Evidence map›Paper›PMID 32144342›Full record

ArticleScientific reports2020

Effect of VCP modulators on gene expression profiles of retinal ganglion cells in an acute injury mouse model.

Tomoko Hasegawa, Hanako Ohashi Ikeda, Norimoto Gotoh, Kei Iida, Sachiko Iwai, Noriko Nakano, Akira Kakizuka, Akitaka Tsujikawa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. 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

8 authors at 1 institution in 1 country.

Tomoko HasegawaDepartment of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, 606-8501, Japan.
Hanako Ohashi IkedaDepartment of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, 606-8501, Japan. hanakoi@kuhp.kyoto-u.ac.jp.
Norimoto GotohDepartment of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, 606-8501, Japan.
Kei IidaMedical Research Support Center, Kyoto University Graduate School of Medicine, Kyoto, 606-8501, Japan.
Sachiko IwaiDepartment of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, 606-8501, Japan.
Noriko NakanoDepartment of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, 606-8501, Japan.
Akira KakizukaLaboratory of Functional Biology, Kyoto University Graduate School of Biostudies & Solution Oriented Research for Science and Technology, Kyoto, 606-8501, Japan.
Akitaka TsujikawaDepartment of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, 606-8501, Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In glaucoma, retinal ganglion cells are damaged, leading to the progressive constriction of the visual field. We have previously shown that the valosin-containing protein (VCP) modulators, Kyoto University Substance (KUS)121 and KUS187, prevent the death of retinal ganglion cells in animal models of glaucoma, including the one generated by N-methyl-D-aspartate (NMDA)-induced neurotoxicity. KUSs appeared to avert endoplasmic reticulum (ER) stress by maintaining ATP levels, resulting in the protection of ganglion cells from cell death. To further elucidate the protective mechanisms of KUSs, we examined gene expression profiles in affected ganglion cells. We first injected KUS-treated mice with NMDA and then isolated the affected retinal ganglion cells using fluorescence-activated cell sorting. Gene expression in the cells was quantified using a next-generation sequencer. Resultantly, we found that KUS121 upregulated several genes involved in energy metabolism. In addition, we observed the upregulation of Zfp667, which has been reported to suppress apoptosis-related genes and prevent cell death. These results further support the suitability of KUS121 as a therapeutic drug in protecting retinal ganglion cells in ophthalmic disorders, such as glaucoma.

Indexed as

Disease SusceptibilityTranscriptomeAcute DiseaseAnimalsApoptosisBiomarkersComputational BiologyDisease Models, AnimalEnergy MetabolismGene Expression ProfilingGene OntologyImmunophenotypingMetabolic Networks and PathwaysMiceN-MethylaspartateRetinal DiseasesBiomarkersN-MethylaspartateValosin Containing ProteinVcp protein, mouse

Identifiers

PMID32144342
PMCPMC7060332
OpenAlexW3010514739

What OpenQuestion holds

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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.