ArticleJournal of neuroinflammation2018
Vascular adhesion protein-1 is actively involved in the development of inflammatory lesions in rat models of multiple sclerosis.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Vascular-adhesion protein 1 in giant cell arteritis and polymyalgia rheumatica.Frontiers in medicine · 2024Review
- Vascular adhesion protein-1-targeted PET imaging in autoimmune myocarditis.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2023Article
- Inhibition of vascular adhesion protein 1 protects dopamine neurons from the effects of acute inflammation and restores habit learning in the striatum.Journal of neuroinflammation · 2021Article
- Physiological and Pathological Factors Affecting Drug Delivery to the Brain by Nanoparticles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- First-in-Humans Study ofJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2021Article
- SSAO/VAP-1 in Cerebrovascular Disorders: A Potential Therapeutic Target for Stroke and Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Article
- Increased Vascular Adhesion Protein 1 (VAP-1) Levels are Associated with Alternative M2 Macrophage Activation and Poor Prognosis for Human Gliomas.Diagnostics (Basel, Switzerland) · 2020Article
- Human Copper-Containing Amine Oxidases in Drug Design and Development.Molecules (Basel, Switzerland) · 2020Review
- MicroRNA-7, synergizes with RORα, negatively controls the pathology of brain tissue inflammation.Journal of neuroinflammation · 2020Article
- Changes in expression profiles of internal jugular vein wall and plasma protein levels in multiple sclerosis.Molecular medicine (Cambridge, Mass.) · 2018Article
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15 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundVascular adhesion protein-1 (VAP-1) is an inflammation-inducible endothelial cell molecule and primary amine oxidase that mediates leukocyte entry to sites of inflammation. However, there is limited knowledge of the inflammation-related expression of VAP-1 in the central nervous system (CNS). Therefore, we investigated the expression of VAP-1 within the CNS vasculature in two focal rat models of experimental autoimmune encephalomyelitis (EAE) mimicking multiple sclerosis (MS).
methodsEAE was induced either with Bacillus Calmette-Guérin, resulting in a delayed-type hypersensitivity-like pathogenesis (fDTH-EAE), or with myelin oligodendrocyte glycoprotein (fMOG-EAE). A subgroup of fMOG-EAE rats were treated daily with a selective VAP-1 inhibitor (LJP1586; 5 mg/kg). On 3 and 14 days after lesion activation, rat brains were assessed using magnetic resonance imaging (MRI), and ex vivo autoradiography was conducted to evaluate the binding of Gallium-68-labelled VAP-1 ligand. Histology and immunohistochemistry (OX-42, VAP-1, intercellular adhesion protein-1 [ICAM-1], P-selectin) supported the ex vivo autoradiography.
resultsEAE lesions showed MRI-detectable signal changes and binding of the VAP-1-targeting radiotracer in both rat models. Some of the VAP-1 positive vessels showed morphological features typical for high endothelial-like venules at sites of inflammation. Inhibition of VAP-1 activity with small molecule inhibitor, LJP1586, decreased lymphocyte density in the acute inflammatory phase of fMOG-EAE lesions (day 3, P = 0.026 vs. untreated), but not in the remission phase (day 14, P = 0.70 vs. untreated), and had no effect on the amount of OX-42-positive cells in either phase. LJP1586 treatment reduced VAP-1 and ICAM-1 expression in the acute inflammatory phase, whereas P-selectin remained not detectable at all studied stages of the disease.
conclusionsOur results revealed that VAP-1 is expressed and functionally active in vasculature within the induced focal EAE lesions during the acute phase of inflammation and remains expressed after the acute inflammation has subsided. The study indicates that VAP-1 is actively involved in the development of inflammatory CNS lesions. During this process, the endothelial cell lesion-related vasculature seem to undergo a structural transformation from regular flat-walled endothelium to HEV-like endothelium.
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