Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1204188 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our study was designed to identify plasma miRNAs specific for rheumatoid arthritis (RA) by a comprehensive array approach. We performed a array-based miRNA analysis on plasma samples from three RA patients and three healthy controls (HCs).
2013-04-13 | GSE46012 | GEO
Project description:The gole of this study was to determine whether circulaitng miRNAs could be used as candidate miRNAs of SLE . In this study a miRNA profile was used to determine aberrant expressed circulating miRNAs in patients with system lupus erythematosus (SLE), compared with rheumatoid arthritis (RA) and healthy control (HCs). To further confirm these microarray data, we identify 8 miRNAs (miR-126, miR-21, miR-451, miR-223, miR-16, miR-125a-3p,miR-155,miR-146a) by real-time quantitative PCR in 20 healthy controls and in 55 cases, of whom 30 were diagnosed with SLE and 25 were diagnosed RA.
2011-12-13 | GSE34391 | GEO
Project description:The gole of this study was to determine whether circulaitng miRNAs could be used as candidate miRNAs of SLE . In this study a miRNA profile was used to determine aberrant expressed circulating miRNAs in patients with system lupus erythematosus (SLE), compared with rheumatoid arthritis (RA) and healthy control (HCs). To further confirm these microarray data, we identify 8 miRNAs (miR-126, miR-21, miR-451, miR-223, miR-16, miR-125a-3p,miR-155,miR-146a) by real-time quantitative PCR in 20 healthy controls and in 55 cases, of whom 30 were diagnosed with SLE and 25 were diagnosed RA. Using microarray-based expression profiling follwed by real-time quantitative polymerase Cycle Reaction (RT-qPCR)validation, we compared the levels of circulating miRNAs in plasma sample from SLE patients, RA patients, and healthy controls
2011-12-13 | E-GEOD-34391 | biostudies-arrayexpress
Project description:Malondialdehyde-modified epitopes (MDA-epitopes) can elicit specific autoantibody that expressed oxidative stress arising in rheumatoid arthritis (RA). The purpose of this study was to discover and validate MDA-peptide adducts as novel biomarkers using concanavalin A affinity chromatography, 1D SDS-PAGE, in-gel digestion, and label-free nano-LC-MS, and evaluate levels of serum MDA, MDA-protein adducts, proteins and autoantibody isotypes against an unmodified and MDA-peptide from Taiwanese female patients with RA and healthy controls (HCs). Levels of serum MDA and MDA-protein adducts were significantly higher in RA patients versus HCs. Four differentially expressed novel MDA-peptides were selected that relative modification ratio were 2-fold differences to examine protein levels and assess autoantibodies to MDA-peptides in RA patients compared with HCs. Four of peptides are autoantigens. Furthermore, 4 MDA-peptides can induce more autoantibody isotypes that are statistical significance in RA patients compared to HCs. Serum IgG and IgM against MDA-peptides showed excellent diagnostic performance in discriminating among RA patients and HCs: area under the curve (AUC, 0.96 ~ 0.98), sensitivity (88.9% ~ 97.8%) and specificity (88.9% ~ 100%). Autoantibodies to MDA-epitopes indicate oxidative modifications occurring in RA, and might be useful as clinical markers fro RA diagnosis if further investigated.
2021-02-25 | PXD004546 | Pride
Project description:Objective: Stem cell-like memory T cells (Tscm) are a subset of memory T cells that have the characteristics of stem cells. The role of Tscm cells in rheumatoid arthritis (RA) is unknown. Methods: The transcriptomes of Tscm cells from RA patients were compared with those from HCs. Results: Transcriptome analysis revealed that Tscm cells from RA patients showed patterns distinct from those of HCs. Conclusion: The percentage of transcriptionally distinct and potentially pathogenic Tscm cells are higher in RA patients than in HCs; these cells may be a continuous source of pathogenic T cells, which perpetuate RA.
2021-12-01 | GSE141836 | GEO
Project description:Our study was designed to identify plasma miRNAs specific for rheumatoid arthritis (RA) by a comprehensive array approach. We performed a array-based miRNA analysis on plasma samples from three RA patients and three healthy controls (HCs). TaqMan Low-Density Array (TLDA) using human miRNA version 3.0A and version 2.0B cards (Applied Biosystems) were applied to examine the global change of miRNA expression levels in plasma from patients with RA and healthy controls. A total of 756 mature miRNA updated in the Sanger miRBase v.15.0 were quantified according to the manufacturer's instructions as previously described. Normalization was carried out with the average Ct value of all miRNAs. Relative quantification of miRNA expression was calculated with the 2−ΔΔCt Ct method. The data was presented as log10 of the relative quantity of each miRNA.
