Evidence map›Paper›PMID 28596825›Full record

ArticleCell & bioscience2017

Kv1.3 channel blocker (ImKTx88) maintains blood-brain barrier in experimental autoimmune encephalomyelitis.

Jie Huang, Song Han, Qi Sun, Yipeng Zhao, Junchen Liu, Xiaolu Yuan, Wenqian Mao, Biwen Peng, Wanhong Liu, Jun Yin and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

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  12. Mechanisms of Blood-Brain Barrier Disruption in Herpes Simplex Encephalitis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Review
  13. Scorpion toxins targeting Kv1.3 channels: insights into immunosuppression.The journal of venomous animals and toxins including tropical diseases · 2019
    Article
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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

11 authors at 1 institution in 1 country.

Jie Huang *Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Song Han *Department of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Qi SunDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Yipeng ZhaoDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Junchen LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Xiaolu YuanDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Wenqian MaoDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Biwen PengHubei Provincial Key Laboratory of Developmentally Originated Disease, School of Basic Medical Sciences, Wuhan University, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Wanhong LiuHubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Jun YinDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Xiaohua HeDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, No. 185, Donghu Road, Wuchang District, Wuhan, 430071 China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDisruption of blood-brain barrier (BBB) and subsequent infiltration of auto-reactive T lymphocytes are major characteristics of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Kv1.3 channel blockers are demonstrated potential therapeutic effects on MS patients and EAE models, maybe via reducing activation of T cells. However, it remains to be explored whether Kv1.3 channel blockers maintain integrity of BBB in MS model.

resultsIn this study, ImKTx88, a highly selective Kv1.3 channel blocker, was used to determine the role of Kv1.3 channel in the pathogenesis of EAE, particularly in the maintenance of BBB. ImKTx88 ameliorated pathological severity in the EAE rats, and reduced extravasation into CNS. ImKTx88 also ameliorated the severity of loss or redistribution of tight junction proteins, and inhibited over-expression of ICAM-1 and VCAM-1 in the brain from EAE rats. Furthermore ImKTx88 protection was associated with activation of Ang-1/Tie-2 axis, and might be due to decreased IL-17 production.

conclusionsImKTx88 may be a novel therapeutic agent for MS treatment by stabilizing the BBB.

Indexed as

Blood–brain barrierExperimental autoimmune encephalomyelitisIL-17Kv1.3 channel blockerMultiple sclerosis

Identifiers

PMID28596825
PMCPMC5463463
OpenAlexW2622886030

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.