Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192276 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Whole blood RNA-sequencing data from 5 AS patients who met 1984 AS criteria and 3 healthy human were obtained to gain insight into the potential mechanism of ankylosing spondylitis.
2021-11-10 | GSE181364 | GEO
Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling. Fifteen knee synovial biopsy tissue samples consisting of six seronegative spondyloarthropy (SpA), two ankylosing spondylitis (AS), three osteoarthritis (OA) and four normal control biopsies were obtained from the Synovial Tissue Bank at the Repatriation General Hospital in Adelaide, South Australia with the appropriate ethical approval (Supplementary Table 1). All patients provided informed written consent.
2012-12-01 | E-GEOD-41038 | biostudies-arrayexpress
Project description:To compare differential effectors of IL-17 pathway between male and female patients with ankylosing spondylitis (AS)
2023-01-02 | GSE221786 | GEO
Project description:We have already demonstrated that mesenchymal stem cells from patients with ankylosing spondylitis (ASMSCs) exhibited greater adipogenic differentiation potential than those from healthy donors (HDMSCs). Here, we further investigated the expression profile of long noncoding RNA (lncRNA) and mRNA, aiming to explore the underlying mechanism of abnormal adipogenic differentiation in ASMSCs.
2022-09-29 | GSE212613 | GEO
Project description:Single-cell transcriptome of >55,000 cells multiplexed into 4 channels obtained from peripheral blood and synovial fluid of two patients with HLA-B27+ ankylosing spondylitis,.
2021-10-18 | E-MTAB-10948 | biostudies-arrayexpress
Project description:CircRNA sequencing in peripheral blood mononuclear cells from Ankylosing Spondylitis patients and healthy controls
| PRJNA738893 | ENA
Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling.
2012-12-01 | GSE41038 | GEO
Project description:In order to recapitulated the primary mechanism of the pathologically enhanced osteogenesis of mesenchymal stem cells from ankylosing spondylitis patients (ASMSCs) over MSCs from healthy donor, we performed multiomic high-throughput sequencing. We analysed the H3K27ac ChIP-seq data according to ROSE algorithm, and identified super enhancers (SEs) in ASMSCs and HDMSCs. The ASMSC-unique SEs (ASUSEs) are associated with osteogenic differentiation and AS pathogenesis. By integrated analysis of H3K27ac ChIP-seq, ankylosing spondylitis (AS) SNPs and RNA-seq data, we discovered the transcription network regulated by AS SNP-adjacent super enhancers (SASEs) during the enhanced osteogenic differentiation of MSCs from AS patients (ASMSCs), which helped us gain insight into the crutial mechanism of AS pathological osteogenesis. And based on the inhibition effect of SE inhibitor JQ1 on the enhanced osteogenic differentiation of ASMSCs, we proposed that SEs may be attractive targets to treat AS pathological osteogenesis.
2021-02-21 | GSE153311 | GEO
Project description:In order to recapitulated the primary mechanism of the pathologically enhanced osteogenesis of mesenchymal stem cells from ankylosing spondylitis patients (ASMSCs) over MSCs from healthy donor, we performed multiomic high-throughput sequencing. We analysed the H3K27ac ChIP-seq data according to ROSE algorithm, and identified super enhancers (SEs) in ASMSCs and HDMSCs. The ASMSC-unique SEs (ASUSEs) are associated with osteogenic differentiation and AS pathogenesis. By integrated analysis of H3K27ac ChIP-seq, ankylosing spondylitis (AS) SNPs and RNA-seq data, we discovered the transcription network regulated by AS SNP-adjacent super enhancers (SASEs) during the enhanced osteogenic differentiation of MSCs from AS patients (ASMSCs), which helped us gain insight into the crutial mechanism of AS pathological osteogenesis. And based on the inhibition effect of SE inhibitor JQ1 on the enhanced osteogenic differentiation of ASMSCs, we proposed that SEs may be attractive targets to treat AS pathological osteogenesis.
2021-02-21 | GSE153310 | GEO
Project description:Mouse thymocytes can be classified into four major subsets based on expression of CD4 and CD8 co-receptors. CD4-CD8- (double negative, DN) cells become CD4+CD8+ (double positive, DP) cells following productive T cell receptor (TCR) beta chain rearrangement. A small proportion of DP cells are selected through interaction of clonal TCRalpha/beta and MHC self peptide complex expressed on thymic stromal cells. DP cell expressing MHC class I-restricted TCR become CD4-CD8+ cells, which will finally differentiate into cytotoxic T cells, while MHC class II restricted selection generates CD4+CD8- helper lineage T cells. We used microarrays to identify genes important for thymocyte differentiation and lineage determination by profiling gene expression in different thymocyte subsets. Mouse thymocytes were divided into four subsets based on CD4, CD8a, and TCRb expression and purified by flw cytometry. FACS purified DN (CD4-CD8a-TCRb-), DP (CD4+CD8a+), CD4SP (CD4+CD8a-TCRbhi) and CD8SP (CD4-CD8a+TCRbhi) populations were lysed in Trizol, and provided to the Genomics Core Facility of the Memorial Sloan-Kettering Cancer Center (MSKCC) for quality control, quantification, reverse transcription, labeling and hybridization to MOE430A 2.0 microarray chips (Affymetrix). Arrays were scanned per the manufacturer’s specifications for the Affymetrix MOE430v2 chip.
2011-08-09 | E-GEOD-31082 | biostudies-arrayexpress