Evidence map›Paper›PMID 24676347›Full record

ArticlePloS one2014

Deafness gene expression patterns in the mouse cochlea found by microarray analysis.

Hidekane Yoshimura, Yutaka Takumi, Shin-ya Nishio, Nobuyoshi Suzuki, Yoh-ichiro Iwasa, Shin-ichi Usami

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 3 pooled it
2.0field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 3 syntheses or guidelines pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Hearing Loss, Tinnitus, and Dizziness in COVID-19: A Systematic Review and Meta-Analysis.The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques · 2022
    Pooled it
  3. Pooled it
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  5. Genetic Diagnosis and Discovery Enabled by Large Language Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  7. Genetic Discovery Enabled by A Large Language Model.bioRxiv : the preprint server for biology · 2023
    Article
  8. Follistatin regulates the specification of the apical cochlea responsible for low-frequency hearing in mammals.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

6 authors at 1 institution in 1 country.

Hidekane YoshimuraDepartment of Otorhinolaryngology, Shinshu University School of Medicine, Matsumoto, Nagano, Japan.
Yutaka TakumiDepartment of Otorhinolaryngology, Shinshu University School of Medicine, Matsumoto, Nagano, Japan.
Shin-ya NishioDepartment of Otorhinolaryngology, Shinshu University School of Medicine, Matsumoto, Nagano, Japan.
Nobuyoshi SuzukiDepartment of Otorhinolaryngology, Shinshu University School of Medicine, Matsumoto, Nagano, Japan.
Yoh-ichiro IwasaDepartment of Otorhinolaryngology, Shinshu University School of Medicine, Matsumoto, Nagano, Japan.
Shin-ichi UsamiDepartment of Otorhinolaryngology, Shinshu University School of Medicine, Matsumoto, Nagano, Japan.
Shinshu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTonotopy is one of the most fundamental principles of auditory function. While gradients in various morphological and physiological characteristics of the cochlea have been reported, little information is available on gradient patterns of gene expression. In addition, the audiograms in autosomal dominant non syndromic hearing loss can be distinctive, however, the mechanism that accounts for that has not been clarified. We thought that it is possible that tonotopic gradients of gene expression within the cochlea account for the distinct audiograms. METHODOLOGY/PRINCIPAL

findingsWe compared expression profiles of genes in the cochlea between the apical, middle, and basal turns of the mouse cochlea by microarray technology and quantitative RT-PCR. Of 24,547 genes, 783 annotated genes expressed more than 2-fold. The most remarkable finding was a gradient of gene expression changes in four genes (Pou4f3, Slc17a8, Tmc1, and Crym) whose mutations cause autosomal dominant deafness. Expression of these genes was greater in the apex than in the base. Interestingly, expression of the Emilin-2 and Tectb genes, which may have crucial roles in the cochlea, was also greater in the apex than in the base. CONCLUSIONS/SIGNIFICANCE: This study provides baseline data of gradient gene expression in the cochlea. Especially for genes whose mutations cause autosomal dominant non syndromic hearing loss (Pou4f3, Slc17a8, Tmc1, and Crym) as well as genes important for cochlear function (Emilin-2 and Tectb), gradual expression changes may help to explain the various pathological conditions.

Indexed as

TranscriptomeAnimalsCalcium ChannelsCochleaComputational BiologyDeafnessDisease Models, AnimalGene Expression ProfilingGene Expression RegulationMicemu-CrystallinsOligonucleotide Array Sequence AnalysisPotassium ChannelsReproducibility of ResultsSodium ChannelsCalcium ChannelsCrym protein, mousemu-CrystallinsPotassium ChannelsSodium Channels

Identifiers

PMID24676347
PMCPMC3967995
OpenAlexW2032591048

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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.