Evidence map›Paper›PMID 28967703›Full record

ArticleAging cell2017

miR-155 induces ROS generation through downregulation of antioxidation-related genes in mesenchymal stem cells.

Yuta Onodera, Takeshi Teramura, Toshiyuki Takehara, Kayoko Obora, Tatsufumi Mori, Kanji Fukuda

Abstract read
In one paragraph

Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Connecting the Dots: How MicroRNAs Link Asthma and Atherosclerosis.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Effects of saponins RbFrontiers in molecular biosciences · 2024
    Article
  9. Article
  10. Article
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  12. Article
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  14. Review
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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.

Yuta OnoderaDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Takeshi TeramuraDivision 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.
Kayoko OboraDepartment of Rehabilitation Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Tatsufumi MoriKindai University Life Science Research Institute, Osaka, Japan.
Kanji FukudaDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation-induced reactive oxygen species (ROS) are implicated in cellular dysfunction and an important trigger for aging- or disease-related tissue degeneration. Inflammation-induced ROS in stem cells lead to deterioration of their properties, altering tissue renewal or regeneration. Pathological ROS generation can be induced by multiple steps, and dysfunction of antioxidant systems is a major cause. The identification of the central molecule mediating the above-mentioned processes would pave the way for the development of novel therapeutics for aging, aging-related diseases, or stem cell therapies. In recent years, microRNAs (miRNAs) have been shown to play important roles in many biological reactions, including inflammation and stem cell functions. In inflammatory conditions, certain miRNAs are highly expressed and mediate some cytotoxic actions. Here, we focused on miR-155, which is one of the most prominent miRNAs in inflammation and hypothesized that miR-155 participates to inflammation-induced ROS generation in stem cells. We observed mesenchymal stem cells (MSCs) from 1.5-year-old aged mice and determined that antioxidants, Nfe2l2, Sod1, and Hmox1, were suppressed, while miR-155-5p was highly expressed. Subsequent in vitro studies demonstrated that miR-155-5p induces ROS generation by suppression of the antioxidant genes by targeting the common transcription factor C/ebpβ. Moreover, this mechanism occurred during the cell transplantation process, in which ROS generation is triggering loss of transplanted stem cells. Finally, attenuation of antioxidants and ROS accumulation were partially prevented in miR-155 knockout MSCs. In conclusion, our study suggests that miR-155 is an important mediator connecting aging, inflammation, and ROS generation in stem cells.

Indexed as

Age FactorsAnimalsCells, CulturedDown-RegulationGene Knockout TechniquesHeme Oxygenase-1HumansMembrane ProteinsMesenchymal Stem CellsMiceMice, Inbred C57BLMicroRNAsNF-E2-Related Factor 2Oxidation-ReductionReactive Oxygen SpeciesSuperoxide Dismutase-1Heme Oxygenase-1HMOX1 protein, humanHmox1 protein, mouseMembrane ProteinsMicroRNAsMIRN155 microRNA, humanMirn155 microRNA, mouseNF-E2-Related Factor 2Reactive Oxygen SpeciesSuperoxide Dismutase-1aginginflammationmesenchymal stem cellsmicroRNAstem cellssuperoxide

Identifiers

PMID28967703
PMCPMC5676067

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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.