ArticleBMC veterinary research2014
Enhanced Wnt/β-catenin and Notch signalling in the activated canine hepatic progenitor cell niche.
Article in BMC veterinary research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Casein kinase 1 epsilon (CK1ε) as a potential therapeutic target in chronic liver disease.Journal of veterinary science · 2025Review
- Article
- Re-Recognizing the Cellular Origin of the Primary Epithelial Tumors of the Liver.Journal of hepatocellular carcinoma · 2021Review
- Nucleoside diphosphate kinase B promotes osteosarcoma proliferation through c-Myc.Cancer biology & therapy · 2018Article
- Hepatic Fibrosis in Dogs.Journal of veterinary internal medicine · 2018Review
- Immunohistochemical evaluation of the activation of hepatic progenitor cells and their niche in feline lymphocytic cholangitis.Journal of feline medicine and surgery · 2018Article
- Tanshinone IIA promotes the proliferation of WB-F344 hepatic oval cells via Wnt/β-catenin signaling.Molecular medicine reports · 2016Article
- Disease Modeling and Gene Therapy of Copper Storage Disease in Canine Hepatic Organoids.Stem cell reports · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe liver has a large regenerative capacity. Hepatocytes can replicate and regenerate a diseased liver. However, as is the case in severe liver diseases, this replication may become insufficient or exhausted and hepatic progenitor cells (HPCs) can be activated in an attempt to restore liver function. Due to their bi-potent differentiation capacity, these HPCs have great potential for regenerative approaches yet over-activation does pose potential health risks. Therefore the mechanisms leading to activation must be elucidated prior to safe implementation in the veterinary clinic. Wnt/β-catenin and Notch signalling have been implicated in the activation of HPCs in mouse models and in humans. Here we assessed the involvement in canine HPC activation. Gene-expression profiles were derived from laser microdissected HPC niches from lobular dissecting hepatitis (LDH) and normal liver tissue, with a focus on Wnt/β-catenin and Notch signalling. Immunohistochemical and immunofluorescent studies were combined to assess the role of the pathways in HPCs during LDH.
resultsGene-expression confirmed higher expression of Wnt/β-catenin and Notch pathway components and target genes in activated HPC niches in diseased liver compared to quiescent HPC niches from normal liver. Immunofluorescence confirmed the activation of these pathways in the HPCs during disease. Immunohistochemistry showed proliferating HPCs during LDH, and double immunofluorescence showed downregulation of Wnt/β-catenin and Notch in differentiating HPCs. Vimentin, a mesenchymal marker, was expressed on a subset of undifferentiated HPCs.
conclusionsTogether these studies clearly revealed that both Wnt/β-catenin and Notch signalling pathways are enhanced in undifferentiated, proliferating and potentially migrating HPCs during severe progressive canine liver disease (LDH).
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