ArticleImmunology2018
Galectin-3 is an amplifier of the interleukin-1β-mediated inflammatory response in corneal keratinocytes.
Article in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Study on the Role of Galectin-3 in Sepsis.Biochemical genetics · 2026Article
- Molecular and cellular processes disrupted in the early postnatal Down syndrome prefrontal cortex.Science (New York, N.Y.) · 2026Article
- Integration of tear fluid biomarkers and machine learning for the early detection of keratoconus.BMC ophthalmology · 2025Article
- Galectin-3 as a possible link between periodontitis and chronic kidney disease: a cross-sectional study.Journal of Yeungnam medical science · 2025Article
- Differential Efficacy of Small Molecules Dynasore and Mdivi-1 for the Treatment of Dry Eye Epitheliopathy or as a Countermeasure for Nitrogen Mustard Exposure of the Ocular Surface.The Journal of pharmacology and experimental therapeutics · 2024Article
- Gingival crevicular fluid galectin-3 and interleukin-1 beta levels in stage 3 periodontitis with grade B and C.Clinical oral investigations · 2023Article
- Targeting disordered-structured domain interactions in Galectin-3 based on NMR and enhanced MD.Biophysical journal · 2022Article
- 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
- Galectin-3 Is a Crucial Immunological Disease Marker in Patients with Fungal Keratitis.Disease markers · 2022Article
- Review
- Diagnostic Significance of Serum Galectin-3 in Hospitalized Patients with COVID-19-A Preliminary Study.Biomolecules · 2021Observational
- Galectin-3 protects against ischemic stroke by promoting neuro-angiogenesis via apoptosis inhibition and Akt/Caspase regulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Galectins as Regulators of Corneal Inflammation.Current opinion in physiology · 2021Article
- Trichinella spiralis co-infection exacerbates Plasmodium berghei malaria-induced hepatopathy.Parasites & vectors · 2020Article
- Serum galectin-3 levels are decreased in schizophrenia.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2020Article
- Article
- Galectin-3 initiates epithelial-stromal paracrine signaling to shape the proteolytic microenvironment during corneal repair.Science signaling · 2019Article
- Lectin-Glycan Interactions in Corneal Infection and Inflammation.Frontiers in immunology · 2018Review
- Galectin-3-Mediated Glial Crosstalk Drives Oligodendrocyte Differentiation and (Re)myelination.Frontiers in cellular neuroscience · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Interleukin-1β (IL-1β) is a potent mediator of innate immunity commonly up-regulated in a broad spectrum of inflammatory diseases. When bound to its cell surface receptor, IL-1β initiates a signalling cascade that cooperatively induces the expression of canonical IL-1 target genes such as IL-8 and IL-6. Here, we present galectin-3 as a novel regulator of IL-1β responses in corneal keratinocytes. Using the SNAP-tag system and digitonin semi-permeabilization, we show that recombinant exogenous galectin-3 binds to the plasma membrane of keratinocytes and is internalized into cytoplasmic compartments. We find that exogenous galectin-3, but not a dominant negative inhibitor of galectin-3 polymerization lacking the N-terminal domain, exacerbates the response to IL-1β by stimulating the secretion of inflammatory cytokines. The activity of galectin-3 could be reduced by a novel d-galactopyranoside derivative targeting the conserved galactoside-binding site of galectins and did not involve interaction with IL-1 receptor 1 or the induction of endogenous IL-1β. Consistent with these observations, we demonstrate that small interfering RNA-mediated suppression of endogenous galectin-3 expression is sufficient to impair the IL-1β-induced secretion of IL-8 and IL-6 in a p38 mitogen-activated protein kinase-independent manner. Collectively, our findings provide a novel role for galectin-3 as an amplifier of IL-1β responses during epithelial inflammation through an as yet unidentified mechanism.
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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.