Evidence map›Paper›PMID 25685928›Full record

ArticleThe Journal of investigative dermatology2015

MicroRNA-31 Promotes Skin Wound Healing by Enhancing Keratinocyte Proliferation and Migration.

Dongqing Li, X I Li, Aoxue Wang, Florian Meisgen, Andor Pivarcsi, Enikö Sonkoly, Mona Ståhle, Ning Xu Landén

Abstract read
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In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 2 pooled it
16.2field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Time to Heal: MicroRNA Temporal Dysregulation in Diabetic Foot Ulcers.International journal of molecular sciences · 2026
    Review
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  8. Therapeutic Potential of Modulating Gene-MicroRNA Crosstalk in Burn Injury.International journal of molecular sciences · 2025
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28 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Dongqing LiMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
X I LiMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Aoxue WangMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Dermatology, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Florian MeisgenMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Andor PivarcsiMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Enikö SonkolyMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Mona StåhleMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Ning Xu LandénMolecular Dermatology Research Group, Unit of Dermatology and Venereology, Centre for Molecular Medicine (CMM), Department of Medicine, Karolinska Institutet, Stockholm, Sweden. Electronic address: ning.xu@ki.se.
Karolinska Institutet · SEDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wound healing is a basic biological process restoring the integrity of the skin. The role of microRNAs during this process remains largely unexplored. By using an in vivo human skin wound healing model, we show here that the expression of miR-31 is gradually upregulated in wound edge keratinocytes in the inflammatory (1 day after injury) through the proliferative phase (7 days after injury) in comparison with intact skin. In human primary keratinocytes, overexpression of miR-31 promoted cell proliferation and migration, whereas inhibition of miR-31 had the opposite effects. Moreover, we identified epithelial membrane protein 1 (EMP-1) as a direct target of miR-31 in keratinocytes. The expression of EMP-1 in the skin was negatively correlated with the level of miR-31 during wound healing. Silencing of EMP-1 mimicked the effects of overexpression of miR-31 on keratinocyte proliferation and migration, indicating that EMP-1 is a critical target mediating the functions of miR-31 in keratinocytes. Finally, we demonstrated that transforming growth factor-β2, which is highly expressed in skin wounds, upregulated miR-31 expression in keratinocytes. Collectively, we identify miR-31 as a key regulator for promoting keratinocyte proliferation and migration during wound healing.

Indexed as

Cell ProliferationWound HealingAdultBiopsyCell MovementCells, CulturedFemaleGene Expression RegulationGene SilencingHumansInflammationKeratinocytesMaleMicroRNAsMiddle AgedNeoplasm Proteinsepithelial membrane protein-1MicroRNAsMIRN31 microRNA, humanNeoplasm ProteinsReceptors, Cell SurfaceTransforming Growth Factor beta2

Identifiers

PMID25685928
OpenAlexW2002393742

What OpenQuestion holds

Textmetadata
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.