Circulating microRNAs: Association with lung function in asthma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE74770 | GEO | 2016/06/09
SECONDARY ACCESSION(S): PRJNA301451
REPOSITORIES: GEO
Similar Datasets
Project description:Blood serum from 160 Childhood Asthma Management Program (CAMP) subjects were microRNA profiles with 13 subjects profiled twice. Each subject has diverse clinical phenotypes notably spirometry related phenotypes. Least squares linear regression was applied with subject phenotypes as the dependent variable, and microRNA Ct values (data matrix quantile normalized) as the independent variable to identify significant associations between subject phenotype and microRNA abundance.
2016-06-09 | E-GEOD-74770 | biostudies-arrayexpress
Project description:Evaluation of the airway transcriptome may reveal patterns of gene expression that are associated with clinical phenotypes of asthma. To define transcriptomic endotypes of asthma (TEA) we analyzed gene expression in induced sputum that correlate with phenotypes of disease. Gene expression was measured in sputum of subjects with asthma using Affymetrix HuGene ST 1.0 microarrays. Unsupervised clustering analysis of genes identified TEA clusters. Clinical characteristics were compared.
2014-04-07 | GSE56396 | GEO
Project description:BACKGROUND: Evaluation of the airway transcriptome may reveal patterns of gene expression that are associated with clinical phenotypes of asthma. To define transcriptomic endotypes of asthma (TEA) we analyzed gene expression in induced sputum that correlate with phenotypes of disease. METHODS: Gene expression was measured in sputum of subjects with asthma using Affymetrix HuGene ST 1.0 microarrays. Unsupervised clustering analysis of genes in pathways selected from the Kyoto Encyclopedia of Genes and Genomes (KEGG) identified TEA clusters. Clinical characteristics were compared and logistic regression analysis of matched blood samples defined an expression profile to determine the TEA cluster assignment in a cohort of children with asthma for validation. RESULTS: Three TEA clusters were identified. TEA cluster 1 had the most subjects with a history of intubation (P = 0.05), a lower pre-bronchodilator FEV1 (P = 0.006), a higher bronchodilator response (P = 0.03), and higher exhaled nitric oxide levels (P = 0.04), compared to the other TEA clusters. TEA cluster 2, the smallest cluster had the most subjects that were hospitalized for asthma (P = 0.04). Subjects in TEA cluster 3, the largest cluster, had normal lung function, low exhaled nitric oxide levels, and lower inhaled steroid requirements. Evaluation of TEA clusters in children confirmed that TEA clusters 1 and 2 are associated with a history of intubation (P = 5.58 x 10-06) and hospitalization (P = 0.01), respectively. CONCLUSIONS: Patterns of gene expression in the sputum and blood reveal TEA clusters that are associated with severe asthma phenotypes in children and adults. Gene expression was measured in sputum of subjects with asthma using Affymetrix HuGene ST 1.0 microarrays. Unsupervised clustering analysis of genes in pathways selected from the Kyoto Encyclopedia of Genes and Genomes (KEGG) identified TEA clusters. Clinical characteristics were compared and logistic regression analysis of matched blood samples defined an expression profile to determine the TEA cluster assignment in a cohort of children with asthma for validation.
2014-04-07 | E-GEOD-56396 | biostudies-arrayexpress
Project description:Bronchial asthma is one of the most common respiratory diseases. Reversible airflow limitation, persistent airway inflammation and airway hyperresponsiveness, and air remodeling is its main characterization. The morbidity and mortality rates of asthma increase due to air pollution. MicroRNAs are small molecules that regulate gene expression playing a part in inflammatory diseases. The designed current study aims to compare and screen circulating microRNAs targeting LIGHT as diagnostic biomarkers during asthma attack through microRNA microarray and Real Time PCR assay. Methods: Serum from 40 patients with asthma attack and 20 normal subjects was collected to detect circulating microRNAs expression profile through miRNA microarray. It is revealed that the significant differences of microRNAs level between asthmatic patients and normal controls. Target gene predictive analysis of differentially expressing microRNAs was performed to screen the miRNAs targeting LIGHT gene basing on the TargetScan bioinformatics software. Real Time PCR was conducted to further verify the realiability of the miRNA microassay and the screened specific miRNAs targeting LIGHT. Results: Asthmatic patients had a significant upper expression of miR-512-3p, miR-513b-5p, miR-5691 and lower level of miR-107, miR-140-5p, miR-17-5p compared with healthy subjects. The level of miR-140-5p and miR-107 in plasma of asthmatic patients were tightly correlated with their eosinophilic inflammation. The plasma miR-140-5p and miR-107 were needed to perform further investigation to evaluate the role as biomarkers in diagnosis of asthma.
