Evidence map›Paper›PMID 30382880›Full record

ArticleClinical epigenetics2018

Multiomics analyses identified epigenetic modulation of the S100A gene family in Kawasaki disease and their significant involvement in neutrophil transendothelial migration.

Lien-Hung Huang, Ho-Chang Kuo, Cheng-Tsung Pan, Yeong-Shin Lin, Ying-Hsien Huang, Sung-Chou Li

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Analysis of the Transcriptional Control ofAnimals : an open access journal from MDPI · 2025
    Article
  4. Review
  5. Article
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  11. Article
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  13. Article
  14. Article
  15. Long-Term Hypermethylation ofJournal of clinical medicine · 2021
    Article
  16. DNA Methylation inChildren (Basel, Switzerland) · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Epigenetics in Kawasaki Disease.Frontiers in pediatrics · 2021
    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

6 authors at 3 institutions in 1 country.

Lien-Hung HuangGenomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital, 12th Floor, Children's Hospital, No.123, Dapi Rd, Niaosong District, Kaohsiung, 83301, Taiwan.
Ho-Chang KuoDepartment of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Cheng-Tsung PanInstitute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsinchu, Taiwan.
Yeong-Shin LinInstitute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsinchu, Taiwan.
Ying-Hsien HuangDepartment of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Sung-Chou LiGenomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital, 12th Floor, Children's Hospital, No.123, Dapi Rd, Niaosong District, Kaohsiung, 83301, Taiwan. raymond.pinus@gmail.com.ORCID 0000-0002-3016-9718
Chang Gung University · TWKaohsiung Chang Gung Memorial Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

Ministry of Science and Technology, Taiwan 106-2311-B-182A-002
6 · The paper itself

Abstract

backgroundKawasaki disease (KD) is a prevalent pediatric disease worldwide and can cause coronary artery aneurysm as a severe complication. Typically, DNA methylation is thought to repress the expression of nearby genes. However, the cases in which DNA methylation promotes gene expression have been reported. In addition, globally, to what extent DNA methylation affects gene expression and how it contributes to the pathogenesis of KD are not yet well understood.

methodsTo address these important biological questions, we enrolled subjects, collected DNA and RNA samples from the subjects' total white blood cells, and performed DNA methylation (M450K) and gene expression (HTA 2.0) microarray assays.

resultsBy analyzing the variation ratios of CpG beta values (methylation percentage) and gene expression intensities, we first concluded that the CpG markers close (- 1500 bp to + 500 bp) to the transcription start sites had higher variation ratios, reflecting significant regulation capacities. Next, we observed that, globally speaking, gene expression was modestly negatively correlated (correlation rho ≈ - 0.2) with the DNA methylation status of both upstream and downstream CpG markers in the promoter region. Third, we found that specific CpG markers were hypo-methylated in disease samples compared with healthy samples and hyper-methylated in convalescent samples compared with disease samples, promoting and repressing S100A genes' expressions, respectively. Finally, using an in vitro cell model, we demonstrated that S100A family proteins enhanced leukocyte transendothelial migration in KD.

conclusionsThis is the first study to integrate genome-wide DNA methylation with gene expression assays in KD and showed that the S100A family plays important roles in the pathogenesis of KD.

Indexed as

DNA MethylationCell LineCpG IslandsEpigenesis, GeneticEpigenomicsFemaleGene Expression ProfilingGene Expression RegulationGenome-Wide Association StudyHumansMucocutaneous Lymph Node SyndromePromoter Regions, GeneticS100 ProteinsSequence Analysis, DNATransendothelial and Transepithelial MigrationS100 ProteinsCorrelationCpG markerDNA methylationGene expressionKawasaki diseaseLeukocyte transendothelial migrationS100A gene family

Identifiers

PMID30382880
PMCPMC6211403
OpenAlexW2899223437

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.