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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome wide-DNA methylation analysis of articular chondrocytes reveals a cluster of osteoarthritic patients

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Juan Fernandez Tajes

PROVIDER: E-GEOD-43270 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide DNA methylation analysis of articular chondrocytes reveals a cluster of osteoarthritic patients.

Fernández-Tajes Juan J Soto-Hermida Angel A Vázquez-Mosquera Maria E ME Cortés-Pereira Estefania E Mosquera Alejandro A Fernández-Moreno Mercedes M Oreiro Natividad N Fernández-López Carlos C Fernández Jose Luis JL Rego-Pérez Ignacio I Blanco Francisco J FJ

Annals of the rheumatic diseases 20130316 4

<h4>Objective</h4>Alterations in DNA methylation patterns have been found to correlate with several diseases including osteoarthritis (OA). The aim of this study was to identify, for the first time, the genome-wide DNA methylation profiles of human articular chondrocytes from OA cartilage and healthy control cartilage samples.<h4>Methods</h4>DNA methylation profiling was performed using Illumina Infinium HumanMethylation27 in 25 patients with OA and 20 healthy controls. Subsequent validation was ...[more]

PMID: 23505229

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Genome wide-DNA methylation analysis of articular chondrocytes reveals a cluster of osteoarthritic patients (methylation)

Project description:The aim of this study is to identify, for the first time, the genome-wide DNA methylation profiles of human articular chondrocytes from OA and healtly cartilage samples. Genome wide DNA methylation profiling of normal and osteoarthritic samples. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in cartilage knee samples. Samples included 18 healthy controls and 23 OA patients. Bisulphite converted DNA from the 31 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2013-04-01 | E-GEOD-43269 | biostudies-arrayexpress

Global methylation analysis of psoriatic (involved and uninvolved) and control skin

Project description:Psoriasis is a chronic inflammatory immune-mediated disorder affecting the skin and other organs including joints. Over 1,300 transcripts are altered in psoriatic involved skin compared to normal skin. Global epigenetic profiles of psoriatic skin have not been described. Here we describe the first genome-wide study of altered CpG methylation in psoriatic skin. We determined the methylation levels at 27,578 CpG sites in skin samples from individuals with psoriasis (12 involved, 8 uninvolved) and 10 unaffected individuals. CpG methylation of involved skin differed from normal skin at 1,108 sites. Twelve mapped to the epidermal differentiation complex, upstream or within genes that are highly up-regulated in psoriasis. Hierarchical clustering of 50 of the top differentially methylated (DM) sites separated psoriatic from normal skin samples. CpG sites where methylation was correlated with gene expression are reported. Sites with inverse correlations between methylation and nearby gene expression include those of KYNU, OAS2, S100A12, and SERPINB3, whose strong transcriptional up-regulation are important discriminators of psoriasis. We observed intrinsic epigenetic differences in uninvolved skin. Pyrosequencing of bisulfite-treated DNA from skin biopsies at three DM loci confirmed earlier findings and revealed a reversion of methylation levels towards the non-psoriatic state after one month of anti-TNF-a therapy. Control n=8 (NN), psoriasis involved n = 19 (PP), psoriasis uninvolved n=8 (PN). Hybridized to Illumina Human 27k methylation array. Paired samples are as follows: PN1 and PP1 PN2 and PP2 PN3 and PP3 PN4 and PP4 PN5 and PP5 PN6 and PP6 PN7 and PP7 PN8 and PP8

2011-11-11 | E-GEOD-31835 | biostudies-arrayexpress

Spatial intratumor heterogeneity of epigenetic alterations in esophageal squamous cell carcinoma

Project description:Esophageal squamous cell carcinoma (ESCC) is among the most common malignancies, but little is known about the spatial intratumor heterogeneity (ITH) and the temporal clonal evolutionary processes in this cancer. Interestingly, the epigenetic profiling also showed strong evidence of spatial ITH, and the phyloepigenetic trees were extremely similar with the phylogenetic ones, indicating the interplay and co-dependency of genetic and epigenetic alterations in ESCC. We found that several genes were both mutated and hypermethylated at their promoters, such as ASXL1 and EPHA7. Our integrated investigations of the spatial ITH and the temporal clonal evolution might provide insights into developing biomarkers for early diagnosis of ESCC, as well as personalized therapeutic targets for treating this malignancy. DNA methylation profiles of 12 tumor regions and 2 matched normal esophageal epithelial tissues from three M-WES-examined ESCC cases (ESCC01, ESCC03 and ESCC05) were performed using Illumina Infinium HumanMethylation450K platform (Illumina, San Diego, CA) at the Epigenome Center of University of Southern California.

