Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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"Köpfe" der aktuellen Meldungen:

Nina Höller

Nariae Baik-Schneditz

Bernhard Schwaberger

Lukas Peter Mileder

Niels Hammer

Gerhard Pichler

Roland Malli

Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid Stoffw Microb

Fickert, P; Fuchsbichler, A; Marschall, HU; Wagner, M; Zollner, G; Krause, R; Zatloukal, K; Jaeschke, H; Denk, H; Trauner, M.
Lithocholic acid feeding induces segmental bile duct obstruction and destructive cholangitis in mice.
Am J Pathol. 2006; 168(2):410-422 Doi: 10.2353/ajpath.2006.050404 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz: Fickert Peter; Trauner Michael
Co-Autor*innen der Med Uni Graz: Denk Helmut; Krause Robert; Wagner Martin; Zatloukal Kurt; Zollner Gernot
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Abstract:: We determined the mechanisms of hepatobiliary injury in the lithocholic acid (LCA)-fed mouse, an increasingly used model of cholestatic liver injury. Swiss albino mice received control diet or 1% (w/w) LCA diet (for 1, 2, and 4 days), followed by assessment of liver morphology and ultrastructure, tight junctions, markers of fibrosis and key proteins of hepatobiliary function, and bile flow and composition. As expected LCA feeding led to bile infarcts, which were followed by a destructive cholangitis with activation and proliferation of periductal myofibroblasts. At the ultrastructural level, small bile ducts were frequently obstructed by crystals. Biliary-excreted fluorescence-labeled ursodeoxycholic acid accumulated in bile infarcts, whereas most infarcts did not stain with India ink injected into the common bile duct; both findings are indicative of partial biliary obstruction. Expression of the main basolateral bile acid uptake proteins (sodium-taurocholate cotransporter and organic anion-transporting polypeptide 1) was reduced, the canalicular transporters bile salt export pump and multidrug-related protein 2 were preserved, and the basolateral transporter multidrug-related protein 3 and the detoxifying enzyme sulfotransferase 2a1 were induced. Thus, we demonstrate that LCA feeding in mice leads to segmental bile duct obstruction, destructive cholangitis, periductal fibrosis, and an adaptive transporter and metabolic enzyme response.
Find related publications in this database (using NLM MeSH Indexing): Animals -; Bile Acids and Salts - metabolism; Biliary Tract Diseases - chemically induced Biliary Tract Diseases - metabolism Biliary Tract Diseases - pathology; Cholangitis - chemically induced Cholangitis - metabolism; Cholestasis - chemically induced Cholestasis - metabolism Cholestasis - pathology; Detergents - toxicity; Diet -; Drug-Induced Liver Injury -; Fibrosis - chemically induced Fibrosis - metabolism Fibrosis - pathology; Fluorescence -; Lithocholic Acid - toxicity; Liver - drug effects Liver - injuries Liver - metabolism; Liver Diseases - metabolism Liver Diseases - pathology; Male -; Membrane Transport Proteins - genetics Membrane Transport Proteins - metabolism; Mice -; Mice, Inbred C57BL -; Multidrug Resistance-Associated Proteins - genetics Multidrug Resistance-Associated Proteins - metabolism; Organic Anion Transporters - genetics Organic Anion Transporters - metabolism; Organic Anion Transporters, Sodium-Dependent - genetics Organic Anion Transporters, Sodium-Dependent - metabolism; RNA, Messenger - genetics RNA, Messenger - metabolism; Reverse Transcriptase Polymerase Chain Reaction -; Sulfotransferases - genetics Sulfotransferases - metabolism; Symporters - genetics Symporters - metabolism