Characterisation of epigenomic changes during chondrogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA529809 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8810700.fastq.gz | Fastqsanger.gz | |||
| SRR8810710.fastq.gz | Fastqsanger.gz | |||
| SRR8810691.fastq.gz | Fastqsanger.gz | |||
| SRR8810701.fastq.gz | Fastqsanger.gz | |||
| SRR8810711.fastq.gz | Fastqsanger.gz |
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Project description:Epigenetic mechanisms are known to regulate gene expression during chondrogenesis. In this study, we have characterised the epigenome during in vitro differentiation of human mesenchymal stem cells (hMSCs) into chondrocytes. Chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) was used to assess a range of N-terminal post-transcriptional modifications (marks) to histone H3 lysines (H3K4me3, H3K4me1, H3K27ac, H3K27me3 and H3K36me3) in both hMSCs and differentiated chondrocytes. Chromatin states were characterised using histone ChIP-seq and cis-regulatory elements were identified in chondrocytes.
2020-03-23 | GSE129031 | GEO
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:Characterisation of DNA methylation during mesenchymal stem cell chondrogenesis
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Project description:Gli1 labels progenitors during chondrogenesis in postnatal mice
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Project description:To reveal the organisation of the cartilage cell chondrocyte genome and identify changes that occur within this organisation during development and due to osteoarthritis (OA). Methods Assay for Transposase -Accessible Chromatin using Sequencing (ATAC-seq) was performed on chondrocytes isolated from 16 patients undergoing total hip replacement because of OA (n=7) or due to a neck of femur fracture (NOF, n=9). ATAC-seq was similarly performed on bone-marrow mesenchymal stem cells (BM-MSC) and differentiated chondrocytes of two donors. DNA sequence reads (av. 50 million/sample) were aligned to human genome Hg38. Peaks were called using MACS2 and differential accessibility identified by DiffBind. Interexperiment comparisons and intersection with published gene expression changes, chondrogenesis ChIP-seq, knee ATAC-seq and human tissue scATAC-seq were performed in Galaxy and R. OA GWAS signal regions were overlapped with our defined chondrocyte ATAC-seq peaks. Results In BM-MSC and derived chondrocytes we mapped 138005 open chromatin regions, of which 20979 and 50699 significantly increased and decreased respectively during cell differentiation. In hip chondrocytes we identified 115295 open chromatin regions, 1383 and 573 were more or less differentially accessible respectively when comparing OA with NOF samples. In both data sets ‘newly accessible regions were enriched at enhancer regions (defined by ChIP-seq). Comparing the data with the ATAC-seq from the single cell ATLAS we identified 11866 open regions exclusive to chondrocytes. Genes associated with these regions were significantly enriched for cartilage-related gene ontology terms. Taking the 420 OA GWAS signals present in the GWAS catalogue, 313 of the OA regions (defined as lead SNP + proxy SNPs with r2 ≥ 0.8) overlapped with a chondrocyte ATAC-seq region. Conclusions Here we have mapped chromatin accessible region changes during chondrogenesis, showing that newly accessible regions are enriched at enhancer regions and positively correlate with gene expression. Open chromatin region changes between OA and NOF cartilage were fewer, and peak differences were subtle. Overall, we have associated OA GWAS loci with accessible regions and defined regions of the genome specific to cartilage and chondrogenesis.
2025-01-01 | GSE270602 | GEO
Project description:Changes in chondrocyte gene expression can contribute to the development of osteoarthritis (OA), and so recognition of the regulative processes during chondrogenesis can lead to a better understanding of OA. microRNAs (miRNAs) are key regulators of gene expression in chondrocytes/OA and we have used a combined experimental, bioinformatic, and systems biology approach to explore the multiple miRNA-mRNA interactions that regulate chondrogenesis. A longitudinal chondrogenesis bioinformatic analysis identified paralogues miR-199a-5p and miR-199b-5p as pro-chondrogenic regulators. Experimental work demonstrated alteration of miR-199a-5p or miR-199b-5p expression led to significant inverse modulation of key chondrogenic genes and extracellular matrix production. miR-199a/b-5p targetsFZD6, ITGA3andCAV1were identified by inhibition experiments and verified as direct targets by luciferase assay. The experimental work was used to generate and parameterize a multi-miRNA 14-day chondrogenesis kinetic model to be used as a repository for the experimental work and as a resource for further investigation of this system. This is the first multi-miRNA model of a chondrogenesis-based system, and highlights the complex relationships between regulatory miRNAs, and their target mRNAs.
2024-08-09 | GSE274379 | GEO
Project description:Limb development is a well-established model for understanding cell fate decisions, and the formation of skeletal elements is coordinated through a sequence of events that control chondrogenesis spatiotemporally. It has been established that epigenetic control participates in cartilage maturation. Our research has shown for the first time that the inhibition of DNA methylation in interdigital tissue with 5-azacytidine results in the formation of an ectopic digit. This discovery suggested that DNA methylation dynamics could regulate the fate of cells between chondrogenesis and cell death during autopod development. We sequenced WGBS libraries from in-vivo interdigital tissue treated with 5-azacytidine or DMSO to identify genome-wide methylation changes during the early stages of 5-azacytidine-induced chondrogenesis.
2024-04-29 | GSE266119 | GEO
Project description:Comparative analysis of chromatin accessibility during chondrogenesis and in osteoarthritis
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Project description:Transcriptional changes in Wnt antagonism- and TGFβ agonism-induced MSC chondrogenesis.
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Project description:This SuperSeries is composed of the following subset Series: GSE24494: cgh_colvsc24_chr4-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE24831: cgh_colvsc24_wg-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE24835: cgh_colvscvi_wg-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25049: h3k4me2_c24_chr4-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25050: h3k27me3_colxcvi-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25051: h3k27me3_cvi-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25052: h3k27me3_col(cvi)-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25053: h3k4me2_colxcvi-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25054: h3k4me2_cvi-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25056: h3k4me2_col(cvi)-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25057: h3k27me3_colxc24-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25058: h3k27me3_c24-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25059: h3k27me3_col(c24)-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25060: h3k4me2_colxc24_chr4-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions GSE25061: h3k4me2_col_chr4-Analysis of epigenomic changes in hybrids Arabidopsis thaliana Col-0, C24 and Cvi accessions Refer to individual Series
2011-05-17 | E-GEOD-24836 | biostudies-arrayexpress