ArticleGlia2016
Loss of galectin-3 decreases the number of immune cells in the subventricular zone and restores proliferation in a viral model of multiple sclerosis.
Article in Glia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Galectin-3 in the Lateral Ventricle Regulates Immune Functions.ASN neuro · 2026Review
- Galectin-3 induces neurodevelopmental apical-basal polarity and regulates gyrification.Science advances · 2025Article
- Limiting endosomal damage sensing reduces inflammation triggered by lipid nanoparticle endosomal escape.Nature nanotechnology · 2025Article
- Investigation of Galectin-3 and Cardiotrophin-1 Concentrations as Biomarkers in Dogs with Neurological Distemper.Veterinary sciences · 2025Article
- Sweet Aging: Glycocalyx and Galectins in CNS Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2025Review
- Proteomic analysis reveals candidate molecules to mediate cortical pathology and identify possible biomarkers in an animal model of multiple sclerosis.Frontiers in immunology · 2025Article
- TIM-3 on myeloid cells promotes pulmonary inflammation through increased production of galectin-3.Communications biology · 2024Article
- The role of galectins in immunity and infection.Nature reviews. Immunology · 2023Review
- Elevated Galectin-3 Is Associated with Aging, Multiple Sclerosis, and Oxidized Phosphatidylcholine-Induced Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Galectins-Potential Therapeutic Targets for Neurodegenerative Disorders.International journal of molecular sciences · 2022Review
- Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration.Cell death & disease · 2022Review
- Intravital Imaging of the Murine Subventricular Zone with Three Photon Microscopy.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Galectin-3 Involvement in Cognitive Processes for New Therapeutic Considerations.Frontiers in cellular neuroscience · 2022Review
- Review
- Galectin-3 possible involvement in antipsychotic-induced metabolic changes of schizophrenia: A minireview.World journal of diabetes · 2021Review
- Therapeutically viable generation of neurons with antisense oligonucleotide suppression of PTB.Nature neuroscience · 2021Article
- Galectins and Their Ligand Glycoconjugates in the Central Nervous System Under Physiological and Pathological Conditions.Frontiers in neuroanatomy · 2021Review
- Galectin-3: Roles in Neurodevelopment, Neuroinflammation, and Behavior.Biomolecules · 2020Review
- Article
- Pharmacological Inhibition of Galectin-3 Ameliorates Diabetes-Associated Cognitive Impairment, Oxidative Stress and Neuroinflammation in vivo and in vitro.Journal of inflammation research · 2020Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Multiple sclerosis (MS) frequently starts near the lateral ventricles, which are lined by subventricular zone (SVZ) progenitor cells that can migrate to lesions and contribute to repair. Because MS-induced inflammation may decrease SVZ proliferation and thus limit repair, we studied the role of galectin-3 (Gal-3), a proinflammatory protein. Gal-3 expression was increased in periventricular regions of human MS in post-mortem brain samples and was also upregulated in periventricular regions in a murine MS model, Theiler's murine encephalomyelitis virus (TMEV) infection. Whereas TMEV increased SVZ chemokine (CCL2, CCL5, CCL, and CXCL10) expression in wild type (WT) mice, this was inhibited in Gal-3(-/-) mice. Though numerous CD45+ immune cells entered the SVZ of WT mice after TMEV infection, their numbers were significantly diminished in Gal-3(-/-) mice. TMEV also reduced neuroblast and proliferative SVZ cell numbers in WT mice but this was restored in Gal-3(-/-) mice and was correlated with increased numbers of doublecortin+ neuroblasts in the corpus callosum. In summary, our data showed that loss of Gal-3 blocked chemokine increases after TMEV, reduced immune cell migration into the SVZ, reestablished SVZ proliferation and increased the number of progenitors in the corpus callosum. These results suggest Gal-3 plays a central role in modulating the SVZ neurogenic niche's response to this model of MS.
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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.