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Genome-wide DNA methylation profiling of multiple sclerosis patients in relapse [CD14]

ABSTRACT: Multiple sclerosis (MS) is a chronic autoimmune and degenerative disease of the central nervous system, which develops in genetically predisposed individuals upon exposure to environmental influences. Environmental triggers of MS, such as viral infections or smoking, were demonstrated to affect DNA methylation, and thus to involve this important epigenetic mechanism in the development of pathological processes. To identify DNA methylation hallmarks, associated with relapse of MS, we performed genome-wide DNA methylation profiling of two cell populations (CD4+ T-lymphocytes and CD14+ monocytes), collected from the same individuals, using Illumina 450K methylation arrays. We revealed changes in DNA methylation for both cell populations of MS patients in relapse when compared wih remission. In CD4+ cells the absolute majority of differentially methylated positions (DMPs) were hypermethylated. In CD4+, but not in CD14+ cells, we found a differentially methylated region within the GNAS complex locus and showed significant differences in the ammount of its transcripts between patients in relapse and remission.

ORGANISM(S): Homo sapiens

PROVIDER: GSE261977 | GEO | 2025/01/01

REPOSITORIES: GEO

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Genome-wide DNA methylation profiling of multiple sclerosis patients in relapse [CD4]

Project description:Multiple sclerosis (MS) is a chronic autoimmune and degenerative disease of the central nervous system, which develops in genetically predisposed individuals upon exposure to environmental influences. Environmental triggers of MS, such as viral infections or smoking, were demonstrated to affect DNA methylation, and thus to involve this important epigenetic mechanism in the development of pathological processes. To identify DNA methylation hallmarks, associated with relapse of MS, we performed genome-wide DNA methylation profiling of two cell populations (CD4+ T-lymphocytes and CD14+ monocytes), collected from the same individuals, using Illumina 450K methylation arrays. We revealed changes in DNA methylation for both cell populations of MS patients in relapse when compared wih remission. In CD4+ cells the absolute majority of differentially methylated positions (DMPs) were hypermethylated. In CD4+, but not in CD14+ cells, we found a differentially methylated region within the GNAS complex locus and showed significant differences in the ammount of its transcripts between patients in relapse and remission.

2025-01-01 | GSE262734 | GEO

Genome-wide DNA methylation profiling identifies epigenetic changes in CD4+ and CD14+ cells of multiple sclerosis patients [CD4]

Project description:Multiple sclerosis (MS) is a chronic autoimmune and degenerative disease of the central nervous system, which develops in genetically predisposed individuals upon exposure to environmental influences. Environmental triggers of MS, such as viral infections or smoking, were demonstrated to affect DNA methylation, and thus to involve this important epigenetic mechanism in the development of pathological processes. To identify DNA methylation hallmarks, associated with MS, we performed genome-wide DNA methylation profiling of two cell populations (CD4+ T-lymphocytes and CD14+ monocytes), collected from the same individuals (relapsing-remitting MS patients and healthy subjects), using Illumina 450K methylation arrays. We revealed significant changes in DNA methylation for both cell populations of studied groups. In CD4+ cells the majority of differentially methylated positions (DMPs) were shown to be hypomethylated, while in CD14+ cells – hypermethylated in MS patients. Noteworthy, in CD4+, but not in CD14+ cells, we found differential methylation of HLA-DRB6 gene from HLA locus, which is known to have the strongest genetic association with MS. Besides, about 20% of DMPs identified in studied cells were identical; they all had the same direction of methylation changes in both cell populations and may be involved in basic epigenetic processes occuring in MS. These findings suggest that the epigenetic mechanism of DNA methylation in immune cells contributes to MS; further studies are now required to validate these results and understand their functional significance.

2022-02-28 | GSE189255 | GEO

Genome-wide DNA methylation profiling identifies epigenetic changes in CD4+ and CD14+ cells of multiple sclerosis patients [CD14]

Project description:Multiple sclerosis (MS) is a chronic autoimmune and degenerative disease of the central nervous system, which develops in genetically predisposed individuals upon exposure to environmental influences. Environmental triggers of MS, such as viral infections or smoking, were demonstrated to affect DNA methylation, and thus to involve this important epigenetic mechanism in the development of pathological processes. To identify DNA methylation hallmarks, associated with MS, we performed genome-wide DNA methylation profiling of two cell populations (CD4+ T-lymphocytes and CD14+ monocytes), collected from the same individuals (relapsing-remitting MS patients and healthy subjects), using Illumina 450K methylation arrays. We revealed significant changes in DNA methylation for both cell populations of studied groups. In CD4+ cells the majority of differentially methylated positions (DMPs) were shown to be hypomethylated, while in CD14+ cells – hypermethylated in MS patients. Noteworthy, in CD4+, but not in CD14+ cells, we found differential methylation of HLA-DRB6 gene from HLA locus, which is known to have the strongest genetic association with MS. Besides, about 20% of DMPs identified in studied cells were identical; they all had the same direction of methylation changes in both cell populations and may be involved in basic epigenetic processes occuring in MS. These findings suggest that the epigenetic mechanism of DNA methylation in immune cells contributes to MS; further studies are now required to validate these results and understand their functional significance.

