ArticlePloS one2015
Galectin-2 induces a proinflammatory, anti-arteriogenic phenotype in monocytes and macrophages.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Systemic reprogramming of monocytes in Crohn's disease promotes their intestinal inflammatory function.JCI insight · 2026Article
- Loss of Chromosome Y Associates With Altered Immune Cell Trajectories and X-Inactivation Features.Aging cell · 2026Article
- Discovery of core genes for systemic lupus erythematosus via genome-wide aggregated trans-effects analysis.Genes and immunity · 2025Article
- Role of Galectin-1 in the Pathogenesis of Melanoma.Journal of cancer science and clinical therapeutics · 2025Article
- Mendelian randomization reveals interactions of the blood proteome and immunome in mitral valve prolapse.Communications medicine · 2024Article
- Galectin-9, a pro-survival factor inducing immunosuppression, leukemic cell transformation and expansion.Molecular biology reports · 2024Review
- Single-cell transcriptomics of the immune system in ME/CFS at baseline and following symptom provocation.Cell reports. Medicine · 2024Article
- Chimera and Tandem-Repeat Type Galectins: The New Targets for Cancer Immunotherapy.Biomolecules · 2023Review
- Galectin functions in cancer-associated inflammation and thrombosis.Frontiers in cardiovascular medicine · 2023Review
- Galectin-2 in Health and Diseases.International journal of molecular sciences · 2022Review
- Galectokines: The Promiscuous Relationship between Galectins and Cytokines.Biomolecules · 2022Review
- Banp regulates DNA damage response and chromosome segregation during the cell cycle in zebrafish retina.eLife · 2022Article
- In vivo multidimensional CRISPR screens identifyScience advances · 2022Article
- Regulation of wound healing and fibrosis by galectins.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Anti-Galectin-2 Antibody Treatment Reduces Atherosclerotic Plaque Size and Alters Macrophage Polarity.Thrombosis and haemostasis · 2022Article
- Galectins dysregulation: A way for cancer cells to invade and pervade.Oncology research · 2022Article
- Placental galectins regulate innate and adaptive immune responses in pregnancy.Frontiers in immunology · 2022Article
- Galectins in Glioma: Current Roles in Cancer Progression and Future Directions for Improving Treatment.Cancers · 2021Review
- Hedgehog-induced PD-L1 on tumor-associated macrophages is critical for suppression of tumor-infiltrating CD8+ T cell function.JCI insight · 2021Article
- Medawar's PostEra: Galectins Emerged as Key Players During Fetal-Maternal Glycoimmune Adaptation.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-2 is a monocyte-expressed carbohydrate-binding lectin, for which increased expression is genetically determined and associated with decreased collateral arteriogenesis in obstructive coronary artery disease patients. The inhibiting effect of galectin-2 on arteriogenesis was confirmed in vivo, but the mechanism is largely unknown. In this study we aimed to explore the effects of galectin-2 on monocyte/macrophage phenotype in vitro and vivo, and to identify the receptor by which galectin-2 exerts these effects. We now show that the binding of galectin-2 to different circulating human monocyte subsets is dependent on monocyte surface expression levels of CD14. The high affinity binding is blocked by an anti-CD14 antibody but not by carbohydrates, indicating a specific protein-protein interaction. Galectin-2 binding to human monocytes modulated their transcriptome by inducing proinflammatory cytokines and inhibiting pro-arteriogenic factors, while attenuating monocyte migration. Using specific knock-out mice, we show that galectin-2 acts through the CD14/toll-like receptor (TLR)-4 pathway. Furthermore, galectin-2 skews human macrophages to a M1-like proinflammatory phenotype, characterized by a reduced motility and expression of an anti-arteriogenic cytokine/growth factor repertoire. This is accompanied by a switch in surface protein expression to CD40-high and CD206-low (M1). In a murine model we show that galectin-2 administration, known to attenuate arteriogenesis, leads to increased numbers of CD40-positive (M1) and reduced numbers of CD206-positive (M2) macrophages surrounding actively remodeling collateral arteries. In conclusion galectin-2 is the first endogenous CD14/TLR4 ligand that induces a proinflammatory, non-arteriogenic phenotype in monocytes/macrophages. Interference with CD14-Galectin-2 interaction may provide a new intervention strategy to stimulate growth of collateral arteries in genetically compromised cardiovascular patients.
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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.