Expression analysis of stable chronic obstructive pulmonary disease and acute exacerbation of chronic obstructive pulmonary disease
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE60399 | GEO | 2014/08/14
SECONDARY ACCESSION(S): PRJNA258183
REPOSITORIES: GEO
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Project description:Investigation of whole genome gene expression level changes of the dynamic gene profiling of peripheral blood mononuclear cells (PBMCs) from patients with AECOPD) on day1, 3 and 10, compared to the normal people and stable COPD patients. A five chip study using total RNA recovered from Peripheral Blood Mononuclear Cell of Peripheral Blood.Evaluating the dynamic gene profiling of peripheral blood mononuclear cells (PBMCs) from patients with AECOPD) on day1, 3 and 10 after the hospital admission, to compared with healthy controls or patients with stable COPD. Slides were scanned at 5 μm/pixel resolution using an Axon GenePix 4000B scanner (Molecular Devices Corporation) piloted by GenePix Pro 6.0 software (Axon). Scanned images (TIFF format) were then imported into NimbleScan software (version 2.5) for grid alignment and expression data analysis. Expression data were normalized through quantile normalization and the Robust Multichip Average (RMA) algorithm included in the NimbleScan software. The Probe level (*_norm_RMA.pair) files and Gene level (*_RMA.calls) files were generated after normalization.
2014-08-14 | E-GEOD-60399 | biostudies-arrayexpress
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2003-07-16 | GSE475 | GEO
Project description:It has been recognized that COPD holds metabolic characteristics. however, at present, the early intervention of COPD is also still insufficient because of lacking effective biomarkers. Therefore, it is necessary to systematically and comprehensively explore the metabolic characteristics of COPD developing acute exacerbation. In the study, a non-targeted metabolomics strategy was used in exploring the metabolic profiling of COPD, AECOPD and heathy controls samples and screening potential biomarkers of metabolic disorders related to AECOPD, to analyze the potential value of these metabolites in predicting the development of COPD. For COPD patients, serum lysine, glutamine, 3-hydroxybutyrate, pyruvate and glutamate levels were significantly higher, while 1-methylhistidine, isoleucine, choline, valine, alanine, histidine and leucine levels were significantly lower in AECOPD patients compared with stable COPD patients after normalization based on the heathy controls. moreover, eight metabolic pathways were significantly altered (P < 0.05) in the serum of AECOPD patients compared with the stable COPD population, including purine metabolism, glutamine and glutamate metabolism, arginine biosynthesis, butyrate metabolism, ketone body synthesis and degradation, and linoleic acid metabolism. In addition, analysis of the correlation between stable COPD and AECOPD patients with pulmonary ventilation function and symptoms demonstrated that the levels of pyruvate, isoleucine, 1-methylhistidine and glutamine were significantly correlated with pulmonary ventilation function in COPD patients. Altogether, the study provides new insights for the early detection, treatment and prognosis monitoring of COPD development.
2023-04-13 | PXD041502 | iProX
Project description:This experiment was carried out to see if there were any miRNA expression differences in pulmonary endothelial cells between patients with and without COPD. COPD is an inflammatory condition and although much work has previously been performed to investigate the inflammatory cells in COPD there has not been as much research looking at the endothelium through which inflammatory cells must pass through to reach the lung tissue. In this experiment pulmonary endothelial cells were extracted from whole lung tissue removed at the time of cardiothoracic surgery. This was performed for patients with and without COPD. RNA was extracted using the Qiagen microRNeasy kits prior to transferring to the University of Birmingham Biosciences department who performed RNA labelling and ran the microarrays. Once the microarrays were performed quality was checked using ArrayQualityMetrics and the COPD group was compared to the non-COPD group using SAM. The experiment was then repeated using another patient group. MiRNAs of interest were validated with qPCR initially before moving on to functional work.
2021-08-01 | E-MTAB-10311 | biostudies-arrayexpress
Project description:Background: Chronic obstructive pulmonary disease (COPD) is a major risk factor for the development of lung adenocarcinoma (AC). AC often develops on underlying COPD, thus the differentiation of both entities by biomarker is challenging. Although survival of AC patients strongly depends on early diagnosis, a biomarker panel for AC detection and differentiation from COPD is still missing. Methods: Plasma samples from 176 patients with AC with or without underlying COPD, COPD patients, and hospital controls were analyzed using mass spectrometry-based proteomics. We performed univariate statistics and additionally evaluated machine learning algorithms regarding the differentiation of AC vs. COPD and AC with COPD vs. COPD. Results: Univariate statistics revealed significantly regulated proteins that were significantly regulated between the patient groups. Furthermore, Random forest classification yielded the best performance for differentiation of AC vs. COPD (area under the curve (AUC) 0.935) and AC with COPD vs. COPD (AUC 0.916). The most influential proteins were identified by permutation feature importance and compared to those identified by univariate testing. Conclusion: We demonstrate the great potential of machine learning for differentiation of highly similar disease entities and present a panel of biomarker candidates that should be considered for the development of a future biomarker panel.
