Evidence map›Paper›PMID 33999356›Full record

ArticleNeurotoxicity research2021

FTY720 Exacerbates Blood-Brain Barrier Dysfunction Induced by IgG Derived from Patients with NMO and MOG Disease.

Shunsuke Yoshimura, Shinsuke Nakagawa, Toshiyuki Takahashi, Keiko Tanaka, Akira Tsujino

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 36% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 1 country.

Shunsuke YoshimuraDepartment of Neurology and Strokology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, 852-8501, Japan.
Shinsuke NakagawaDepartment of Medical Pharmacology, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki, 852-8523, Japan. shin3@fukuoka-u.ac.jp.ORCID http://orcid.org/0000-0001-7945-9719
Toshiyuki TakahashiDepartment of Neurology, Tohoku University Graduate School of Medicine, 2-1 Seiryomachi, Aoba-ku, Sendai, Miyagi, 980-0872, Japan.
Keiko TanakaDepartment of Animal Model Development, Brain Research Institute, Niigata University, 757 Asahimachidori, Niigata Chuo-ku, Niigata, 951-8122, Japan.
Akira TsujinoDepartment of Neurology and Strokology, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki, 852-8501, Japan.
Nagasaki University Hospital · JPFukuoka University · JPNiigata University · JPTohoku University · JP

Funding

an Society for the Promotion of Science (JP) 26462167Japan Society for the Promotion of Science (JP) 17K10838
6 · The paper itself

Abstract

Neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein (MOG) antibody-related disease (MOG disease) are inflammatory demyelinating diseases of the central nervous system (CNS). The disruption of the blood-brain barrier (BBB) is considered a key step in the pathogenesis of NMO and MOG disease. Although a previous report indicated that circulating immunoglobulin G (IgG) from NMO patients disrupts the BBB, the effect of IgG from patients with MOG disease has not been elucidated. In addition, it has been reported that some disease-modifying drugs for multiple sclerosis are harmful to NMO by an unknown mechanism. This study aimed to examine the effects of IgG from patients with NMO or MOG disease on BBB integrity. We also examined the effects of disease-modifying drugs (fingolimod [FTY720] and dimethyl fumarate [DMF]) on IgG-treated brain capillary endothelial cells. We used in vitro BBB models constructed with rat brain capillary endothelial cells (RBECs) to examine the effects on BBB function. The integrity of the RBECs was assessed by measuring transendothelial resistance (TEER) and cell viability. NMO or MOG-IgG treatment decreased TEER and cell viability in the endothelial monolayer model. Although FTY720 and DMF did not affect barrier function or cell viability under normal conditions, disease IgG-induced barrier dysfunctions were worsened by the presence of FTY720. These data indicate that circulating IgG in patients with NMO or MOG disease worsens BBB function. Furthermore, in patients with NMO or MOG disease treated with FTY720, changes in the integrity of the BBB were found to exacerbate the disease.

Indexed as

Neuromyelitis OpticaAnimalsBlood-Brain BarrierCells, CulturedDose-Response Relationship, DrugFingolimod HydrochlorideHumansImmunoglobulin GMaleMyelin-Oligodendrocyte GlycoproteinRatsRats, WistarSphingosine 1 Phosphate Receptor ModulatorsFingolimod HydrochlorideImmunoglobulin GMOG protein, humanMyelin-Oligodendrocyte GlycoproteinSphingosine 1 Phosphate Receptor ModulatorsBlood–brain barrierFTY720MOG-related diseaseNeuromyelitis optica

Identifiers

PMID33999356
OpenAlexW3161946523

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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.