Evidence map›Paper›PMID 28240738›Full record

ArticleScientific reports2017

Inflammation-induced miRNA-155 inhibits self-renewal of neural stem cells via suppression of CCAAT/enhancer binding protein β (C/EBPβ) expression.

Kayoko Obora, Yuta Onodera, Toshiyuki Takehara, John Frampton, Joe Hasei, Toshifumi Ozaki, Takeshi Teramura, Kanji Fukuda

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  5. Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025
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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 2 countries.

Kayoko OboraDepartment of Rehabilitation Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Yuta OnoderaDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Toshiyuki TakeharaDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
John FramptonSchool of Biomedical Engineering, Dalhousie University. Halifax, Nova Scotia, Canada.
Joe HaseiScience of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Toshifumi OzakiScience of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Takeshi TeramuraDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Kanji FukudaDepartment of Rehabilitation Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Kindai University · JPOkayama University · JPDalhousie University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracerebral inflammation resulting from injury or disease is implicated in disruption of neural regeneration and may lead to irreversible neuronal dysfunction. Analysis of inflammation-related microRNA profiles in various tissues, including the brain, has identified miR-155 among the most prominent miRNAs linked to inflammation. Here, we hypothesize that miR-155 mediates inflammation-induced suppression of neural stem cell (NSC) self-renewal. Using primary mouse NSCs and human NSCs derived from induced pluripotent stem (iPS) cells, we demonstrate that three important genes involved in NSC self-renewal (Msi1, Hes1 and Bmi1) are suppressed by miR-155. We also demonstrate that suppression of self-renewal genes is mediated by the common transcription factor C/EBPβ, which is a direct target of miR-155. Our study describes an axis linking inflammation and miR-155 to expression of genes related to NSC self-renewal, suggesting that regulation of miR-155 may hold potential as a novel therapeutic strategy for treating neuroinflammatory diseases.

Indexed as

Gene Expression RegulationRNA InterferenceAnimalsBiomarkersCCAAT-Enhancer-Binding Protein-betaCell Self RenewalHumansInflammationInterleukin-1betaMiceMicroRNAsNerve Tissue ProteinsNeural Stem CellsRNA-Binding ProteinsTranscription Factor HES-1BiomarkersCCAAT-Enhancer-Binding Protein-betaHES1 protein, humanInterleukin-1betaMicroRNAsMIRN155 microRNA, humanMirn155 microRNA, mouseMSI1 protein, humanNerve Tissue ProteinsRNA-Binding ProteinsTranscription Factor HES-1

Identifiers

PMID28240738
PMCPMC5378916
OpenAlexW2594135991

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.