ArticleGut2015
Osteopontin neutralisation abrogates the liver progenitor cell response and fibrogenesis in mice.
Article in Gut, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 99 citations in OpenAlex.
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- Osteopontin in Chronic Inflammatory Diseases: Mechanisms, Biomarker Potential, and Therapeutic Strategies.Biology · 2025Review
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- Osteopontin: an indispensable component in common liver, pancreatic, and biliary related disease.Journal of cancer research and clinical oncology · 2024Review
- Liver macrophages revisited: The expanding universe of versatile responses in a spatiotemporal context.Hepatology communications · 2024Review
- GDF11: An emerging therapeutic target for liver diseases and fibrosis.Journal of cellular and molecular medicine · 2024Review
- Transcriptional Control: A Directional Sign at the Crossroads of Adult Hepatic Progenitor Cells' Fates.International journal of biological sciences · 2024Review
- Repopulating Kupffer cells originate directly from hematopoietic stem cells.Stem cell research & therapy · 2023Article
- Single-cell transcriptome analysis reveals liver injury induced by glyphosate in mice.Cellular & molecular biology letters · 2023Article
- Triptolide increases resistance to bile duct ligation-induced liver injury and fibrosis in mice by inhibiting RELB.Frontiers in nutrition · 2022Article
- Cancer-associated mesothelial cells promote ovarian cancer chemoresistance through paracrine osteopontin signaling.The Journal of clinical investigation · 2021Article
- Molecular Crosstalk between the Hepatitis C Virus and the Extracellular Matrix in Liver Fibrogenesis and Early Carcinogenesis.Cancers · 2021Review
- Quantitative Expression of Key Cancer Markers in the AS-30D Hepatocarcinoma Model.Frontiers in oncology · 2021Article
- Review
- Liver osteopontin is required to prevent the progression of age-related nonalcoholic fatty liver disease.Aging cell · 2020Article
- Emerging Roles of Matricellular Proteins in Systemic Sclerosis.International journal of molecular sciences · 2020Review
- Growth differentiation factor 11 attenuates liver fibrosis via expansion of liver progenitor cells.Gut · 2020Article
- Hepatocyte Injury and Hepatic Stem Cell Niche in the Progression of Non-Alcoholic Steatohepatitis.Cells · 2020Review
Corrections and comments
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Authors and funding
21 authors at 10 institutions in 5 countries.
Funding
Abstract
backgroundChronic liver injury triggers a progenitor cell repair response, and liver fibrosis occurs when repair becomes deregulated. Previously, we reported that reactivation of the hedgehog pathway promotes fibrogenic liver repair. Osteopontin (OPN) is a hedgehog-target, and a cytokine that is highly upregulated in fibrotic tissues, and regulates stem-cell fate. Thus, we hypothesised that OPN may modulate liver progenitor cell response, and thereby, modulate fibrotic outcomes. We further evaluated the impact of OPN-neutralisation on murine liver fibrosis.
methodsLiver progenitors (603B and bipotential mouse oval liver) were treated with OPN-neutralising aptamers in the presence or absence of transforming growth factor (TGF)-β, to determine if (and how) OPN modulates liver progenitor function. Effects of OPN-neutralisation (using OPN-aptamers or OPN-neutralising antibodies) on liver progenitor cell response and fibrogenesis were assessed in three models of liver fibrosis (carbon tetrachloride, methionine-choline deficient diet, 3,5,-diethoxycarbonyl-1,4-dihydrocollidine diet) by quantitative real time (qRT) PCR, Sirius-Red staining, hydroxyproline assay, and semiquantitative double-immunohistochemistry. Finally, OPN expression and liver progenitor response were corroborated in liver tissues obtained from patients with chronic liver disease.
resultsOPN is overexpressed by liver progenitors in humans and mice. In cultured progenitors, OPN enhances viability and wound healing by modulating TGF-β signalling. In vivo, OPN-neutralisation attenuates the liver progenitor cell response, reverses epithelial-mesenchymal-transition in Sox9+ cells, and abrogates liver fibrogenesis.
conclusionsOPN upregulation during liver injury is a conserved repair response, and influences liver progenitor cell function. OPN-neutralisation abrogates the liver progenitor cell response and fibrogenesis in mouse models of liver fibrosis.
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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.