Evidence map›Paper›PMID 35562622›Full record

ArticleClinical rheumatology2022

Exploration of the pathogenesis of Sjögren's syndrome via DNA methylation and transcriptome analyses.

Yu Du, Jie Li, Jianhong Wu, Fanxin Zeng, Chengsong He

Abstract read
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In one paragraph

Article in Clinical rheumatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Yu DuDepartment of Rheumatology and Immunology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Jie LiDepartment of Clinical Research Center, Dazhou Central Hospital, Dazhou, China.
Jianhong WuDepartment of Rheumatology and Immunology, Dazhou Central Hospital, Dazhou, China.
Fanxin ZengDepartment of Clinical Research Center, Dazhou Central Hospital, Dazhou, China.
Chengsong HeDepartment of Rheumatology and Immunology, The Affiliated Hospital of Southwest Medical University, Luzhou, China. hcs0878@163.com.ORCID http://orcid.org/0000-0003-4984-8814
Dazhou Central Hospital · CNAffiliated Hospital of Southwest Medical University · CN

Funding

Sichuan Science and Technology and Luzhou Municipal people's Government and Luzhou Medical College Joint Scientific Research Special Fund [2014]1074
6 · The paper itself

Abstract

objectivesSjögren's syndrome (SS), a systemic autoimmune disorder, is characterized by dry mouth and eyes. However, SS pathogenesis is poorly understood. We performed bioinformatics analysis to investigate the potential targets and molecular pathogenesis of SS.

methodsGene expression profiles (GSE157159) and methylation data (GSE110007) associated with SS patients were obtained from the Gene Expression Omnibus (GEO) database. Differentially methylated positions (DMPs) and differentially expressed genes (DEGs) were identified by the R package limma. The potential biological functions of DEGs were determined using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Key DMPs were selected by overlap and the shrunken centroid algorithm, and corresponding genes were identified as hub genes, with their diagnostic value assessed by receiver operating characteristic (ROC) curves. The potential molecular mechanisms of hub genes were analyzed by protein-protein interaction (PPI) networks and single-gene gene set enrichment analysis (GSEA). Peripheral blood mononuclear cells (PBMCs) were collected from control and SS patients at The Affiliated Hospital of Southwest Medical University and Dazhou Central Hospital. The mRNA levels of hub genes were verified by quantitative real-time polymerase chain reaction (qRT-PCR).

resultsWe identified 788 DMPs and 2457 DEGs between the two groups. Functional enrichment analysis suggested that the DEGs were significantly enriched in T cell activation, leukocyte cell-cell adhesion, and cytokine-cytokine receptor interaction. TSS200, TSS1500, and 1stExon were identified as highly enriched areas of differentially methylated promoter CpG islands (DMCIs). In total, 61 differentially methylated genes (DMGs) were identified by the overlap of 2457 DEGs and 507 genes related to DMPs (DMPGs), of which 21 genes located near TSS200, TSS1500, and 1stExon were selected. Then, three key DMPs and the corresponding hub genes (RUNX3, HLA-DPA1, and CD6) were screened by the shrunken centroid algorithm and calculated to have areas under the ROC curve of 1.000, 0.931, and 0.986, respectively, indicating good diagnostic value. The GSEA results suggested that all three hub genes were highly associated with the immune response. Finally, positive mRNA expression of the three hub genes in clinical SS samples was verified by qRT-PCR, consistent with the GSE157159 data.

conclusionsThe identification of three hub genes provides novel insight into molecular mechanisms and therapeutic targets for SS. Key Points • Hub genes were screened by DNA methylation and transcriptome analyses. • The relative expression of hub genes in peripheral blood samples was verified by qRT-PCR. • HLA-DPA1 was correlated with the pathogenic mechanism of SS.

Indexed as

DNA MethylationSjogren's SyndromeComputational BiologyGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansLeukocytes, MononuclearRNA, MessengerTranscriptomeRNA, MessengerBioinformaticsDNA methylationHub genesSjögren’s syndrome (SS)

Identifiers

PMID35562622
OpenAlexW4280522171

What OpenQuestion holds

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Registered trials

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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.