ArticleScientific reports2016
Deletion of Galectin-3 Enhances Xenobiotic Induced Murine Primary Biliary Cholangitis by Facilitating Apoptosis of BECs and Release of Autoantigens.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Galectin-3 Mediates Heme-Induced Multi-Organ Dysfunction by Modulating the Splenic Immune Microenvironment.Diseases (Basel, Switzerland) · 2026Article
- Review
- Galectin-3-Insights from Inflammatory Bowel Disease and Primary Sclerosing Cholangitis.International journal of molecular sciences · 2025Review
- Galectin-3 inhibition ameliorates hepatic steatosis in a multilineage 3D spheroid model.PloS one · 2025Article
- Inflammasome and pyroptosis in autoimmune liver diseases.Frontiers in immunology · 2023Review
- The Expression of IL-1β Correlates with the Expression of Galectin-3 in the Tissue at the Maternal-Fetal Interface during the Term and Preterm Labor.Journal of clinical medicine · 2022Article
- Role of galectin-3 in the pathogenesis and progression of biliary atresia.Clinical liver disease · 2022Review
- Galectin-3, Possible Role in Pathogenesis of Periodontal Diseases and Potential Therapeutic Target.Frontiers in pharmacology · 2021Review
- Galectin-3 in Inflammasome Activation and Primary Biliary Cholangitis Development.International journal of molecular sciences · 2020Review
- Galectin-3: Roles in Neurodevelopment, Neuroinflammation, and Behavior.Biomolecules · 2020Review
- Metabolic syndrome attenuates ulcerative colitis: Correlation with interleukin-10 and galectin-3 expression.World journal of gastroenterology · 2019Article
- Galectin 3 protects from cisplatin-induced acute kidney injury by promoting TLR-2-dependent activation of IDO1/Kynurenine pathway in renal DCs.Theranostics · 2019Article
- Gal-3 Deficiency SuppressesFrontiers in immunology · 2019Article
- Galectin-3 Deficiency Facilitates TNF-α-Dependent Hepatocyte Death and Liver Inflammation in MCMV Infection.Frontiers in microbiology · 2019Article
- Therapeutic and immunological interventions in primary biliary cholangitis: from mouse models to humans.Archives of medical science : AMS · 2018Article
- Galectin-3 and cancer stemness.Glycobiology · 2018Review
- Anti-drug Antibodies Against a Novel Humanized Anti-CD20 Antibody Impair Its Therapeutic Effect on Primary Biliary Cholangitis in Human CD20- and FcγR-Expressing Mice.Frontiers in immunology · 2018Article
- Mesenchymal Stem Cells as New Therapeutic Agents for the Treatment of Primary Biliary Cholangitis.Analytical cellular pathology (Amsterdam) · 2017Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Galectin-3 (Gal-3) is a carbohydrate binding lectin, with multiple roles in inflammatory diseases and autoimmunity including its antiapoptotic effect on epithelial cells. In particular, increased expression of Gal-3 in epithelial cells is protective from apoptosis. Based on the thesis that apoptosis of biliary epithelial cells (BECs) is critical to the pathogenesis of Primary Biliary Cholangitis (PBC), we have analyzed the role of Gal-3 in the murine model of autoimmune cholangitis. We took advantage of Gal-3 knockout mice and immunized them with a mimotope of the major mitochondrial autoantigen of PBC, 2-octynoic acid (2-OA) coupled to BSA (2OA-BSA) and evaluated the natural history of subsequent disease, compared to control wild-type mice, by measuring levels of antibodies to PDC-E2, immunohistology of liver, and expression of Gal-3. We report herein that deletion of Gal-3 significantly exacerbates autoimmune cholangitis in these mice. This is manifested by increased periportal infiltrations, bile duct damage, granulomas and fibrosis. Interestingly, the BECs of Gal-3 knockout mice had a higher response to apoptotic stimuli and there were more pro-inflammatory lymphocytes and dendritic cells (DCs) in the livers of Gal-3 knockout mice. In conclusion, Gal-3 plays a protective role in the pathways that lead to the inflammatory destruction of biliary epithelial cells.
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