ArticleScientific reports2016
Galectin-3 Induces a Pro-degradative/inflammatory Gene Signature in Human Chondrocytes, Teaming Up with Galectin-1 in Osteoarthritis Pathogenesis.
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 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- SOX9 represses the human galectin-3 promoter in SW1353 cells: potential implications for osteoarthritis.Scientific reports · 2026Article
- Identification of novel protein biomarkers for knee osteoarthritis by integrating human plasma proteome: evidence from Mendelian randomization and preliminaryFrontiers in medicine · 2026Article
- Article
- Targeting the Galectin Axis in Osteoarthritis: Chondroprotective Effects of Dietary and Pharmacological Phytochemicals.Molecules (Basel, Switzerland) · 2025Article
- Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- A multi-tissue human knee single-cell atlas identifies that osteoarthritis reduces regenerative tissue stem cells while increasing inflammatory pain macrophages.Communications biology · 2025Article
- Gingival crevicular fluid galectin-3 and interleukin-1 beta levels in stage 3 periodontitis with grade B and C.Clinical oral investigations · 2023Article
- Age-related changes in human bone marrow mesenchymal stromal cells: morphology, gene expression profile, immunomodulatory activity and miRNA expression.Frontiers in immunology · 2023Article
- Galectins as pivotal components in oncogenesis and immune exclusion in human malignancies.Frontiers in immunology · 2023Review
- Potential Protective Role of Galectin-3 in Patients with Gonarthrosis and Diabetes Mellitus: A Cross-Sectional Study.International journal of environmental research and public health · 2022Article
- What is the Sugar Code?Chembiochem : a European journal of chemical biology · 2022Review
- Galectin network in osteoarthritis: galectin-4 programs a pathogenic signature of gene and effector expression in human chondrocytes in vitro.Histochemistry and cell biology · 2022Article
- N-Glycan profiling of chondrocytes and fibroblast-like synoviocytes: Towards functional glycomics in osteoarthritis.Proteomics. Clinical applications · 2021Article
- Adult neural stem cells have latent inflammatory potential that is kept suppressed byScience advances · 2021Article
- The Dysregulated Galectin Network Activates NF-κB to Induce Disease Markers and Matrix Degeneration in 3D Pellet Cultures of Osteoarthritic Chondrocytes.Calcified tissue international · 2021Article
- Human galectin‑3: Molecular switch of gene expression in dermal fibroblasts in vitro and of skin collagen organization in open wounds and tensile strength in incisionsMolecular medicine reports · 2021Article
- Decrease of core 2The Journal of biological chemistry · 2020Article
- How galectins have become multifunctional proteins.Histology and histopathology · 2020Review
- Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory chemo- and cytokines and matrix-degrading proteases underlie the progression of osteoarthritis (OA). Aiming to define upstream regulators for these disease markers, we pursued initial evidence for an upregulation of members of the adhesion/growth-regulatory galectin family. Immunohistochemical localization of galectin-3 (Gal-3) in sections of human cartilage with increasing levels of degeneration revealed a linear correlation reaching a chondrocyte positivity of 60%. Presence in situ was cytoplasmic, the lectin was secreted from OA chondrocytes in culture and binding of Gal-3 yielded lactose-inhibitable surface staining. Exposure of cells to the lectin led to enhanced gene expression and secretion of functional disease markers. Genome-wide transcriptomic analysis broadened this result to reveal a pro-degradative/inflammatory gene signature under the control of NF-κB. Fittingly, targeting this route of activation by inhibitors impaired the unfavourable response to Gal-3 binding, as also seen by shortening the lectin's collagen-like repeat region. Gal-3's activation profile overlaps with that of homodimeric galectin-1 (Gal-1) and also has distinctive (supplementing) features. Tested at subsaturating concentrations in a mixture, we found cooperation between the two galectins, apparently able to team up to promote OA pathogenesis. In summary, our results suggest that a network of endogenous lectins is relevant for initiating this process cascade.
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