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Series GSE111183 Query DataSets for GSE111183
Status Public on Jul 23, 2018
Title Identification of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome-associated DNA methylation patterns
Organism Homo sapiens
Experiment type Methylation profiling by array
Summary Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex condition that involves multiple organ systems and is characterized by an abrupt or delayed onset of persistent/relapsing symptomatology such as debilitating fatigue, immune dysfunction, neurological problems, and other symptoms not curable for at least 6 months. Disruption of DNA methylation patterns has been tied to various immune and neurological diseases; however, the status of this epigenetic mark in ME/CFS remains uncertain. This study aimed at identifying changes in the DNA methylation patterns that are causative of changes in the regulation of gene expression in ME/CSF patients. Such changes may be also used for diagnostic purposes and be indicative of potential therapeutic targets.
Methods: Peripheral blood mononuclear cells (PBMCs) from 13 ME/CFS patients and 12 healthy controls (HC) were used to extract genomic DNA and measure global DNA methylation, and the methylation status at 850,000 CpG sites was assessed using Illumina MethylationEPIC microarrays.
Results: Global DNA methylation levels of ME/CFS patients were similar to those of HC. However, microarray-based genome-wide technology allowed detection of 17,296 differentially methylated CpG sites in 6,368 genes across promoters, gene regulatory elements and within coding regions of genes. Analysis of DNA methylation in promoter regions found 307 differentially methylated promoters (DMP); genes associated with DMP participate in at least 15 different pathways mostly related to cell signaling with a strong immune component.
Conclusions: This is the first study that has explored genome-wide epigenetic changes associated with ME/CFS using the new MethylationEPIC microarrays covering about 850,000 CpG sites. Our results are consistent with dysregulation of the immune system in ME/CFS and suggest a role of this epigenetic modification on the DNA pathobiology of ME/CFS.
 
Overall design Genomic DNA from 25 peripheral blood mononuclear cells (PBMC) samples (13 ME/CFS, 12 controls) were bisulfite-converted and hybridised to the Illumina MethylationEPIC microarrays. GenomeStudio idat files were generated and the data was analyzed using the RnBeads R package.
 
Contributor(s) Trivedi MS, Oltra E, Sarria L, Rose N, Beljanski V, Fletcher MA, Klimas NG, Nathanson L
Citation(s) 30036399
NIH grant(s)
Grant ID Grant title Affiliation Name
R15 NS087604 Genomic approach to find novel biomarkers and mechanisms of CFS/ME NOVA SOUTHEASTERN UNIVERSITY Lubov Nathanson
Submission date Feb 27, 2018
Last update date Jan 20, 2019
Contact name Lubov Nathanson
E-mail(s) lnathanson@nova.edu
Organization name Nova Southeastern University
Department INIM
Street address 3321 College Ave.
City Fort Lauderdale
State/province Florida
ZIP/Postal code 33314
Country USA
 
Platforms (1)
GPL21145 Infinium MethylationEPIC
Samples (25)
GSM3024927 PBMC genomic DNA ME/CFS 1
GSM3024928 PBMC genomic DNA Healthy Control (HC) 1
GSM3024929 PBMC genomic DNA ME/CFS 2
Relations
BioProject PRJNA436126

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE111183_RAW.tar 161.2 Mb (http)(custom) TAR
GSE111183_signal_intensities.txt.gz 102.5 Mb (ftp)(http) TXT
Processed data included within Sample table

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