokeratin 18 as a biomarker of mouse and human hepatosplenic schistosomiasis.Infection and immunity · 2011Article
- Difference in expression of hepatic microRNAs miR-29c, miR-34a, miR-155, and miR-200b is associated with strain-specific susceptibility to dietary nonalcoholic steatohepatitis in mice.Laboratory investigation; a journal of technical methods and pathology · 2010Article
- Intermediate filaments take the heat as stress proteins.Trends in cell biology · 2010Review
- Toward unraveling the complexity of simple epithelial keratins in human disease.The Journal of clinical investigation · 2009Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsKeratins 8 and 18 (K8/K18) are important hepatoprotective proteins. Animals expressing K8/K18 mutants show a marked susceptibility to acute/subacute liver injury. K8/K18 variants predispose to human end-stage liver disease and associate with fibrosis progression during chronic hepatitis C infection. We sought direct evidence for a keratin mutation-related predisposition to liver fibrosis using transgenic mouse models because the relationship between keratin mutations and cirrhosis is based primarily on human association studies.
methodsMouse hepatofibrosis was induced by carbon tetrachloride (CCl(4)) or thioacetamide. Nontransgenic mice, or mice that over express either human Arg89-to-Cys (R89C mice) or wild-type K18 (WT mice) were used. The extent of fibrosis was evaluated by quantitative real-time reverse-transcription polymerase chain reaction of fibrosis-related genes, liver hydroxyproline measurement, and Picro-Sirius red staining and collagen immunofluorescence staining.
resultsCompared with control animals, CCl(4) led to similar liver fibrosis but increased injury in K18 R89C mice. In contrast, thioacetamide caused more severe liver injury and fibrosis in K18 R89C as compared with WT and nontransgenic mice and resulted in increased messenger RNA levels of collagen, tissue inhibitor of metalloproteinase 1, matrix metalloproteinase 2, and matrix metalloproteinase 13. Analysis in nontransgenic mice showed that thioacetamide and CCl(4) have dramatically different molecular expression responses involving cytoskeletal and chaperone proteins.
conclusionsOver expression of K18 R89C predisposes transgenic mice to thioacetamide- but not CCl(4)-induced liver fibrosis. Differences in the keratin mutation-associated fibrosis response among the 2 models raise the hypothesis that keratin variants may preferentially predispose to fibrosis in unique human liver diseases. Findings herein highlight distinct differences in the 2 widely used fibrosis models.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.