2016-08-20 | E-GEOD-79366 | biostudies-arrayexpress

Identification of p38 beta as a therapeutic target for the treatment of Sézary Syndrome

Project description:Cutaneous T-Cell Lymphomas (CTCL) represent a group of hematopoietic malignancies that home to the skin and have no known molecular basis for disease pathogenesis. Sézary syndrome (SS) is the leukemic variant of CTCL. Currently, CTCL is incurable, highlighting the need for new therapeutic modalities. We have previously observed that combined small-molecule inhibition of protein kinase C (PKC) β and glycogen synthase kinase 3 (GSK3) causes synergistic apoptosis in CTCL cell lines and patient cells. Through microarray analysis of a SS cell line, we surveyed global gene expression following combined PKCβ-GSK3 treatment to elucidate therapeutic targets responsible for cell death. Clinically relevant targets were defined as genes differentially expressed in SS patients that were modulated by combination-drug treatment of SS cells. Gene set enrichment analysis uncovered candidate genes enriched for an immune cell signature, specifically the T-cell receptor and MAPK signaling pathways. Further analysis identified p38 as a potential therapeutic target that is over-expressed in SS patients and decreased by synergistic-inhibitor treatment. This target was verified through small-molecule inhibition of p38 leading to cell death in both SS cell lines and patient cells. These data establish p38 as a new SS biomarker and potential therapeutic target for the treatment of CTCL. Hut78 cells were treated with 4μM Enzastaurin, 5μM AR-A014418, 4μM Enzastaurin & 5μM AR-A014418, DMSO, or no treatment for three days. RNA was extracted and hybridized to Illumina microarrays.

2015-07-01 | E-GEOD-59179 | biostudies-arrayexpress

Global methylation analysis of development and progression of colorectal carcinoma

Project description:Colorectal tumorigenesis proceedes through well defined clinical stages assoicated with charateristic mutations. Besides genetic alterations, epi-driver genes that are aberrantly expressed in cancers in a fashion that confers a seletive growth advantage can also contribute to tumor evolution. To gain a global view of methylation patterns in normal and maliganant colorectal epithelia, we performed genome-wide DNA methylation analysis on DNAs from 48 fresh frozen CRC samples at different stages of CRC progression. We used IlluminaHumanMethylation450 Beadchip to get a broad view of genome-wide DNA methylationdata during CRC progression and identified significantly differentially methylated genes during CRC progression A total of 48 macro-dissected tissues including normal colon tissue, adenomas, carcinomas and metastases were collected by the Department of Pathology at the University of Virginia under the supervision of an experienced pathologist. DNA was extracted and run on IlluminaHumanMethylation450 Beadchip by Expression Analyisis.

2016-05-13 | E-GEOD-77954 | biostudies-arrayexpress

Global gene expression and methylation analysis of development and progression of colorectal carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-13 | E-GEOD-77955 | biostudies-arrayexpress

Microenvironment-driven resistance to B-Raf inhibition in a melanoma patient is accompanied by broad changes of gene methylation and expression in distal fibroblasts. Genome methylation study.

Project description:In this study, we compared gene expression and genome methylation of diverse fibroblast populations from a patient suffering from acrolentiginous melanoma (Breslow 4.0 mm, Clark IV, B-Raf V600E mutated). Stromal cells from the metastasis, i.e., melanoma associated fibroblasts (MAF), were positive for smooth muscle actin (SMA). Autologous control fibroblasts (ACF) isolated from distant uninvolved skin of the same patient during B-Raf inhibitor therapy and before clinical progression of the disease exhibited also strong SMA expression. Similar phenotype was observed in control dermal fibroblasts (CDF) from different donors yet exclusively after stimulation by TGF-Î²1. The identified differences in gene transcription as well as in DNA methylation indicate systemic activation of dermal fibroblasts in a patient with malignant melanoma. This dataset contains genome methylation profiling data, complementary transcriptome profiling data are available under accession E-MTAB-4964.

