Evidence map›Paper›PMID 28798331›Full record

ArticleScientific reports2017

MicroRNA-132 promotes fibroblast migration via regulating RAS p21 protein activator 1 in skin wound healing.

Xi Li, Dongqing Li, Jakob D Wikstrom, Andor Pivarcsi, Enikö Sonkoly, Mona Ståhle, Ning Xu Landén

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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Highly expressed TRIM32 promoted traumatic wound healing by mediating ubiquitination of PIAS1.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  2. Article
  3. Review
  4. Article
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  6. Review
  7. Role of Transcription Factors and MicroRNAs in Regulating Fibroblast Reprogramming in Wound Healing.Journal of bioinformatics and systems biology : Open access · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Beyond the Code: Noncoding RNAs in Skin Wound Healing.Cold Spring Harbor perspectives in biology · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
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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

7 authors at 2 institutions in 1 country.

Xi LiUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Dongqing LiUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Jakob D WikstromUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Andor PivarcsiUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Enikö SonkolyUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Mona StåhleUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Ning Xu LandénUnit of Dermatology and Venereology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. ning.xu@ki.se.
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA (miR)-132 has been identified as a top up-regulated miRNA during skin wound healing and its inhibition impairs wound repair. In a human in vivo surgical wound model, we showed that miR-132 was induced in epidermal as well as in dermal wound-edge compartments during healing. Moreover, in a panel of cells isolated from human skin wounds, miR-132 was found highly expressed in human dermal fibroblasts (HDFs). In HDFs, miR-132 expression was upregulated by TGF-β1. By overexpression or inhibition of miR-132, we showed that miR-132 promoted HDF migration. Mechanistically, global transcriptome analysis revealed that RAS signaling pathway was regulated by miR-132 in HDFs. We found that RAS p21 protein activator 1 (RASA1), a known target of miR-132, was downregulated in HDFs upon miR-132 overexpression. Silencing of RASA1 phenocopied the pro-migratory effect of miR-132. Collectively, our study reveals an important role for miR-132 in HDFs during wound healing and indicates a therapeutic potential of miR-132 in hard-to-heal skin wounds.

Indexed as

Cell MovementCells, CulturedDown-RegulationFibroblastsGene Expression ProfilingHumansMicroRNAsOligonucleotide Array Sequence Analysisp120 GTPase Activating ProteinSignal TransductionSurgical WoundTransforming Growth Factor beta1Up-RegulationWound HealingMicroRNAsMIRN132 microRNA, humanp120 GTPase Activating ProteinRASA1 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID28798331
PMCPMC5552762
OpenAlexW2742884469

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.