Evidence map›Paper›PMID 32605309›Full record

ArticleBiomedicines2020

Identification of Differentially Methylated CpG Sites in Fibroblasts from Keloid Scars.

Mansour A Alghamdi, Hilary J Wallace, Phillip E Melton, Eric K Moses, Andrew Stevenson, Laith N Al-Eitan, Suzanne Rea, Janine M Duke, Patricia L Danielsen, Cecilia M Prêle and 2 more

Abstract read
In one paragraph

Article in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. 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

12 authors.

Mansour A AlghamdiDepartment of Anatomy, College of Medicine, King Khalid University, Abha 61421, Saudi Arabia.
Hilary J WallaceSchool of Medicine, the University of Notre Dame Australia, Fremantle 6959, Australia.
Phillip E MeltonCentre for Genetic Origins of Health and Disease, Faculty of Health and Medical Sciences, the University of Western Australia, Perth 6009, Australia.
Eric K MosesCentre for Genetic Origins of Health and Disease, Faculty of Health and Medical Sciences, the University of Western Australia, Perth 6009, Australia.
Andrew StevensonBurn Injury Research Unit, School of Biomedical Sciences, Faculty of Health and Medical Sciences, the University of Western Australia, Perth 6009, Australia.
Laith N Al-EitanDepartment of Applied Biological Sciences, Jordan University of Science and Technology, Irbid 22110, Jordan.
Suzanne ReaBurns Service of Western Australia, Perth Children's Hospital and Fiona Stanley Hospital, Department of Health, Perth 6009, Australia.
Janine M DukeBurn Injury Research Unit, School of Biomedical Sciences, Faculty of Health and Medical Sciences, the University of Western Australia, Perth 6009, Australia.
Patricia L DanielsenDepartment of Dermatology and Copenhagen Wound Healing Center, Copenhagen University Hospital, DK-2400 Copenhagen NV, Denmark.
Cecilia M PrêleInstitute for Respiratory Health, Faculty of Health and Medical Sciences, the University of Western Australia, Perth 6009, Australia.
Fiona M WoodBurn Injury Research Unit, School of Biomedical Sciences, Faculty of Health and Medical Sciences, the University of Western Australia, Perth 6009, Australia.
Mark W FearBurn Injury Research Unit, School of Biomedical Sciences, Faculty of Health and Medical Sciences, the University of Western Australia, Perth 6009, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a part of an abnormal healing process of dermal injuries and irritation, keloid scars arise on the skin as benign fibroproliferative tumors. Although the etiology of keloid scarring remains unsettled, considerable recent evidence suggested that keloidogenesis may be driven by epigenetic changes, particularly, DNA methylation. Therefore, genome-wide scanning of methylated cytosine-phosphoguanine (CpG) sites in extracted DNA from 12 keloid scar fibroblasts (KF) and 12 control skin fibroblasts (CF) (six normal skin fibroblasts and six normotrophic fibroblasts) was conducted using the Illumina Human Methylation 450K BeadChip in two replicates for each sample. Comparing KF and CF used a Linear Models for Microarray Data (Limma) model revealed 100,000 differentially methylated (DM) CpG sites, 20,695 of which were found to be hypomethylated and 79,305 were hypermethylated. The top DM CpG sites were associated with

Indexed as

DNA methylationepigeneticskeloid scarswound healing

Identifiers

PMID32605309
PMCPMC7400180

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.