ArticleJournal of hepatology2016
Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers.
Article in Journal of hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 148 citations in OpenAlex.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Cholangiocyte biology in primary sclerosing cholangitis and other cholangiopathies: pathogenesis, clinical insights, and experimental tools.Physiological reviews · 2026Review
- Single-cell and spatial transcriptomics reveal Thbs1-CD36 crosstalk between Kupffer and hepatic stellate cells following mesenchymal stem cell-derived small extracellular vesicles transplantation, alleviating liver fibrosis.Journal of nanobiotechnology · 2026Article
- ECM1 produced by hepatic stellate cells serves as a gatekeeper of liver homeostasis in hepatic fibrosis.Hepatology (Baltimore, Md.) · 2026Article
- Cellular senescence in human liver under normal aging and cancer.Cell genomics · 2026Article
- Conserved Ductular Reaction Mechanisms in Biliary Atresia and Primary Sclerosing Cholangitis Derived From Single-Cell and Spatial Transcriptomics.Cellular and molecular gastroenterology and hepatology · 2026Review
- Global Trends in Hepatocellular Carcinoma and TGF-β Research: A Bibliometric and Visualization Analysis from 2000 to 2024.Current protein & peptide science · 2026Article
- Effects of embryonic origin, tissue cues and pathological signals on fibroblast diversity in humans.Nature cell biology · 2025Review
- Periductal fibroblasts participate in liver homeostasis, fibrosis, and tumorigenesis.The Journal of experimental medicine · 2025Article
- Cancer-associated fibroblasts in hepatocellular carcinoma: origins, heterogeneity, and therapeutic implications.Frontiers in immunology · 2025Review
- Challenges ofFrontiers in cell and developmental biology · 2025Review
- Jag1 insufficiency alters liver fibrosis via T cell and hepatocyte differentiation defects.EMBO molecular medicine · 2024Article
- The possible pathogenesis of liver fibrosis: therapeutic potential of natural polyphenols.Pharmacological reports : PR · 2024Review
- Article
- The effects of TGF-β-induced activation and starvation of vitamin A and palmitic acid on human stem cell-derived hepatic stellate cells.Stem cell research & therapy · 2024Article
- Heterogeneity of primary and metastatic CAFs: From differential treatment outcomes to treatment opportunities (Review).International journal of oncology · 2024Article
- JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis.Clinical and molecular hepatology · 2024Article
- XIAP-mediated degradation of IFT88 disrupts HSC cilia to stimulate HSC activation and liver fibrosis.EMBO reports · 2024Article
- Modulation of canonical Wnt signaling regulates peribiliary mesenchymal identity during homeostasis and injury.Hepatology communications · 2024Article
- Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsContribution of hepatic stellate cells (HSCs), portal fibroblasts (PFs), and mesothelial cells (MCs) to myofibroblasts is not fully understood due to insufficient availability of markers and isolation methods. The present study aimed to isolate these cells, characterize their phenotypes, and examine their contribution to myofibroblasts in liver fibrosis.
methodsLiver fibrosis was induced in Collagen1a1-green fluorescent protein (Col1a1(GFP)) mice by bile duct ligation (BDL), 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet, or CCl4 injections. Combining vitamin A (VitA) lipid autofluorescence and expression of GFP and glycoprotein M6a (GPM6A), we separated HSCs, PFs, and MCs from normal and fibrotic livers by fluorescence-activated cell sorting (FACS).
resultsNormal Col1a1(GFP) livers broadly expressed GFP in HSCs, PFs, and MCs. Isolated VitA+ HSCs expressed reelin, whereas VitA-GFP+GPM6A- PFs expressed ectonucleoside triphosphate diphosphohydrolase-2 and elastin. VitA-GFP+GPM6A+ MCs expressed keratin 19, mesothelin, and uroplakin 1b. Transforming growth factor (TGF)-β1 treatment induced the transformation of HSCs, PFs, and MCs into myofibroblasts in culture. TGF-β1 suppressed cyclin D1 mRNA expression in PFs but not in HSCs and MCs. In biliary fibrosis, PFs adjacent to the bile duct expressed α-smooth muscle actin. FACS analysis revealed that HSCs are the major source of GFP+ myofibroblasts in the injured Col1a1(GFP) mice after DDC or CCl4 treatment. Although PFs partly contributed to GFP+ myofibroblasts in the BDL model, HSCs were still dominant source of myofibroblasts.
conclusionHSCs, PFs, and MCs have distinct phenotypes, and PFs partly contribute to myofibroblasts in the portal triad in biliary fibrosis.
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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.