ArticleHepatology (Baltimore, Md.)2014
Expansion of prominin-1-expressing cells in association with fibrosis of biliary atresia.
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 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- A clinically deployed dual-compartment biochemical monitoring platform for human liver perfusion.Nature communications · 2026Article
- BiliQML: a supervised machine-learning model to quantify biliary forms from digitized whole slide liver histopathological images.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Review
- Pathological role of methionine in the initiation and progression of biliary atresia.Frontiers in pediatrics · 2023Review
- Reduced peroxisome proliferator-activated receptor-α and bile acid nuclear receptor NR1H4/FXR may affect the hepatic immune microenvironment of biliary atresia.Frontiers in immunology · 2022Article
- Blockade of phosphotyrosine pathways suggesting SH2 superbinder as a novel therapy for pulmonary fibrosis.Theranostics · 2022Article
- Developmental histology of the portal plate in biliary atresia: observations and implications.Pediatric surgery international · 2021Article
- Urea-based amino sugar agent clears murine liver and preserves protein fluorescence and lipophilic dyes.BioTechniques · 2021Article
- Prominin-1-expressing hepatic progenitor cells induce fibrogenesis in murine cholestatic liver injury.Physiological reports · 2020Article
- The Emerging Roles of Cancer Stem Cells and Wnt/Beta-Catenin Signaling in Hepatoblastoma.Cancers · 2019Review
- Prominin-1 Promotes Biliary Fibrosis Associated With Biliary Atresia.Hepatology (Baltimore, Md.) · 2019Article
- Liver fibrosis in biliary atresia.World journal of pediatrics : WJP · 2019Review
- Prohibitin 1 Acts As a Negative Regulator of Wingless/Integrated-Beta-Catenin Signaling in Murine Liver and Human Liver Cancer Cells.Hepatology communications · 2018Article
- Contribution of Resident Stem Cells to Liver and Biliary Tree Regeneration in Human Diseases.International journal of molecular sciences · 2018Review
- Cholangiopathies - Towards a molecular understanding.EBioMedicine · 2018Review
- Inhibition of CREB binding protein-beta-catenin signaling down regulates CD133 expression and activates PP2A-PTEN signaling in tumor initiating liver cancer cells.Cell communication and signaling : CCS · 2018Article
- Role of A-Kinase Anchoring Protein Phosphorylation in Alcohol-Induced Liver Injury and Hepatic Stellate Cell Activation.The American journal of pathology · 2018Article
- Newborn screening for biliary atresia in the United States.Pediatric surgery international · 2017Review
- Adjuvant therapy in biliary atresia: hopelessly optimistic or potential for change?Pediatric surgery international · 2017Review
- The let-7/Lin28 axis regulates activation of hepatic stellate cells in alcoholic liver injury.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
unlabelledBiliary atresia (BA), the most common cause of end-stage liver disease and the leading indication for pediatric liver transplantation, is associated with intrahepatic ductular reactions within regions of rapidly expanding periportal biliary fibrosis. Whereas the extent of such biliary fibrosis is a negative predictor of long-term transplant-free survival, the cellular phenotypes involved in the fibrosis are not well established. Using a rhesus rotavirus-induced mouse model of BA, we demonstrate significant expansion of a cell population expressing the putative stem/progenitor cell marker, PROMININ-1 (PROM1), adjacent to ductular reactions within regions of periportal fibrosis. PROM1positive (pos) cells express Collagen-1α1. Subsets of PROM1pos cells coexpress progenitor cell marker CD49f, epithelial marker E-CADHERIN, biliary marker CYTOKERATIN-19, and mesenchymal markers VIMENTIN and alpha-SMOOTH MUSCLE ACTIN (αSMA). Expansion of the PROM1pos cell population is associated with activation of Fibroblast Growth Factor (FGF) and Transforming Growth Factor-beta (TGFβ) signaling. In vitro cotreatment of PROM1-expressing Mat1a-/- hepatic progenitor cells with recombinant human FGF10 and TGFβ1 promotes morphologic transformation toward a myofibroblastic cell phenotype with increased expression of myofibroblastic genes Collagen-1α1, Fibronectin, and α-Sma. Infants with BA demonstrate similar expansion of periportal PROM1pos cells with activated Mothers Against Decapentaplegic Homolog 3 (SMAD3) signaling in association with increased hepatic expression of FGF10, FGFR1, and FGFR2 as well as mesenchymal genes SLUG and SNAIL. Infants with perinatal subtype of BA have higher tissue levels of PROM1 expression than those with embryonic subtype.
conclusionExpansion of collagen-producing PROM1pos cells within regions of periportal fibrosis is associated with activated FGF and TGFβ pathways in both experimental and human BA. PROM1pos cells may therefore play an important role in the biliary fibrosis of BA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.