Invasive Ductular Reaction Operates Hepatobiliary Junctions upon Hepatocellular Injury in Rodents and Humans.
- Clerbaux LA Laboratory of Gastroenterology, Université Catholique de Louvain, Brussels, Belgium.
- Manco R Laboratory of Gastroenterology, Université Catholique de Louvain, Brussels, Belgium.
- Van Hul N Department of Biosciences and Nutrition, Karolinska Institute, Stockholm, Sweden.
- Bouzin C Imaging Platform, Institute of clinical and Experimental Research, Université Catholique de Louvain, Brussels, Belgium.
- Sciarra A Service of Clinical Pathology, Lausanne University Hospital, Institute of Pathology, Lausanne, Switzerland.
- Sempoux C Service of Clinical Pathology, Lausanne University Hospital, Institute of Pathology, Lausanne, Switzerland.
- Theise ND Department of Pathology, New York University School of Medicine, New York, New York.
- Leclercq IA Laboratory of Gastroenterology, Université Catholique de Louvain, Brussels, Belgium. Electronic address: isabelle.leclercq@uclouvain.be.
- 2019-05-21
Published in:
- The American journal of pathology. - 2019
English
Ductular reaction (DR) is observed in virtually all liver diseases in both humans and rodents. Depending on the injury, DR is confined within the periportal area or invades the parenchyma. On severe hepatocellular injury, invasive DR has been proposed to arise for supplying the liver with new hepatocytes. However, experimental data evidenced that DR contribution to hepatocyte repopulation is at the most modest, unless replicative capacity of hepatocytes is abrogated. Herein, we proposed that invasive DR could contribute to operating hepatobiliary junctions on hepatocellular injury. The choline-deficient ethionine-supplemented mouse model of hepatocellular injury and human liver samples were used to evaluate the hepatobiliary junctional role of the invasive form of DR. Choline-deficient ethionine-supplemented-induced DR expanded as biliary epithelium into the lobule and established new junctions with the canaliculi. By contrast, no new ductular-canalicular junctions were observed in mouse models of biliary obstructive injury exhibiting noninvasive DR. Similarly, in humans, an increased number of hepatobiliary junctions were observed in hepatocellular diseases (viral, drug induced, or metabolic) in which DR invaded the lobule but not in biliary diseases (obstruction or cholangitis) in which DR was contained within the portal mesenchyme. In conclusion, our data in rodents and humans support that invasive DR plays a hepatobiliary junctional role to maintain structural continuity between hepatocytes and ducts in disorders affecting hepatocytes.
- Language
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- English
- Open access status
- bronze
- Identifiers
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- DOI 10.1016/j.ajpath.2019.04.011
- PMID 31108103
- Persistent URL
- https://sonar.ch/global/documents/126239
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