2022-10-17 | PXD035120 | Pride
Project description:Chronic obstructive pulmonary disease (COPD) Metagenome
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Project description:This experiment was carried out to see if there were any miRNA expression differences in pulmonary endothelial cells between patients with and without COPD. COPD is an inflammatory condition and although much work has previously been performed to investigate the inflammatory cells in COPD there has not been as much research looking at the endothelium through which inflammatory cells must pass through to reach the lung tissue. In this experiment pulmonary endothelial cells were extracted from whole lung tissue removed at the time of cardiothoracic surgery. This was performed for patients with and without COPD. RNA was extracted using the Qiagen microRNeasy kits prior to transferring to the University of Birmingham Biosciences department who performed RNA labelling and ran the microarrays. Once the microarrays were performed quality was checked using ArrayQualityMetrics and the COPD group was compared to the non-COPD group using SAM. The experiment was then repeated using another patient group. MiRNAs of interest were validated with qPCR initially before moving on to functional work.
2018-09-10 | E-MTAB-7141 | biostudies-arrayexpress
Project description:Identifying protein biomarkers for chronic obstructive pulmonary disease (COPD) has been challenging. Most previous studies have utilized individual proteins or pre-selected protein panels measured in blood samples. To identify COPD protein biomarkers by applying comprehensive mass spectrometry proteomics in lung tissue samples. We utilized mass spectrometry proteomic approaches to identify protein biomarkers from 152 lung tissue samples representing COPD cases and controls.
2022-01-07 | PXD024124 | Pride
Project description:Purpose:To identify whether accelerated aging can be observed in the airways of PLWH with COPD, manifest by a unique DNA methylation signature. Methods: Bronchial epithelial brushings from PLWH with and without COPD and HIV-uninfected adults with and without COPD (n=76) were profiled for DNA methylation and gene expression. We evaluated global Alu and LINE-1 methylation and calculated the epigenetic age using the Horvath clock and the methylation telomere length estimator. To identify genome-wide differential DNA methylation and gene expression associated with HIV and COPD, robust linear models were used followed by an expression quantitative trait methylation (eQTM) analysis. Results:Epigenetic age acceleration and shorter methylation estimates of telomere length were found in PLWH with COPD compared to PLWH without COPD and uninfected patients with and without COPD. We identified CpG sites, genes, and eQTM-gene pairs associated with the interaction between HIV and COPD. Conclusions: Methylation age acceleration is observed in the airway epithelium of PLWH with COPD, a process that may be responsible for the heightened risk of COPD in this population. Their distinct methylation profile, differing from that observed in patients with COPD alone, suggests a unique pathogenesis to HIV-associated COPD that warrants investigation into the candidate genes identified.
2022-03-18 | GSE178808 | GEO
Project description:Purpose:To identify whether accelerated aging can be observed in the airways of PLWH with COPD, manifest by a unique DNA methylation signature. Methods: Bronchial epithelial brushings from PLWH with and without COPD and HIV-uninfected adults with and without COPD (n=76) were profiled for DNA methylation and gene expression. We evaluated global Alu and LINE-1 methylation and calculated the epigenetic age using the Horvath clock and the methylation telomere length estimator. To identify genome-wide differential DNA methylation and gene expression associated with HIV and COPD, robust linear models were used followed by an expression quantitative trait methylation (eQTM) analysis. Results:Epigenetic age acceleration and shorter methylation estimates of telomere length were found in PLWH with COPD compared to PLWH without COPD and uninfected patients with and without COPD. We identified CpG sites, genes, and eQTM-gene pairs associated with the interaction between HIV and COPD. Conclusions: Methylation age acceleration is observed in the airway epithelium of PLWH with COPD, a process that may be responsible for the heightened risk of COPD in this population. Their distinct methylation profile, differing from that observed in patients with COPD alone, suggests a unique pathogenesis to HIV-associated COPD that warrants investigation into the candidate genes identified.
2022-03-18 | GSE178807 | GEO