Evidence map›Paper›PMID 28157839›Full record

ArticlePediatric research2017

Establishment of a method for evaluating endothelial cell injury by TNF-α in vitro for clarifying the pathophysiology of virus-associated acute encephalopathy.

Kyohei Miyazaki, Koichi Hashimoto, Masatoki Sato, Masahiro Watanabe, Naoki Tomikawa, Shuto Kanno, Yukihiko Kawasaki, Nobuo Momoi, Mitsuaki Hosoya

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Pediatric research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

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  7. Cholinergic regulation of vascular endothelial function by human ChATProceedings of the National Academy of Sciences of the United States of America · 2023
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  11. The Role of RASGRP2 in Vascular Endothelial Cells-A Mini Review.International journal of molecular sciences · 2021
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  18. CRISPR-Based Activation of Endogenous Expression ofFrontiers in cell and developmental biology · 2021
    Article
  19. Article
  20. Article
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

9 authors at 1 institution in 1 country.

Kyohei MiyazakiDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Koichi HashimotoDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Masatoki SatoDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Masahiro WatanabeDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Naoki TomikawaDepartment of Basic Pathology, Fukushima Medical University, Fukushima, Japan.
Shuto KannoDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Yukihiko KawasakiDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Nobuo MomoiDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Mitsuaki HosoyaDepartment of Pediatrics, Fukushima Medical University, Fukushima, Japan.
Fukushima Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVirus-associated acute encephalopathy (VAE) is a severe central nervous system complication caused by common viral infections in children. The pathophysiology of VAE is thought to be endothelial injury. This study was designed to establish an in vitro VAE model for evaluating endothelial injury caused by the proinflammatory cytokine TNF-α.

methodsTranswell-grown human umbilical vein endothelial cells (HUVECs) monolayers were incubated with serially diluted TNF-α. Transendothelial electrical resistance (TER) was measured using impedance spectroscopy. Permeability changes of HUVECs after TNF-α treatment were determined by fluorescein isothiocyanate (FITC)-conjugated dextran. Moreover, TNF-α-induced morphological changes in claudin-5 and apoptosis were observed by immunofluorescent staining.

resultsThe decrease in TER, time of TER recovery to baseline, and increase in permeability were all dependent on TNF-α concentration. Immunofluorescent staining showed that claudin-5 was delocalized after TNF-α treatment in a dose-dependent manner. In addition, some apoptotic cells were observed at high TNF-α concentrations.

conclusionTER measurement combined with a permeability assay could be useful for evaluating vascular endothelial cell permeability in an in vitro model. These evaluation methods will contribute to both the development of specific treatments focusing on vascular permeability, and the search for a novel therapeutic strategy in VAE treatment.

Indexed as

ApoptosisBrain DiseasesChildClaudin-5Dose-Response Relationship, DrugEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsIn Vitro TechniquesPermeabilityTumor Necrosis Factor-alphaClaudin-5CLDN5 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID28157839
OpenAlexW2583108044

What OpenQuestion holds

Textmetadata
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.