DNA methylation in osteoarthritis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA730429 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Illumina Infinium Epic Human DNA Methylation Beadchip V1.2.8 The Illumina Infinium Epic Human DNA Methylation Beadchip V1.2.8 is used to obtain DNA methylation profiles of about 850k CpG in osteoarthritis and normal cells to find differences, approximately 850k CpGs in osteoarthritis and normal cell
2021-05-18 | GSE174525 | GEO
Project description:Osteoarthritis (OA) is a chronic disease of the joint characterized by a progressive degradation of articular cartilage and subchondral bone. In healthy tissue, specialized cells called chondrocytes are regulating a balanced cartilage catabolism and anabolism. By contrast osteoarthritic joints are characterized by a dramatic increase of cartilage catabolism, due to changes of gene expression patterns within chondrocytes. To identify potential epigenetic differences regulating this process a genome-wide methylation screening of paired unaffected and osteoarthritic knee cartilage samples was performed. Therefore samples of macroscopic arthritic and non-arthritic cartilage areas of the femoral condyle of five female patients were collected and DNA isolation was performed. For being able to investigate methylation changes on a genome-wide scale using only limited amounts of DNA a specific amplification protocol for mainly methylated DNA has been established, based on combinations of different methylation-sensitive and M-bM-^@M-^Sindependent restriction digestions. The amplified DNA was then labeled and hybridized onto Agilent M-bM-^@M-^\Human Promoter Whole GenomeM-bM-^@M-^] microarrays. A random variance t-test for paired (per patient) samples was performed, identifying 1214 differentially methylated genetic targets between arthritic and non-arthritic samples. The biological relevance of these genes was then further investigated via Gene Ontology (GO) and KEGG pathway analysis. DNA isolated of paired arthritic and non-arthritic knee cartilage samples of five different female osteoarthritis patients (10 samples) was methylation-specifically amplified using combinations of methylation-sensitive and -insensitive restriction enzymes. Amplicons were dye labeled (Cy3) and hybridized onto 2x244k Agilent Human Promoter microarrays.
2014-07-01 | E-GEOD-48422 | biostudies-arrayexpress
Project description:Osteoarthritis (OA) is a chronic disease of the joint characterized by a progressive degradation of articular cartilage and subchondral bone. In healthy tissue, specialized cells called chondrocytes are regulating a balanced cartilage catabolism and anabolism. By contrast osteoarthritic joints are characterized by a dramatic increase of cartilage catabolism, due to changes of gene expression patterns within chondrocytes. To identify potential epigenetic differences regulating this process a genome-wide methylation screening of paired unaffected and osteoarthritic knee cartilage samples was performed. Therefore samples of macroscopic arthritic and non-arthritic cartilage areas of the femoral condyle of five female patients were collected and DNA isolation was performed. For being able to investigate methylation changes on a genome-wide scale using only limited amounts of DNA a specific amplification protocol for mainly methylated DNA has been established, based on combinations of different methylation-sensitive and –independent restriction digestions. The amplified DNA was then labeled and hybridized onto Agilent “Human Promoter Whole Genome” microarrays. A random variance t-test for paired (per patient) samples was performed, identifying 1214 differentially methylated genetic targets between arthritic and non-arthritic samples. The biological relevance of these genes was then further investigated via Gene Ontology (GO) and KEGG pathway analysis.
2014-07-01 | GSE48422 | GEO
Project description:A study of colorectal cancer screening using stool DNA-based SDC2 methylation test
| 2332763 | ecrin-mdr-crc
Project description:Regulation of transcription occurs in a cell type specific manner orchestrated by epigenetic mechanisms including DNA methylation. Methylation changes may also play a key role in lineage specification during stem cell differentiation. To further our understanding of epigenetic regulation in chondrocytes we characterised DNA methylation changes during chondrogenesis of mesenchymal stem cells (MSCs) by Infinium 450K methylation array. Significant DNA hypomethylation was identified during chondrogenesic differentiation including changes at many key cartilage gene loci. Integration with chondrogenesis gene expression data revealed an enrichment of significant CpGs in upregulated genes, while characterisation of significant CpG loci indicated their predominant localisation to enhancer regions. Comparison with methylation profiles of other tissues, including healthy and diseased adult cartilage, identified chondrocyte-specific regions of hypomethylation and the overlap with differentially methylated CpGs in osteoarthritis. Taken together we have associated DNA methylation levels with the chondrocyte phenotype. The consequences of which has potential to improve cartilage generation for tissue engineering purposes and also to provide context for observed methylation changes in cartilage diseases such as osteoarthritis
2019-05-24 | GSE129266 | GEO
Project description:The main goal of the study was to measure the epigenetic age (also known as DNA methylation age) of human bone tissue and to relate it to chronological age. Toward this end, we used the epigenetic clock software described in Horvath S (2013) DNA methylation age of human tissues and cell types. Genome Biology.2013, 14:R115. DOI: 10.1186/10.1186/gb-2013-14-10-r115 PMID: 24138928 Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 486,000 CpGs. The trabecular bone pieces were obtained from the central part of the femoral head of Spanish (Caucasian) patients with hip fractures (due to osteoporosis) or subjects with osteoarthritis. About 85% of the cell population in this bone tissue are osteocytes and the remainder are osteoblasts, bone marrow, etc.
2015-06-03 | E-GEOD-64490 | biostudies-arrayexpress
Project description:We want to determine if there is a difference in the DNA methylation status of liver and Bone marrow in Cbs-/- mice under + or - ZnH20.
2016-01-28 | ST000341 | MetabolomicsWorkbench
Project description:Interventions: Gold Standard:colonoscopy;Index test:Stool DNA methylation biomarkers.
Primary outcome(s): accuracy
Study Design: Diagnostic test for accuracy
| 2680588 | ecrin-mdr-crc
Project description:In mammals, the acquisition of the germline from the soma provides the germline with an essential challenge, the necessity to erase and reset genomic methylation. In the male germline RNA-directed DNA methylation silences young active transposable elements (TEs). The PIWI protein MIWI2 (PIWIL4) and its associated PIWI-interacting RNAs (piRNAs) are proposed to tether MIWI2 to nascent TE transcripts and instruct DNA methylation. The mechanism by which MIWI2 directs de novo TE methylation is poorly understood but central to the immortality of the germline. Here, we define the interactome of MIWI2 in foetal gonocytes that are undergoing de novo genome methylation and identify a novel MIWI2-associated factor, SPOCD1, that is essential for young TE methylation and silencing. The loss of Spocd1 in mice results in male specific infertility and does not impact on piRNA biogenesis nor localization of MIWI2 to the nucleus. SPOCD1 is a nuclear protein and its expression is restricted to the period of de novo genome methylation. We found SPOCD1 co-purified in vivo with DNMT3L and DNMT3A, components of the de novo methylation machinery as well as constituents of the NURD and BAF chromatin remodelling complexes. We propose a model whereby tethering of MIWI2 to a nascent TE transcript recruits repressive chromatin remodelling activities and the de novo methylation apparatus through its association with SPOCD1. In summary, we have identified a novel and essential executor of mammalian piRNA-directed DNA methylation.
2020-06-22 | PXD016701 | Pride