ArticleThe American journal of pathology2002
Bile acid-induced Mallory body formation in drug-primed mouse liver.
Article in The American journal of pathology, 2002. 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, 47 citations in OpenAlex.
- Bile acids regulation of cellular stress responses in liver physiology and diseases.eGastroenterology · 2024Article
- Recent discoveries in microbiota dysbiosis, cholangiocytic factors, and models for studying the pathogenesis of primary sclerosing cholangitis.Open medicine (Warsaw, Poland) · 2022Review
- Review
- Loss of hepatocyte β-catenin protects mice from experimental porphyria-associated liver injury.Journal of hepatology · 2019Article
- Calnexin Depletion by Endoplasmic Reticulum Stress During Cholestasis Inhibits the NaHepatology communications · 2018Article
- Dysregulated Bile Transporters and Impaired Tight Junctions During Chronic Liver Injury in Mice.Gastroenterology · 2018Article
- NaHepatology (Baltimore, Md.) · 2018Article
- Animal models of biliary injury and altered bile acid metabolism.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Expression and localization of sterile alpha motif domain containing 5 is associated with cell type and malignancy of biliary tree.PloS one · 2017Article
- Bile acids promote diethylnitrosamine-induced hepatocellular carcinoma via increased inflammatory signaling.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Cardiomyopathy reverses with recovery of liver injury, cholestasis and cholanemia in mouse model of biliary fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2015Article
- Autophagy and apoptosis in liver injury.Cell cycle (Georgetown, Tex.) · 2015Review
- Impaired bile acid handling and aggravated liver injury in mice expressing a hepatocyte-specific RXRα variant lacking the DNA-binding domain.Journal of hepatology · 2014Article
- Role of p62/SQSTM1 in liver physiology and pathogenesis.Experimental biology and medicine (Maywood, N.J.) · 2013Review
- The establishment and characterization of immortal hepatocyte cell lines from a mouse liver injury model.In vitro cellular & developmental biology. Animal · 2011Article
- Hypertrophic cardiomyopathy and dysregulation of cardiac energetics in a mouse model of biliary fibrosis.Hepatology (Baltimore, Md.) · 2010Article
- Farnesoid X receptor critically determines the fibrotic response in mice but is expressed to a low extent in human hepatic stellate cells and periductal myofibroblasts.The American journal of pathology · 2009Article
- Hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis.PloS one · 2008Article
- Intermediate filament cytoskeleton of the liver in health and disease.Histochemistry and cell biology · 2008Review
- Epigenetic mechanisms regulate Mallory Denk body formation in the livers of drug-primed mice.Experimental and molecular pathology · 2008Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic cholestasis is associated with retention of bile acids and profound cytoskeletal alterations in hepatocytes including Mallory body (MB) formation. The mechanisms responsible for MB formation in cholestatic liver diseases are unclear. The aim of our study was to determine the relevance of cholestasis and bile acids for MB formation. For this purpose mice received a 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-supplemented diet for 2.5 months to induce MB formation. After recovery from DDC intoxication for 4 weeks followed by disappearance of MBs, these drug-primed mice were subjected to DDC refeeding, common bile duct ligation (CBDL), and feeding of a cholic acid (CA)-supplemented diet for 7 days, respectively. Cytokeratin (CK) 8 and CK 18 expression was studied by competitive reverse transcriptase-polymerase chain reaction and Western blot analysis. Cytoskeletal alterations of hepatocytes and MB formation were monitored by immunofluorescence microscopy and immunohistochemistry using CK-, ubiquitin-, and MB-specific antibodies. Like DDC refeeding, both CBDL and CA feeding of drug-primed mice significantly increased CK 8 and CK 18 mRNA and protein levels (with excess of CK 8) and resulted in ubiquitination and abnormal phosphorylation of CKs. Furthermore, CBDL and CA feeding resulted in rapid neoformation of MBs in drug-primed mice. It is concluded that MB formation in cholestatic liver diseases may be triggered by the action of potentially toxic bile acids.
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