ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
The extracellular matrix protein laminin α2 regulates the maturation and function of the blood-brain barrier.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 2 of them syntheses that pooled it.
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Who cites it
131 citing papers in PubMed, 2 syntheses or guidelines pooled it, 218 citations in OpenAlex.
- Laminin as a Biomarker of Blood-Brain Barrier Disruption under Neuroinflammation: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Genetic basis of lacunar stroke: a pooled analysis of individual patient data and genome-wide association studies.The Lancet. Neurology · 2021Pooled it
- Human blood-brain barrier tissue model to characterize lipid nanoparticle delivery and transport mechanisms.Biomaterials · 2026Article
- Cell-to-Cell Signaling Networks at the Blood-Brain Barrier in Health and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Cellular and signalling mechanisms that regulate the blood-brain barrier.Nature reviews. Molecular cell biology · 2026Review
- Dissecting the aberrant vasculature of glioblastoma: mechanisms and therapeutic targets.Cancer metastasis reviews · 2026Review
- Development of the blood-brain barrier.Development (Cambridge, England) · 2026Review
- Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression.Molecular neurodegeneration advances · 2026Article
- Dynamic modulation of the blood-brain barrier in the healthy brain.Nature reviews. Neuroscience · 2025Review
- Overexpression of endothelial β4 integrin has no impact on blood-brain barrier integrity or the pathogenesis of experimental autoimmune encephalomyelitis.Experimental neurology · 2025Article
- Development and functional characterization of a tissue-engineered blood-air barrier model forNanomedicine (London, England) · 2025Article
- A novel mouse model foreLife · 2025Article
- Dietary Influence on Urolithiasis Risk Mediated by Plasma Metabolites: A Mendelian Randomization and Experimental Study Linking Genes, Metabolites, and Clinical Outcomes.Food science & nutrition · 2025Article
- Distinct functional domains of Dystroglycan regulate inhibitory synapse formation and maintenance in cerebellar Purkinje cells.Communications biology · 2025Article
- Laminins and the blood-brain barrier.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Article
- AKAP12 Variant 1 Knockout Enhances Vascular Endothelial Cell Motility.Journal of vascular research · 2025Article
- Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025Review
- Basement membranes' role in immune cell recruitment to the central nervous system.Journal of inflammation (London, England) · 2024Article
- Single-cell DNA methylome and 3D genome atlas of the human subcutaneous adipose tissue.bioRxiv : the preprint server for biology · 2024Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Laminins are major constituents of the gliovascular basal lamina of the blood-brain barrier (BBB); however, the role of laminins in BBB development remains unclear. Here we report that Lama2(-/-) mice, lacking expression of the laminin α2 subunit of the laminin-211 heterotrimer expressed by astrocytes and pericytes, have a defective BBB in which systemically circulated tracer leaks into the brain parenchyma. The Lama2(-/-) vascular endothelium had significant abnormalities, including altered integrity and composition of the endothelial basal lamina, inappropriate expression of embryonic vascular endothelial protein MECA32, substantially reduced pericyte coverage, and tight junction abnormalities. Additionally, astrocytic endfeet were hypertrophic and lacked appropriately polarized aquaporin4 channels. Laminin-211 appears to mediate these effects at least in part by dystroglycan receptor interactions, as preventing dystroglycan expression in neural cells led to a similar set of BBB abnormalities and gliovascular disturbances, which additionally included perturbed vascular endothelial glucose transporter-1 localization. These findings provide insight into the cell and molecular changes that occur in congenital muscular dystrophies caused by Lama2 mutations or inappropriate dystroglycan post-translational modifications, which have accompanying brain abnormalities, including seizures. Our results indicate a novel role for laminin-dystroglycan interactions in the cooperative integration of astrocytes, endothelial cells, and pericytes in regulating the BBB.
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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.