ArticleHepatology (Baltimore, Md.)2014
Polysialic acid/neural cell adhesion molecule modulates the formation of ductular reactions in liver injury.
Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- ST8Sia2 polysialyltransferase protects against infection by Trypanosoma cruzi.PLoS neglected tropical diseases · 2024Article
- Article
- The intact parasympathetic nerve promotes submandibular gland regeneration through ductal cell proliferation.Cell proliferation · 2021Article
- Liver stem cells: Plasticity of the liver epithelium.World journal of gastroenterology · 2019Review
- Diverse perspectives to address for the future treatment of heterogeneous hepatocellular carcinoma.Heliyon · 2019Review
- Contribution of Resident Stem Cells to Liver and Biliary Tree Regeneration in Human Diseases.International journal of molecular sciences · 2018Review
- Polysialic acid is a cellular receptor for human adenovirus 52.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Candidate genes investigation for severe nonalcoholic fatty liver disease based on bioinformatics analysis.Medicine · 2017Article
- Is Polysialylated NCAM Not Only a Regulator during Brain Development But also during the Formation of Other Organs?Biology · 2017Review
- The Polybasic Region of the Polysialyltransferase ST8Sia-IV Binds Directly to the Neural Cell Adhesion Molecule, NCAM.Biochemistry · 2017Article
- Sialylation of N-glycans: mechanism, cellular compartmentalization and function.Histochemistry and cell biology · 2017Review
- Status of and candidates for cell therapy in liver cirrhosis: overcoming the "point of no return" in advanced liver cirrhosis.Journal of gastroenterology · 2017Review
- Expression kinetics of hepatic progenitor markers in cellular models of human liver development recapitulating hepatocyte and biliary cell fate commitment.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Engineering of complex protein sialylation in plants.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Stem/Progenitor Cell Niches Involved in Hepatic and Biliary Regeneration.Stem cells international · 2016Review
- Regenerating the liver: not so simple after all?F1000Research · 2016Review
- Revisiting Epithelial-to-Mesenchymal Transition in Liver Fibrosis: Clues for a Better Understanding of the "Reactive" Biliary Epithelial Phenotype.Stem cells international · 2016Review
- Novel insights into the function and dynamics of extracellular matrix in liver fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- EpCAM and the biology of hepatic stem/progenitor cells.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- Neural cell adhesion molecule and polysialic acid in ductular reaction: the puzzle is far from completed, but the picture is becoming more clear.Hepatology (Baltimore, Md.) · 2014Article
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15 authors at 5 institutions in 3 countries.
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Abstract
unlabelledIn severe liver injury, ductular reactions (DRs) containing bipotential hepatic progenitor cells (HPCs) branch from the portal tract. Neural cell adhesion molecule (NCAM) marks bile ducts and DRs, but not mature hepatocytes. NCAM mediates interactions between cells and surrounding matrix; however, its role in liver development and regeneration is undefined. Polysialic acid (polySia), a unique posttranslational modifier of NCAM, is produced by the enzymes, ST8SiaII and ST8SiaIV, and weakens NCAM interactions. The role of polySia with NCAM synthesizing enzymes ST8SiaII and ST8SiaIV were examined in HPCs in vivo using the choline-deficient ethionine-supplemented and 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet models of liver injury and regeneration, in vitro using models of proliferation, differentiation, and migration, and by use of mouse models with gene defects in the polysialyltransferases (St8sia 2+/-4+/-, and St8sia2-/-4-/-). We show that, during liver development, polySia is required for the correct formation of bile ducts because gene defects in both the polysialyltransferases (St8sia2+/-4+/- and St8sia2-/-4-/- mice) caused abnormal bile duct development. In normal liver, there is minimal polySia production and few ductular NCAM+ cells. Subsequent to injury, NCAM+ cells expand and polySia is produced by DRs/HPCs through ST8SiaIV. PolySia weakens cell-cell and cell-matrix interactions, facilitating HGF-induced migration. Differentiation of HPCs to hepatocytes in vitro results in both transcriptional down-regulation of polySia and cleavage of polySia-NCAM. Cleavage of polySia by endosialidase (endoN) during liver regeneration reduces migration of DRs into parenchyma.
conclusionPolySia modification of NCAM+ ductules weakens cell-cell and cell-matrix interactions, allowing DRs/HPCs to migrate for normal development and regeneration. Modulation of polySia levels may provide a therapeutic option in liver regeneration.
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