ArticleJournal of neuroinflammation2012
Inflammation modulates expression of laminin in the central nervous system following ischemic injury.
Article in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Laminin as a Biomarker of Blood-Brain Barrier Disruption under Neuroinflammation: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Roles and therapeutic prospects of the laminin family in disorders of the nervous system.Journal of translational medicine · 2026Review
- Glycocalyx and basal lamina in neurological disorders.Matrix biology : journal of the International Society for Matrix Biology · 2026Review
- Detection of inflammation-related blood-brain barrier dysfunction using PET and MR imaging: a pilot study.Scientific reports · 2026Article
- Laminins and the blood-brain barrier.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Review
- The dual nature of neuroinflammation in networked brain.Frontiers in immunology · 2025Review
- Basement membranes' role in immune cell recruitment to the central nervous system.Journal of inflammation (London, England) · 2024Article
- Development of a cell-free strategy to recover aged skeletal muscle after disuse.The Journal of physiology · 2023Article
- Increasing reproducibility in preclinical stroke research: the correlation of immunofluorescence intensity measurements and Western blot analyses strongly depends on antibody clonality and tissue pre-treatment in a mouse model of focal cerebral ischemia.Frontiers in cellular neuroscience · 2023Article
- Early Rehabilitation Exercise after Stroke Improves Neurological Recovery through Enhancing Angiogenesis in Patients and Cerebral Ischemia Rat Model.International journal of molecular sciences · 2022Article
- Infiltration of meningeal macrophages into the Virchow-Robin space after ischemic stroke in rats: Correlation with activated PDGFR-β-positive adventitial fibroblasts.Frontiers in molecular neuroscience · 2022Article
- Astrocyte depletion alters extracellular matrix composition in the demyelinating phase of Theiler's murine encephalomyelitis.PloS one · 2022Article
- Review
- Chemically defined human vascular laminins for biologically relevant culture of hiPSC-derived brain microvascular endothelial cells.Fluids and barriers of the CNS · 2020Article
- Comparison of proteome alterations during aging in the temporal lobe of humans and rhesus macaques.Experimental brain research · 2020Article
- Demonstrating a reduced capacity for removal of fluid from cerebral white matter and hypoxia in areas of white matter hyperintensity associated with age and dementia.Acta neuropathologica communications · 2020Article
- Basement Membrane Changes in Ischemic Stroke.Stroke · 2020Review
- Targeting the HIV-infected brain to improve ischemic stroke outcome.Nature communications · 2019Article
- Involvement of Epigenetic Mechanisms and Non-coding RNAs in Blood-Brain Barrier and Neurovascular Unit Injury and Recovery After Stroke.Frontiers in neuroscience · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIschemic stroke induces neuronal death in the core of the infarct within a few hours and the secondary damage in the surrounding regions over a long period of time. Reduction of inflammation using pharmacological reagents has become a target of research for the treatment of stroke. Cyclooxygenase 2 (COX-2), a marker of inflammation, is induced during stroke and enhances inflammatory reactions through the release of enzymatic products, such as prostaglandin (PG) E2.
methodsWild-type (WT) and COX-2 knockout (COX-2KO) mice were subjected to middle cerebral artery occlusion (MCAO). Additionally, brain slices derived from these mice or brain microvascular endothelial cells (BMECs) were exposed to oxygen-glucose deprivation (OGD) conditions. The expression levels of extracellular matrix (ECM) proteins were assessed and correlated with the state of inflammation.
resultsWe found that components of the ECM, and specifically laminin, are transiently highly upregulated on endothelial cells after MCAO or OGD. This upregulation is not observed in COX-2KO mice or WT mice treated with COX-2 inhibitor, celecoxib, suggesting that COX-2 is associated with changes in the levels of laminins.
conclusionsTaken together, we report that transient ECM remodeling takes place early after stroke and suggest that this increase in ECM protein expression may constitute an effort to revascularize and oxygenate the tissue.
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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.