2022-02-28 | GSE189256 | GEO

Small nucleolar RNA and microRNA expression data from multiple sclerosis patients in relapse and remission.

Project description:Multiple sclerosis is a common inflammatory and degenerative disease that causes neurological disability. It affects young adults and its prevalence is higher in women. The most common form is manifested as a series of acute episodes of neurological disability (relapses) followed by a recovery phase (remission). Recently, non-coding RNAs have emerged as new players in transcriptome regulation, and in turn, they could have a significant role in MS pathogenesis. In this context, our aim was to investigate the involvement of microRNAs and snoRNAs in the relapse-remission dynamics of MS in peripheral blood leucocytes, to shed light on the molecular and regulatory mechanisms that underlie this complex process. With this approach, we found that a subset of small non-coding RNAs (sncRNA) is altered in relapse and remission, revealing unexpected opposite changes that are sex dependent. Furthermore, we found that a relapse-related miRNA signature regulated general metabolism processes in leucocytes, and miRNA altered in remission are involved in the regulation of innate immunity. We observed that sncRNA dysregulation is different in relapse and remission leading to differences in transcriptome regulation, and that this process is sex dependent. In conclusion, relapse and remission have a different molecular background in men and women. 24 multiple sclerosis patients with samples both in remission and relapse (2 samples for each patient; 48 blood samples in total) and 24 healthy controls were included in the study, for a total of 72 samples.

2015-11-03 | E-GEOD-74579 | biostudies-arrayexpress

Combining evidence from four immune cell types identifies DNA methylation patterns that implicate functionally distinct pathways during Multiple Sclerosis progression (CD8+ T cells)

Project description:Background Multiple Sclerosis (MS) is a chronic inflammatory disease and a leading cause of progressive neurological disability among young adults. DNA methylation, which intersects genes and environment to control cellular functions on a molecular level, may provide insights into MS pathogenesis. Methods We measured DNA methylation in CD4+ T cells (n=31), CD8+ T cells (n=28), CD14+ monocytes (n=35) and CD19+ B cells (n=27) from relapsing-remitting (RRMS), secondary progressive (SPMS) patients and healthy controls (HC) using Infinium HumanMethylation450 arrays. Monocyte (n=25) and whole blood (n=275) cohorts were used for validations. Findings B cells from MS patients displayed most significant differentially methylated positions (DMPs), followed by monocytes, while only few DMPs were detected in T cells. We implemented a non-parametric combination framework (omicsNPC) to increase discovery power by combining evidence from all four cell types. Identified shared DMPs co-localized at MS risk loci and clustered into distinct groups. Functional exploration of changes discriminating RRMS and SPMS from HC implicated lymphocyte signaling, T cell activation and migration. SPMS-specific changes, on the other hand, implicated myeloid cell functions and metabolism. Interestingly, neuronal and neurodegenerative genes and pathways were also specifically enriched in the SPMS cluster. Interpretation We utilized a statistical framework (omicsNPC) that combines multiple layers of evidence to identify DNA methylation changes that provide new insights into MS pathogenesis in general, and disease progression, in particular.

2019-06-01 | GSE130030 | GEO

Combining evidence from four immune cell types identifies DNA methylation patterns that implicate functionally distinct pathways during Multiple Sclerosis progression (CD4+ T cells)

2019-06-01 | GSE130029 | GEO

Small nucleolar RNA and microRNA expression data from an MS patient's and a healthy control's PBMC cultures stimulated with phytohemagglutinin.

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Small nucleolar RNA and microRNA expression data from multiple sclerosis patients in relapse and remission.

2015-11-03 | GSE74579 | GEO

Genome-wide methylation analysis of an Acute Myeloid Leukemia (AML) case with complex mutational DNMT3A profile.

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2022-05-10 | GSE202488 | GEO

Epigenomic Evolution of Diffuse Large B-cell Relapse

Project description:Here we characterize an association between disease progression and DNA methylation in Diffuse Large B cell Lymphoma (DLBCL). By profiling genome-wide DNA methylation at single base-pair resolution in thirteen DLBCL diagnosis-relapse sample pairs, we show DLBCL patients exhibit heterogeneous evolution of tumor methylomes during relapse. We identify differentially methylated regulatory elements and determine a relapse–associated methylation signature converging on key pathways such as transforming growth factor beta (TGF-beta) receptor activity. We also observe decreased intra-tumor methylation heterogeneity from diagnosis to relapsed tumor samples. Relapse-free patients display lower intra-tumor methylation heterogeneity at diagnosis compared to relapsed patients in an independent validation cohort. Furthermore, intra-tumor methylation heterogeneity is predictive of time to relapse. Therefore, we propose that epigenomic heterogeneity may support or drive the relapse phenotype and can be used to predict DLBCL relapse. Using ERRBS, we profiled genome-wide DNA methylation patterns of non-relapse DLBCL tumor samples at diagnosis, relaspe DLBCL patient samples at diagnosis and relaspe.

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