Evidence map›Paper›PMID 29682525›Full record

ArticleBioMed research international2018

Blood-Brain Barrier Damage as the Starting Point of Leukoaraiosis Caused by Cerebral Chronic Hypoperfusion and Its Involved Mechanisms: Effect of Agrin and Aquaporin-4.

Jing Huang, Junwen Li, Chao Feng, Xi Huang, Liping Wong, Xueyuan Liu, Zhiyu Nie, Gangming Xi

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Precision Medicine for Blood Glutamate Grabbing in Ischemic Stroke.International journal of molecular sciences · 2024
    Observational
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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

8 authors at 3 institutions in 1 country.

Jing HuangDepartment of Neurology, Shanghai Xuhui Central Hospital, 996 Middle Huaihai Road, Shanghai 200031, China.
Junwen LiDepartment of Neurology, Yangpu Hospital, Tongji University School of Medicine, 450 Tengyue Road, Shanghai 200092, China.
Chao FengDepartment of Internal Medicine, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, N1 Shangcheng Avenue, Yiwu 322000, China.ORCID 0000-0003-0155-9159
Xi HuangDepartment of Medicine, The First Affiliated Hospital, Suzhou University School of Medicine, 188 Shizi Street, Suzhou 215006, China.
Liping WongDepartment of Neurology, Shanghai Xuhui Central Hospital, 996 Middle Huaihai Road, Shanghai 200031, China.
Xueyuan LiuDepartment of Neurology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Middle Yanchang Road, Shanghai 200072, China.
Zhiyu NieDepartment of Neurology, Tongji Hospital, Tongji University School of Medicine, 389 Village Road, Shanghai 200065, China.ORCID 0000-0003-3616-0180
Gangming XiDepartment of Neurology, Shanghai Xuhui Central Hospital, 996 Middle Huaihai Road, Shanghai 200031, China.ORCID 0000-0003-4462-1477
Shanghai Xuhui Central Hospital · CNTongji University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

White matter lesion (WML) is popular in the patients aged over 65. Brain edema and blood-brain barrier (BBB) dysfunction due to cerebral chronic hypoperfusion (CCH) contributed to WML. Preserving astrocyte polarity is vital for BBB integrity. In our experiment, CCH model is established by bilateral carotid arteries occlusion (2VO). Leukoaraiosis was verified by fiber density stain, and brain edema was evaluated using brain water content measuring. The expressions of agrin and aquaporin-4 (AQP4) were evaluated, as well as the integrity of BBB. Astrocyte polarity was assessed by visualizing the distribution of AQP4 on astrocyte end-feet membranes. The results showed that expression of AQP4 firstly increased and then decreased, as agrin expression decreased gradually. At 3 days after 2VO, AQP4 and agrin displayed the most opposite expression with the former increasing and the latter decreasing; at the same time, brain edema reached high point as well as BBB permeability, and astrocyte polarity was degeneration. In the later phase, brain edema and BBB permeability were getting recovered, but WML was getting more evident. In accordance with that, agrin and AQP4 expression decreased significantly with astrocyte polarity reducing. We speculated that agrin and AQP4 played key roles in development of WML by mediating BBB damage in CCH, and BBB dysfunction due to reduced astrocyte polarity is the starting point of WMH.

Indexed as

AgrinAnimalsAquaporin 4AstrocytesBiological TransportBlood-Brain BarrierBrainBrain EdemaBrain IschemiaCell PolarityLeukoaraiosisMalePermeabilityRatsRats, WistarAgrinAquaporin 4

Identifiers

PMID29682525
PMCPMC5846350
OpenAlexW2794235198

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.