1995
DOI: 10.1006/faat.1995.1074
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Biliary Epithelial Cell Proliferation Following α-Naphthylisothiocyanate (ANIT) Treatment: Relationship to Bile Duct Obstruction

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Cited by 44 publications
(23 citation statements)
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“…The identity of the proliferating cell type responsible for bile duct epithelial cell hyperplasia is somewhat controversial with hepatocytes, putative stem cells, and the pre-existing biliary epithelium all being candidates. 12,13,22,23,33,34 A number of in situ and in vitro studies support the conclusion that after bile duct ligation cholangiocytes most likely arise from different portions of the intrahepatic biliary tree and are morphologically and functionally similar to the subpopulation of cholangiocytes obtained from normal rat liver and do not acquire phenotypes of hepatocyte lineage. 14,22,24,33 Studies in the rat have shown that the pre-existing biliary epithelium is the source of proliferating bile duct cells and that bile Figure 6.…”
Section: Discussionmentioning
confidence: 89%
See 1 more Smart Citation
“…The identity of the proliferating cell type responsible for bile duct epithelial cell hyperplasia is somewhat controversial with hepatocytes, putative stem cells, and the pre-existing biliary epithelium all being candidates. 12,13,22,23,33,34 A number of in situ and in vitro studies support the conclusion that after bile duct ligation cholangiocytes most likely arise from different portions of the intrahepatic biliary tree and are morphologically and functionally similar to the subpopulation of cholangiocytes obtained from normal rat liver and do not acquire phenotypes of hepatocyte lineage. 14,22,24,33 Studies in the rat have shown that the pre-existing biliary epithelium is the source of proliferating bile duct cells and that bile Figure 6.…”
Section: Discussionmentioning
confidence: 89%
“…19 -22,32 Thus the pathogenesis of ANIT-induced cholestasis is biphasic; the onset of cholestasis is associated with changes in hepatocanalicular function, whereas bile duct epithelial cell proliferation follows later. 20,22,23 Continuous ANIT feeding is characterized by the development of time-and dose-dependent ductular hyperplasia. 21,24 Typical ductular hyperplasia produced by either ANIT feeding or common bile duct ligation results in cholangiocyte proliferation confined to the portal areas.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, we examined whether the synthetic FXR agonist GW4064 might protect against hepatotoxicity in rodent models of cholestasis. We first tested GW4064 in rats treated with ANIT, which damages biliary epithelial cells and induces intrahepatic cholestasis (23)(24)(25). Adult male rats were treated for 4 days with vehicle alone (corn oil), GW4064, or TUDCA.…”
Section: Fxr Activation Is Hepatoprotective In Intrahepatic Cholestasismentioning
confidence: 99%
“…16 ANIT is a toxin that targets bile ducts. 17,18 Animals were kept individually in metabolic cages in a light-controlled room. These studies were approved by the University of Calgary Animal Care Committee following guidelines of the Canadian Council on Animal Care.…”
mentioning
confidence: 99%