ArticlePloS one2014
Sera from remitting and secondary progressive multiple sclerosis patients disrupt the blood-brain barrier.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Multiple sclerosis: etiology in the context of neurovascular unit and immune system involvement and advancements withFrontiers in immunology · 2025Review
- The Fibrotic Response in Pericyte Culture Upon Exposure to Multiple Sclerosis Sera.Noro psikiyatri arsivi · 2025Article
- Plasma IgG aggregates as biomarkers for multiple sclerosis.Clinical immunology (Orlando, Fla.) · 2023Article
- Multiple sclerosis plasma IgG aggregates induce complement-dependent neuronal apoptosis.Cell death & disease · 2023Article
- Brain Barriers and Multiple Sclerosis: Novel Treatment Approaches from a Brain Barriers Perspective.Handbook of experimental pharmacology · 2022Article
- GRP78 Antibodies Are Associated With Blood-Brain Barrier Breakdown in Anti-Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder.Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- FTY720 Exacerbates Blood-Brain Barrier Dysfunction Induced by IgG Derived from Patients with NMO and MOG Disease.Neurotoxicity research · 2021Article
- Blood-Brain Barrier Dysfunction Amplifies the Development of Neuroinflammation: Understanding of Cellular Events in Brain Microvascular Endothelial Cells for Prevention and Treatment of BBB Dysfunction.Frontiers in cellular neuroscience · 2021Review
- The Role of Antibodies in the Pathogenesis of Multiple Sclerosis.Frontiers in neurology · 2020Review
- Gut microbiota-dependent CCR9+CD4+ T cells are altered in secondary progressive multiple sclerosis.Brain : a journal of neurology · 2019Article
- Article
- Endothelial Response to Glucocorticoids in Inflammatory Diseases.Frontiers in immunology · 2016Review
- Fingolimod (FTY720-P) Does Not Stabilize the Blood-Brain Barrier under Inflammatory Conditions in an in Vitro Model.International journal of molecular sciences · 2015Article
- Pro-inflammatory TNFα and IL-1β differentially regulate the inflammatory phenotype of brain microvascular endothelial cells.Journal of neuroinflammation · 2015Article
- Article
- Disruption in the Blood-Brain Barrier: The Missing Link between Brain and Body Inflammation in Bipolar Disorder?Neural plasticity · 2015Review
- Fingolimod prevents blood-brain barrier disruption induced by the sera from patients with multiple sclerosis.PloS one · 2015Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPathological destruction of blood-brain barrier (BBB) has been thought to be the initial key event in the process of developing multiple sclerosis (MS). The purpose of the present study was to clarify the possible molecular mechanisms responsible for the malfunction of BBB by sera from relapse-remitting MS (RRMS) and secondary progressive MS (SPMS) patients.
methodsWe evaluated the effects of sera from the patients in the relapse phase of RRMS (RRMS-R), stable phase of RRMS (RRMS-S) and SPMS on the expression of tight junction proteins and vascular cell adhesion protein-1 (VCAM-1), and on the transendothelial electrical resistance (TEER) in human brain microvascular endothelial cells (BMECs).
resultsSera from the RRMS-R or SPMS patients decreased the claudin-5 protein expression and the TEER in BMECs. In RRMS-R, this effect was restored after adding an MMP inhibitor, and the MMP-2/9 secretion by BMECs was significantly increased after the application of patients' sera. In SPMS, the immunoglobulin G (IgG) purified from patients' sera also decreased the claudin-5 protein expression and the TEER in BMECs. The sera and purified IgG from all MS patients increased the VCAM-1 protein expression in BMECs.
conclusionsThe up-regulation of autocrine MMP-2/9 by BMECs after exposure to sera from RRMS-R patients or the autoantibodies against BMECs from SPMS patients can compromise the BBB. Both RRMS-S and SPMS sera increased the VCAM-1 expression in the BBB, thus indicating that targeting the VCAM-1 in the BBB could represent a possible therapeutic strategy for even the stable phase of MS and SPMS.
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