ArticleScientific reports2016
Galectin-3 causes enteric neuronal loss in mice after left sided permanent middle cerebral artery occlusion, a model of stroke.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Gut microbiota-mediated neuroinflammation following stroke: mechanisms and intervention strategies.Journal of translational medicine · 2026Review
- Function of the large intestine and its interaction with the brain after ischemic stroke: a comprehensive literature review.Frontiers in cellular neuroscience · 2026Review
- Microbiota-gut-brain-axis: a new target of acupuncture therapy for post-stroke cognitive impairment.Frontiers in microbiology · 2025Review
- Systematic Insights into the Relationship between the Microbiota-Gut-Brain Axis and Stroke with the Focus on Tryptophan Metabolism.Metabolites · 2024Review
- The interaction between intestinal microenvironment and stroke.CNS neuroscience & therapeutics · 2023Review
- Short-Chain Fatty Acids as Bacterial Enterocytes and Therapeutic Target in Diabetes Mellitus Type 2.Biomedicines · 2022Review
- APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer's disease pathology and brain diseases.Molecular neurodegeneration · 2022Review
- Short-term exposure to urban PMPhysiological reports · 2022Article
- Disorders of the enteric nervous system - a holistic view.Nature reviews. Gastroenterology & hepatology · 2021Review
- The serum galectin-3 levels are associated with the severity and prognosis of ischemic stroke.Aging · 2021Article
- Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process.Journal of immunology research · 2021Review
- Mitochondria-Microbiota Interaction in Neurodegeneration.Frontiers in aging neuroscience · 2021Review
- Bidirectional Brain-gut-microbiota Axis in increased intestinal permeability induced by central nervous system injury.CNS neuroscience & therapeutics · 2020Review
- Galectin-3: Roles in Neurodevelopment, Neuroinflammation, and Behavior.Biomolecules · 2020Review
- Post-stroke remodeling processes in animal models and humans.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Review
- Focal, but not global, cerebral ischaemia causes loss of myenteric neurons and upregulation of vasoactive intestinal peptide in mouse ileum.International journal of experimental pathology · 2018Article
- Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z.International journal of molecular sciences · 2018Review
- Galectin-3-Mediated Glial Crosstalk Drives Oligodendrocyte Differentiation and (Re)myelination.Frontiers in cellular neuroscience · 2018Review
- Microglial Lectins in Health and Neurological Diseases.Frontiers in molecular neuroscience · 2018Review
- Endoscopic full-thickness biopsy, a novel method in the work up of complicated abdominal symptoms.Therapeutic advances in gastroenterology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to brain injury stroke patients often suffer gastrointestinal complications. Neuroimmune interactions involving galectin-3, released from microglia in the brain, mediates the post-stroke pro-inflammatory response. We investigated possible consequences of stroke on the enteric nervous system and the involvement of galectin-3. We show that permanent middle cerebral artery occlusion (pMCAO) induces loss of enteric neurons in ileum and colon in galectin-3(+/+), but not in galectin-3(-/-), mice. In vitro we show that serum from galectin-3(+/+), but not from galectin-3(-/-), mice subjected to pMCAO, caused loss of C57BL/6J myenteric neurons, while myenteric neurons derived from TLR4(-/-) mice were unaffected. Further purified galectin-3 (10(-6) M) caused loss of cultured C57BL/6J myenteric neurons. Inhibitors of transforming growth factor β-activated kinase 1 (TAK1) or AMP activated kinase (AMPK) counteracted both the purified galectin-3 and the galectin-3(+/+) pMCAO serum-induced loss in vitro. Combined we show that stroke (pMCAO) triggers central and peripheral galectin-3 release causing enteric neuronal loss through a TLR4 mediated mechanism involving TAK1 and AMPK. Galectin-3 is suggested a target for treatment of post-stroke complications.
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