2018-12-30 | E-MTAB-4965 | biostudies-arrayexpress

CD40-mediated amplification of local immunity by keratinocytes in impaired by HPV

Project description:The interaction between the transmembrane glycoprotein surface receptor CD40 expressed by skin keratinocytes (KCs) and its T cell-expressed ligand CD154 was suggested to exacerbate inflammatory skin diseases. However, the full spectrum of CD40-mediated effects by KCs underlying this observation is unknown. Therefore, changes in gene expression after CD40 ligation of KCs were studied by microarrays. CD40-mediated activation for 2 hours stimulated the expression of a coordinated network of immune-involved genes strongly interconnected by IL8 and TNF, while after 24 hours anti-proliferative and anti-apoptotic genes were upregulated. CD40 ligation stimulated the production of chemokines that attracted lymphocytes and myeloid cells from peripheral blood mononuclear cells (PBMCs). Thus, CD40-mediated activation of KCs resulted in a highly coordinated response of genes required for the local development and sustainment of adaptive immune responses. The importance of this process was confirmed by a study on the effects of human papilloma virus (HPV) infection to the KCâs response to CD40 ligation. HPV infection clearly attenuated the magnitude of the response to CD40 ligation and consequently the KCâs capacity to attract PBMCs. The fact that HPV attenuates CD40 signalling in KCs indicates the importance of the CD40-CD154 immune pathway in boosting cellular immunity within epithelia. Total RNA from eight 72 hours 50 IU/ml IFNgamma pre-stimulated primary undifferentiated keratinocyte cultures, four uninfected and four HPV-positive, that were either left unstimulated, or stimulated for 2 hours with IFNgamma and Control- or CD40L-expressing L-cells (mouse fibroblasts), or stimulated for 24 hours with IFNgamma and Control- or CD40L-expressing L-cells. The stimulated samples were generated in duplo. 72 samples were generated in total.

2015-10-26 | E-GEOD-54181 | biostudies-arrayexpress

Brain transcriptional and epigenetic associations with the autistic phenotype (methylation data)

Project description:Autism is a common neurodevelopmental syndrome. Numerous rare genetic etiologies are reported; most cases are idiopathic. To uncover important gene dysregulation in autism, we analyzed carefully selected idiopathic autistic and control cerebellar and BA19 (occipital) brain tissues using high-resolution whole genome gene expression and DNA methylation microarrays. No changes in DNA methylation were identified in autistic brain but gene expression abnormalities in two areas of metabolism were apparent: down-regulation of genes of mitochondrial oxidative phosphorylation and of protein translation. We also found associations between specific behavioral domains of autism and specific brain gene expression modules related to myelin/myelination, inflammation/immune response and purinergic signaling. This work highlights two largely unrecognized molecular pathophysiological themes in autism and suggests differing molecular bases for autism behavioral endophenotypes. In this set of DNA methylation data, 9 cerebellar autism, 9 cerebellar control, 8 BA19 (occipital cortex) autism, and 8 BA19 control samples were used. Samples are labeled with a B followed by a unique number and letter identifying the subject and brain region, followed by an optional hyphenated number indicating the technical replicates performed on sample 1.

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N17 Modifies Mutant Huntingtin Nuclear Pathogenesis and Severity of Disease in HD BAC Transgenic Mice

Project description:Longitudinal microarray data from BACHD-M-NM-^TN17 mice with wildtype littermate controls Total RNA from cortex and striatum of wildtype and BACHD-M-NM-^TN17 mice collected at 2mo, 7mo, and 11mo was used for microarray on the Illumina MouseRef8v.2 platform.

2015-02-05 | E-GEOD-64386 | biostudies-arrayexpress

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