2023-01-14 | GSE222894 | GEO
Project description:We carried out a genomewide association study by genotyping 10,365 persons with physician-diagnosed asthma and 16,110 unaffected persons, all of whom were matched for ancestry. We used random-effects pooled analysis to test for association in the overall study population and in subgroups of subjects with childhood-onset asthma (defined as asthma developing before 16 years of age), later-onset asthma, severe asthma, and occupational asthma.
| EGAS00000000077 | EGA
Project description:Airway epithelial brushings were obtained for microarray analysis by research bronchoscopy in 62 subjects with mild-to-moderate asthma not on inhaled steroids and 43 healthy controls. Asthma subjects were stratified into 2 subgroups, Th2 high and Th2 low asthma, based on their expression of a three-gene signature of Type 2 inflammation: POSTN, SERPINB2, and CLCA1.
2015-04-01 | GSE67472 | GEO
Project description:Airway epithelial brushings were obtained for microarray analysis by research bronchoscopy in 62 subjects with mild-to-moderate asthma not on inhaled steroids and 43 healthy controls. Asthma subjects were stratified into 2 subgroups, Th2 high and Th2 low asthma, based on their expression of a three-gene signature of Type 2 inflammation: POSTN, SERPINB2, and CLCA1. Gene expression comparisons were made between: 1. asthmatics and healthy controls, and 2. Th2 high asthma and Th2 Low asthma/Healthy controls. The gene expression alterations most associated with asthma were then used in gene set enrichment analyses and gene signature development to compare this asthma dataset to COPD gene expression datasets.
2015-04-01 | E-GEOD-67472 | biostudies-arrayexpress
Project description:Allergic asthma and rhinitis are two common chronic allergic diseases that affect the lungs and nose, respectively. Both diseases share clinical and pathological features characteristic of excessive allergen-induced type 2 inflammation, orchestrated by memory CD4+ T cells that produce type 2 cytokines (TH2 cells). However, a large majority of subjects with allergic rhinitis do not develop asthma, suggesting divergence in disease mechanisms. Since TH2 cells play a pathogenic role in both these diseases and are also present in healthy non-allergic subjects, we performed global transcriptional profiling to determine whether there are qualitative differences in TH2 cells from subjects with allergic asthma, rhinitis and healthy controls. TH2 cells from asthmatic subjects expressed higher levels of several genes that promote their survival as well as alter their metabolic pathways to favor persistence at sites of allergic inflammation. In addition, genes that enhanced TH2 polarization and TH2 cytokine production were also upregulated in asthma. Several genes that oppose T cell activation were downregulated in asthma, suggesting enhanced activation potential of TH2 cells from asthmatic subjects. Many novel genes with poorly defined functions were also differentially expressed in asthma. Thus, our transcriptomic analysis of circulating TH2 cells has identified several molecules that are likely to confer pathogenic features to TH2 cells that are either unique or common to both asthma and rhinitis.
2016-06-01 | GSE75011 | GEO
Project description:<p>SNP Health Association Resource (SHARe) Asthma Resource project (SHARP) is conducting a genome-wide analysis in adults and children
who have participated in National Heart, Lung, and Blood Institute's clinical research trials on asthma. This includes 1041 children
with asthma who participated in the Childhood Asthma Management Program (CAMP), 994 children who participated in one or five clinical
trials conducted by the Childhood Asthma Research and Education (CARE) network, and 701 adults who participated in one of six clinical
trials conducted by the Asthma Clinical Research Network (ACRN).</p>
<p>There are three study types. The longitudinal clinical trials can be subsetted for population-based and/or case-control analyses.
Each of the childhood asthma studies has a majority of children participating as part of a parent-child trio. The ACRN (adult)
studies are probands alone. Control genotypes will be provided for case-control analyses.</p>
| phs000166.v2.p1 | EGA
Project description:<p>The SNP Typing for Association with Multiple Phenotypes from Existing Epidemiologic (STAMPEED) asthma project includes subjects with asthma and controls from the Chicago Asthma Genetics Study (CAG), NHLBI multicenter Severe Asthma Research Program (SARP) and NHLBI Collaborative Studies on the Genetics of Asthma CSGA (Wake Forest). All studies included European American and African American children and adults with asthma ranging from mild to severe and adult controls. CAG participants were collected at the University of Chicago. SARP participants were recruited at the NHLBI SARP sites with an emphasis on recruiting severe asthmatics (Moore et al, Am J Respir Crit Care Med, 2010, PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/19892860" target="_blank">19892860</a>). CSGA cases and controls collected by the Wake Forest investigators were also included. Asthma status was based on both a physician's diagnosis and either bronchodilator reversibility or hyper-responsiveness to methacholine as well as less than 5 pack years of smoking. Genotyping was performed on the Illumina 1Mv1 platform, with individual genotypes called using clustering algorithms as implemented in the BeadStudio software by Illumina. The total number of markers following standard QC was 1,025,129. Imputation was performed using the HapMap phase 2, release 21 SNPs using MACH with the phased HapMap CEU and YRI haplotypes as a reference. Case/control association tests for asthma status were performed using logistic regression in R (<a href="http://CRAN.R-project.org/" target="_blank">http://CRAN.R-project.org/</a>) on genotype dosages, and adjusting for the first principal component from EIGENSTRAT.</p>
| phs000355.v1.p1 | EGA