Evidence map›Paper›PMID 31019085›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Human skin long noncoding RNA WAKMAR1 regulates wound healing by enhancing keratinocyte migration.

Dongqing Li, Lara Kular, Manika Vij, Eva K Herter, Xi Li, Aoxue Wang, Tongbin Chu, Maria-Alexandra Toma, Letian Zhang, Eleni Liapi and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

21 authors at 6 institutions in 2 countries.

Dongqing LiDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Lara KularDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Manika VijDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Eva K HerterDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Xi LiDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Aoxue WangDepartment of Dermatology, The Second Hospital of Dalian Medical University, 116023 Dalian, China.
Tongbin ChuDepartment of Wound Repair, The Second Hospital of Dalian Medical University, 116023 Dalian, China.
Maria-Alexandra TomaDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Letian ZhangDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Eleni LiapiDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Ana MotaScience for Life Laboratory, Department of Medical Biochemistry and Biophysics, Karolinska Institute, 17165 Stockholm, Sweden.
Lennart BlomqvistDepartment of Medicine Huddinge, Karolinska Institute, 14186 Stockholm, Sweden.
Irène Gallais SérézalDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Ola RollmanDepartment of Dermatology, Academic University Hospital, 75185 Uppsala, Sweden.
Jakob D WikstromDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Magda BienkoScience for Life Laboratory, Department of Medical Biochemistry and Biophysics, Karolinska Institute, 17165 Stockholm, Sweden.
David BerglundSection of Clinical Immunology, Department of Immunology, Genetics and Pathology, Uppsala University, 75105 Uppsala, Sweden.
Mona StåhleDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Pehr SommarDepartment of Reconstructive Plastic Surgery, Karolinska University Hospital, 17176 Stockholm, Sweden.
Maja JagodicDepartment of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden.
Ning Xu LandénDermatology and Venereology Division, Department of Medicine (Solna), Center for Molecular Medicine, Karolinska Institute, 17176 Stockholm, Sweden; ning.xu@ki.se.ORCID 0000-0003-4868-3798
Karolinska Institutet · SEKarolinska University Hospital · SEDalian Medical University · CNScience for Life Laboratory · SEUppsala University · SEUppsala University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increasing number of studies reveal the importance of long noncoding RNAs (lncRNAs) in gene expression control underlying many physiological and pathological processes. However, their role in skin wound healing remains poorly understood. Our study focused on a skin-specific lncRNA, LOC105372576, whose expression was increased during physiological wound healing. In human nonhealing wounds, however, its level was significantly lower compared with normal wounds under reepithelialization. We characterized LOC105372576 as a nuclear-localized, RNAPII-transcribed, and polyadenylated lncRNA. In keratinocytes, its expression was induced by TGF-β signaling. Knockdown of LOC105372576 and activation of its endogenous transcription, respectively, reduced and increased the motility of keratinocytes and reepithelialization of human ex vivo skin wounds. Therefore, LOC105372576 was termed "wound and keratinocyte migration-associated lncRNA 1" (WAKMAR1). Further study revealed that WAKMAR1 regulated a network of protein-coding genes important for cell migration, most of which were under the control of transcription factor E2F1. Mechanistically, WAKMAR1 enhanced E2F1 expression by interfering with E2F1 promoter methylation through the sequestration of DNA methyltransferases. Collectively, we have identified a lncRNA important for keratinocyte migration, whose deficiency may be involved in the pathogenesis of chronic wounds.

Indexed as

Cell MovementSignal TransductionWound HealingChronic DiseaseE2F1 Transcription FactorGene Expression RegulationHumansKeratinocytesRNA, Long NoncodingSkinTransforming Growth Factor betaWounds and InjuriesE2F1 protein, humanE2F1 Transcription FactorRNA, Long NoncodingTransforming Growth Factor betakeratinocyte migrationlong noncoding RNAwound healing

Identifiers

PMID31019085
PMCPMC6511036
OpenAlexW2940660074

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.