Evidence map›Paper›PMID 30670717›Full record

ArticleScientific reports2019

Abrogated Caveolin-1 expression via histone modification enzyme Setdb2 regulates brain edema in a mouse model of influenza-associated encephalopathy.

Natsuko Imakita, Masahiro Kitabatake, Noriko Ouji-Sageshima, Atsushi Hara, Shoko Morita-Takemura, Kei Kasahara, Akihiro Matsukawa, Akio Wanaka, Keiichi Mikasa, Toshihiro Ito

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  11. Epigenetics in blood-brain barrier disruption.Fluids and barriers of the CNS · 2021
    Review
  12. Tight junctions and their regulation by non-coding RNAs.International journal of biological sciences · 2021
    Review
  13. Article
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  15. Review
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

10 authors at 2 institutions in 1 country.

Natsuko ImakitaDepartment of Immunology, Nara Medical University, Kashihara, Nara, Japan.
Masahiro KitabatakeDepartment of Immunology, Nara Medical University, Kashihara, Nara, Japan.
Noriko Ouji-SageshimaDepartment of Immunology, Nara Medical University, Kashihara, Nara, Japan.
Atsushi HaraDepartment of Immunology, Nara Medical University, Kashihara, Nara, Japan.
Shoko Morita-TakemuraDepartment of Anatomy & Neuroscience, Nara Medical University, Kashihara, Nara, Japan.
Kei KasaharaCenter for Infectious Diseases, Nara Medical University, Kashihara, Nara, Japan.
Akihiro MatsukawaDepartment of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Akio WanakaDepartment of Anatomy & Neuroscience, Nara Medical University, Kashihara, Nara, Japan.
Keiichi MikasaCenter for Infectious Diseases, Nara Medical University, Kashihara, Nara, Japan.
Toshihiro ItoDepartment of Immunology, Nara Medical University, Kashihara, Nara, Japan. toshi-ito@naramed-u.ac.jp.
Nara Medical University · JPOkayama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza-associated encephalopathy (IAE) is a serious complication that can follow influenza virus infection. Once a cytokine storm is induced during influenza virus infection, tight junction protein disruption occurs, which consequently leads to blood-brain barrier (BBB) breakdown. However, the details of IAE pathogenesis are not well understood. Here, we established a murine IAE model by administration of lipopolysaccharide following influenza virus infection. Brains from IAE model mice had significantly higher expression of type I interferons and inflammatory cytokines. In addition, the expression of Caveolin-1, one of the key proteins that correlate with protection of the BBB, was significantly lower in brains from the IAE group compared with the control group. We also found that, among 84 different histone modification enzymes, only SET domain bifurcated 2 (Setdb2), one of the histone methyltransferases that methylates the lysine 9 of histone H3, showed significantly higher expression in the IAE group compared with the control group. Furthermore, chromatin immunoprecipitation revealed that methylation of histone H3 lysine 9 was correlated with repression of the Caveolin-1 promoter region. These studies identify Caveolin-1 as a key regulator of BBB permeability in IAE and reveal that it acts through histone modification induced by Setdb2.

Indexed as

AnimalsBlood-Brain BarrierBrain DiseasesBrain EdemaCaveolin 1CytokinesDisease Models, AnimalHistone-Lysine N-MethyltransferaseInterferon Type ILipopolysaccharidesMethylationMiceOrthomyxoviridaeOrthomyxoviridae InfectionsCaveolin 1CytokinesHistone-Lysine N-MethyltransferaseInterferon Type ILipopolysaccharidesSetdb2 protein, mouse

Identifiers

PMID30670717
PMCPMC6342998
OpenAlexW2913727230

What OpenQuestion holds

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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.