ArticleGastroenterology2015
Ablation of Foxl1-Cre-labeled hepatic progenitor cells and their descendants impairs recovery of mice from liver injury.
Article in Gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Pooled it
- Comprehensive circRNA expression profile and hub genes screening during human liver development.Annals of medicine · 2025Article
- Rbpj deletion in hepatic progenitor cells attenuates endothelial responses and fibrosis in DDC-fed mice.Hepatology communications · 2025Article
- Cellular Plasticity in Gut and Liver Regeneration.Gut and liver · 2024Review
- Development of a hepatic cryoinjury model to study liver regeneration.Development (Cambridge, England) · 2024Article
- Development of a hepatic cryoinjury model to study liver regeneration.bioRxiv : the preprint server for biology · 2024Article
- GITRL impairs hepatocyte repopulation by liver progenitor cells to aggravate inflammation and fibrosis by GITRCell death & disease · 2024Article
- Transcriptional Control: A Directional Sign at the Crossroads of Adult Hepatic Progenitor Cells' Fates.International journal of biological sciences · 2024Review
- Establishment of a Fah-LSL mouse model to study BEC-to-hepatocyte conversion.Biophysics reports · 2023Article
- Distinct hepatocyte identities in liver homeostasis and regeneration.JHEP reports : innovation in hepatology · 2023Review
- [Research progress in lineage tracing to explore hepatic parenchymal cell regeneration and repair mechanisms].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Review
- Bipotent transitional liver progenitor cells contribute to liver regeneration.Nature genetics · 2023Article
- Update on Hepatobiliary Plasticity.Seminars in liver disease · 2023Article
- Mechanism of paracrine communications between hepatic progenitor cells and endothelial cells.Cellular signalling · 2022Article
- Repolarization Precedes Oval Cell-mediated Hepatocytic Regeneration in the CDE Diet Mouse Model.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- Cellular origins of regenerating liver and hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2022Review
- Role of Immune Cells in Biliary Repair.Frontiers in immunology · 2022Review
- Recent advances in tissue stem cells.Science China. Life sciences · 2021Review
- Cell-Based Regeneration and Treatment of Liver Diseases.International journal of molecular sciences · 2021Review
- Liver regeneration and inflammation: from fundamental science to clinical applications.Nature reviews. Molecular cell biology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsFoxl1(+) hepatic progenitor cells (HPCs) differentiate into cholangiocytes and hepatocytes after liver injury. We investigated the requirement for Foxl1(+) HPCs in recovery from liver injury in mice.
methodsWe developed mice in which we could trace and delete Foxl1-expressing HPCs and their descendants (Foxl1-Cre;Rosa(YFP/iDTR)-inducible diphtheria toxin receptor [iDTR] mice). Foxl1-Cre-negative mice were used as controls. Liver damage was induced in male mice by placing them on choline-deficient, ethionine-supplemented (CDE) diets for 15 days; mice then were placed on normal diets and allowed to recover. Liver damage was induced in female mice by placing them on 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-containing diets, followed by a recovery period. Some mice were given injections of diphtheria toxin during the recovery phase to delete Foxl1-Cre-marked HPCs and their descendants. Livers were collected from all mice and analyzed by immunofluorescence, quantitative reverse-transcription polymerase chain reaction, flow cytometry, and histologic analyses.
resultsFoxl1-Cre-marked HPCs were required for the development of cholangiocytes and hepatocytes in livers after CDE diet-induced injury. A smaller percentage of yellow fluorescent protein-positive (YFP(+)) hepatocytes contained markers of oxidative stress, DNA damage, or cell death than YFP-negative hepatocytes, indicating that YFP(+) hepatocytes are newly formed cells. Injection of diphtheria toxin deleted YFP(+) cells from Foxl1-Cre;Rosa(YFP/iDTR) mice and prevented the resolution of hepatic steatosis. In mice recovering from DDC diet-induced injury, most cholangiocytes arose from Foxl1-Cre-marked HPCs. Deletion of YFP(+) cells did not alter levels of markers of liver injury or liver function.
conclusionsBased on studies of Foxl1-Cre;Rosa(YFP/iDTR) mice, Foxl1(+) HPCs and/or their descendants are required for the development of cholangiocytes and hepatocytes in liver after CDE diet-induced injury.
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