ArticleHepatology (Baltimore, Md.)2014
Clonal tracing of Sox9+ liver progenitors in mouse oval cell 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 132 papers.
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Who cites it
132 citing papers in PubMed.
- Retrorsine impairs liver regeneration by inducing progenitor cell-senescenceAnnals of medicine · 2026Article
- Advances and challenges in developing expandable human hepatocytes for regenerative medicine.Histology and histopathology · 2026Review
- Spatial hepatology: Decoding liver zonation for metabolic and regenerative therapeutics (Review).International journal of molecular medicine · 2026Review
- Chromatin State Distinguishes Injury-Responsive from State-Stabilizing Transcriptional Programs in Hybrid Hepatocytes.bioRxiv : the preprint server for biology · 2026Article
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- Cell Therapy in Advanced Cirrhosis: From Preclinical Evidence to Clinical Application.Gastro hep advances · 2026Review
- Next-Generation Hydrogels for Biliary Organoid Engineering.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Numb-exon3 and full length Numb equivalently alleviate cholestatic liver fibrosis by inhibiting ductular reaction.Scientific reports · 2025Article
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- Liver Progenitor Cells: Cellular Origins, Plasticity, and Signaling Pathways in Liver Regeneration.Biology · 2025Review
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- Breaking the rules of cell biology: Lessons from the liver's exceptional regenerative capacity.Molecular biology of the cell · 2025Review
- The FBXW7-RPAP2 Axis Controls the Growth of Hepatocellular Carcinoma Cells and Determines the Fate of Liver Cell Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Diverse functions of SOX9 in liver development and homeostasis and hepatobiliary diseases.Genes & diseases · 2024Review
- Aberrant differentiation and proliferation of hepatocytes in chronic liver injury and liver tumors.Pathology international · 2024Review
- Article
- GITRL impairs hepatocyte repopulation by liver progenitor cells to aggravate inflammation and fibrosis by GITRCell death & disease · 2024Article
- Repopulating Kupffer cells originate directly from hematopoietic stem cells.Stem cell research & therapy · 2023Article
72 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors.
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Abstract
unlabelledProliferating ducts, termed "oval cells," have long been thought to be bipotential, that is, produce both biliary ducts and hepatocytes during chronic liver injury. The precursor to oval cells is considered to be a facultative liver stem cell (LSC). Recent lineage tracing experiments indicated that the LSC is SRY-related HMG box transcription factor 9 positive (Sox9(+) ) and can replace the bulk of hepatocyte mass in several settings. However, no clonal relationship between Sox9(+) cells and the two epithelial liver lineages was established. We labeled Sox9(+) mouse liver cells at low density with a multicolor fluorescent confetti reporter. Organoid formation validated the progenitor activity of the labeled population. Sox9(+) cells were traced in multiple oval cell injury models using both histology and fluorescence-activated cell sorting. Surprisingly, only rare clones containing both hepatocytes and oval cells were found in any experiment. Quantitative analysis showed that Sox9(+) cells contributed only minimally (<1%) to the hepatocyte pool, even in classic oval cell injury models. In contrast, clonally marked mature hepatocytes demonstrated the ability to self-renew in all classic mouse oval cell activation injuries. A hepatocyte chimera model to trace hepatocytes and nonparenchymal cells also demonstrated the prevalence of hepatocyte-driven regeneration in mouse oval cell injury models.
conclusionSox9(+) ductal progenitor cells give rise to clonal oval cell proliferation and bipotential organoids, but rarely produce hepatocytes in vivo. Hepatocytes themselves are the predominant source of new parenchyma cells in prototypical mouse models of oval cell activation.
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