ArticleThe American journal of pathology2008
von-Willebrand factor influences blood brain barrier permeability and brain inflammation in experimental allergic encephalomyelitis.
Article in The American journal of pathology, 2008. 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, 52 citations in OpenAlex.
- Mouse models to study von Willebrand factor in inflammation: a scoping review.Intensive care medicine experimental · 2026Review
- Spatiotemporal Angiogenic Patterns in the Development of the Mouse Fetal Blood-Brain Barrier System During Pregnancy.International journal of molecular sciences · 2025Article
- ADAMTS-13 and HMGB1-induced oxidative stress in Taenia multiceps-infected animals.Scientific reports · 2023Article
- Transcriptome Profile in the Mouse Brain of Hepatic Encephalopathy and Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Peripheral apoE4 enhances Alzheimer's pathology and impairs cognition by compromising cerebrovascular function.Nature neuroscience · 2022Article
- What is the role of Von Willebrand factor in chronic hepatitis B virus infection to hepatocellular carcinoma: a review article.Therapeutic advances in chronic disease · 2022Review
- Rictor maintains endothelial integrity under shear stress.Frontiers in cell and developmental biology · 2022Article
- Determination of CSF GFAP, CCN5, and vWF Levels Enhances the Diagnostic Accuracy of Clinically Defined MS From Non-MS Patients With CSF Oligoclonal Bands.Frontiers in immunology · 2021Article
- ADAMTS13 ameliorates inflammatory responses in experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2020Article
- Differential Expression of CD31 and Von Willebrand Factor on Endothelial Cells in Different Regions of the Human Brain: Potential Implications for Cerebral Malaria Pathogenesis.Brain sciences · 2020Article
- Role of the Golgi Apparatus in the Blood-Brain Barrier: Golgi Protection May Be a Targeted Therapy for Neurological Diseases.Molecular neurobiology · 2018Review
- von Willebrand factor contributes to poor outcome in a mouse model of intracerebral haemorrhage.Scientific reports · 2016Article
- A novel role for von Willebrand factor in the pathogenesis of experimental cerebral malaria.Blood · 2016Article
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- Analysis of neurogenesis during experimental autoimmune encephalomyelitis reveals pitfalls of bioluminescence imaging.PloS one · 2015Article
- Endothelial Von Willebrand factor promotes blood-brain barrier flexibility and provides protection from hypoxia and seizures in mice.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- On the versatility of von Willebrand factor.Mediterranean journal of hematology and infectious diseases · 2013Article
- Combinatorial roles for histamine H1-H2 and H3-H4 receptors in autoimmune inflammatory disease of the central nervous system.European journal of immunology · 2012Article
- Endothelial histamine H1 receptor signaling reduces blood-brain barrier permeability and susceptibility to autoimmune encephalomyelitis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Weibel-Palade bodies within endothelial cells are secretory granules known to release von Willebrand Factor (VWF), P-selectin, chemokines, and other stored molecules following histamine exposure. Mice with a disrupted VWF gene (VWFKO) have endothelial cells that are deficient in Weibel-Palade bodies. These mice were used to evaluate the role of VWF and/or Weibel-Palade bodies in Bordetella pertussis toxin-induced hypersensitivity to histamine, a subphenotype of experimental allergic encephalomyelitis, the principal autoimmune model of multiple sclerosis. No significant differences in susceptibility to histamine between wild-type and VWFKO mice were detected after 3 days; however, histamine sensitivity persisted significantly longer in VWFKO mice. Correspondingly, encephalomyelitis onset was earlier, disease was more severe, and blood brain barrier (BBB) permeability was significantly increased in VWFKO mice, as compared with wild-type mice. Moreover, inflammation was selectively increased in the brains, but not spinal cords, of VWFKO mice as compared with wild-type mice. Early increases in BBB permeability in VWFKO mice were not due to increased encephalitogenic T-cell activity since BBB permeability did not differ in adjuvant-treated VWFKO mice as compared with littermates immunized with encephalitogenic peptide plus adjuvant. Taken together, these data indicate that VWF and/or Weibel-Palade bodies negatively regulate BBB permeability changes and autoimmune inflammatory lesion formation within the brain elicited by peripheral inflammatory stimuli.
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