2013-04-13 | E-GEOD-46012 | biostudies-arrayexpress
Project description:The emerging evidences support that exosome cargo miRNAs function as important regulators in cell differentiation. Therefore, in order to figure out the mechanism that Exo-AT mediated adipogenesis, we profiled miRNAs in Exo-AT using high-throughput sequencing (miRNA-seq). After trimming low-quality reads, contaminants, adaptors, and reads smaller than 15 nt, the remaining reads were mapped to merged pre-miRNA data bases. To identify the conserved miRNAs in Exo exosomes, miRNAs were aligned to miRBase v21. 148 and 154 types of known miRNAs in Exo-ADSCs and Exo-AT, respectively, were identified in the two replicates. Among these miRNAs, 103 miRNAs were simultaneously detected in both Exo-ADSCs and Exo-AT. Compared to Exo-ADSCs, 45 conserved miRNAs were enriched (expressed ≥ 2 folds, FDR<0.05) in Exo-AT. KEGG Pathway analysis was performed for the targets of the most 20 enriched miRNAs in Exo-AT (compared with Exo-ADSCs) to determine their potential function. Data showed that pathways that regulate adipogenesis such as Wnt signaling pathway, Insulin signaling pathway, MAPK signaling pathway, TGF-ß signaling pathway were enriched significantly for targets of Exo-AT miRNAs. Furthermore, 14 of 45 enriched miRNAs in Exo-AT (31.11%, such as miR-30a-5p, miR-148a-3p) were reported to participate in regulation of adipogenesis while 8 miRNAs (17.78%, such as miR-93-5p, miR-150-3p) that negatively control osteoblastic differentiation of MSC have been described.
2018-12-01 | GSE92313 | GEO
Project description:Using NGS approach we performed the search of multiple sclerosis-related miRNAs. We used PBMC as an informative and easily accessible biological material. To exclude bias in miRNA expression levels caused by disease modifying therapies, miRNA profiling was performed in treatment-naïve RRMS patients. Taking into account hypothetic gender specificity in disease pathogenesis we compared miRNA expression in RRMS patients and HCs separately for men and women. MiRNA profiling in men identified 32 differentially expressed miRNAs, which passed threshold for multiple corrections and may be attributed to MS-related. At the same time we did not find well-defined MS-specific miRNA expression signatures in women using NGS
2019-01-11 | GSE124900 | GEO
Project description:BMSC-derived exosomes from ovariectomized rats (OVX-Exo) and sham-operated rats (Sham-Exo) were co-cultured with bone marrow-derived macrophages to study their effects on osteoclast differentiation. Next-generation sequencing was utilized to identify the differentially expressed miRNAs (DE-miRNAs) in OVX-Exo and Sham-Exo, while target genes were analyzed using bioinformatics. The regulatory effects of miR-27a-3p and miR-196b-5p on osteogenic differentiation of BMSCs and osteoclast differentiation were verified by gain-of-function and loss-of-function analyses.Osteoclast differentiation was significantly enhanced in the OVX-Exo treatment group compared to the Sham-Exo group. Twenty DE-miRNAs were identified in OVX-Exo and Sham-Exo, among which miR-27a-3p and miR-196b-5p promoted the expressions of osteogenic genes in BMSCs. In contrast, knockdown of miR-27a-3p and miR-196b-5p increased the expressions of osteoclastic genes in osteoclasts. These 20 DE-miRNAs were found to target 11435 mRNAs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that these target genes were involved in several biological processes and osteoporosis-related signaling pathways.
2022-07-07 | GSE197085 | GEO
Project description:Premature infants have a high risk of bronchopulmonary dysplasia (BPD), which is characterized by abnormal development of alveoli and pulmonary vessels. Exosomes and exosomal miRNAs (EXO-miRNAs) from bronchoalveolar lavage fluid are involved in the development of BPD and might serve as predictive biomarkers for BPD. However, the roles of exosomes and EXO-miRNAs from umbilical cord blood of BPD infants in regulating angiogenesis are yet to be elucidated. In this study, we showed that umbilical cord blood-derived exosomes from BPD infants impaired angiogenesis in vitro. Next generation sequencing of EXO-miRNAs from preterm infants without (NBPD group) or with BPD (BPD group) uncovered a total of 418 differentially expressed (DE) EXO-miRNAs. These DE EXO-miRNAs were primarily enriched in cellular function-associated pathways including the PI3K/Akt and angiogenesis- related signaling pathways. Among those EXO-miRNAs which are associated with PI3K/Akt and angiogenesis-related signaling pathways, BPD reduced expression of hsa-miR-103a-3p and hsa-miR-185-5p exhibiting most significant reduction (14.3% and 23.1% of NBPD group, respectively); BPD increased hsa-miR-200a-3p expression by 2.64 folds of NBPD group. Furthermore, overexpression of hsa-miR-103a-3p and hsa-miR-185-5p in normal human umbilical vein endothelial cells (HUVECs) significantly enhanced endothelial cell proliferation, tube formation and cell migration, whereas overexpressing hsa-miR-200a-3p inhibited these cellular responses. This study demonstrates that exosomes derived from umbilical cord blood of BPD infants impair angiogenesis, possibly via DE EXO-miRNAs, which might contribute to the development of BPD.
2021-02-16 | GSE166762 | GEO