Results of differentially expressed lncRNAs in COPD and healthy smoker using the Arraystar Human LncRNA Microarray
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ABSTRACT:
PROVIDER: PRJNA420055 | ENA |
REPOSITORIES: ENA
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Project description:A total of 3,359 lncRNAs revealed by microarray analysis have been differentially expressed between the two groups, 1,995 lncRNAs identified to be up-regulated in COPD, whereas 1,364 lncRNAs have been down-regulated. Meanwhile，a total of 3,283 mRNAs have been differentially expressed, 2,589 mRNAs identified to be up-regulated in COPD, whereas 694 mRNAs were down-regulated.
2017-11-29 | GSE107426 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is a progressive disease that obstructs the airflow from the lungs, and tobacco smoking is the major cause of COPD. Here, we applied single-cell RNA sequencing to analyze COPD pathogenesis in COPD patients, non-COPD smokers and never-smokers and investigated the disease progression at single-cell resolution. By single-cell transcriptome analysis, we identified a novel subpopulation of Alveolar Type 2 epithelial cells that emerged in smokers, such as COPD patients, and specifically expressed a series of chemokines and PD-L1. Since the number of cells in the basal cell clusters increased in only the COPD lungs but not in the non-COPD smoker or never-smoker lungs, we also tried to clarify the difference in phenotype between COPD and other basal cells with single-cell RNA-seq. However, due to the small number of cells in each, no clear difference could be found. To further investigate the functional properties of basal cells in COPD, we isolated small airway epithelial cells from surgical samples of COPD or never-smoker lungs and expanded the cells in vitro.Total RNA was extracted from early passaged cells , and bulk RNA-seq was performed to characterize these cells in detail. Finally, we found that the COPD basal cells retained the inflammatory response and basal/stem-related signals, even after a few passages in culture, and it might cause basal cell expansion in vivo.
2021-06-10 | GSE162154 | GEO
Project description:Rationale: COPD is characterized by an abnormal regulatory T cell (Treg) response and increases in Th1 and Th17 cell responses. It is unclear if dysregulation of miRNAs within Treg alters the adaptive immunophenotype in COPD. Objectives: To compare the miRNA profile of COPD Treg cells with that of healthy controls and to explore the function of differentially expressed miRNAs. Methods: Treg cells (CD4+CD25+CD49-CD127-) and T effector (CD4+CD25-) cells were obtained from the peripheral blood of 4 nonsmokers, 4 healthy current smokers, and 4 COPD current smokers for analysis of miRNA expression, matching them for age and sex. We assessed expression initially by microarray analysis on the Illumina miRNA platform then conducted real time RT-PCR validation of the microarray results. 24 samples were analyzed. 8 from each patient group of healthy Normal, Healthy Smoker, and COPD Smoker.
2014-04-19 | E-GEOD-56923 | biostudies-arrayexpress
Project description:Metagenomic analysis of the induced sputum samples from non-smoker COPD, smoker-COPD, and healthy rural Indian subjects
| PRJEB20464 | ENA
Project description:Using Geomx's Digital Space Profiling method for WTA RNA transcriptomics in lung tertiary lymphoid structures (TLS, follicles), we assessed paraffin-embedded and OCT-embedded lung sections from 48 patients, which were classified as Never Smoker Controls (NSC, n=8), Smoker Controls (SC, n=13), and COPD GOLD1-4 patients (n=27 patients). we identified 19 patients with tertiary lymphoid structures (TLS), distributed as 13 COPD patients and 6 SC subjects, with 115 TLS data used for the final data analysis.
2023-11-21 | GSE237120 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is one of the most prevalent lung diseases, and involves persistent airflow limitation and incorporates both emphysema and chronic bronchitis. Cigarette smoking has been identified as the main risk factor for disease development and progression. In a basic model of COPD, the disease is initiated when the physiologic response mechanisms to cigarette smoke exposure are overwhelmed; for example, because of long-term exposure effects or other aging-related changes. In this parallel-group case-controlled clinical study we asked to what extent the different transitions in a chronic-exposure-to-disease model are reflected in the proteome and cellular transcriptome of induced sputum samples from the lung. For this, we selected 60 age- and gender-matched individuals for each of four study groups: current healthy smokers, current-smoker COPD patients, former smokers, and never smokers (a total of 240 individuals). Induced sputum was collected, the cell-free supernatant was analyzed by quantitative proteomics (isobaric-tag based), and the cellular mRNA fraction was analyzed by microarray-based expression profiling. The sputum proteome of current smokers (healthy or COPD patients) clearly reflected the common physiological responses to smoke exposure, including alterations in mucin/trefoil proteins (e.g., MUC5AC and TFF1/3up-regulation), peptidase regulators (e.g., TIMP1 up-regulation), and a prominent xenobiotic/oxidative stress response (e.g., NQO1 and ALDH3A1 up-regulation). The latter response also was observed in the sputum transcriptome, which additionally demonstrated an immune-related polarization change (toward a M2 signature). The (long-term) former smoker group showed nearly complete reversal of the observable biological effects. Thirteen differentially abundant proteins between the COPD and healthy smoker groups were identified. These abundant proteins included previously reported COPD-associated proteins (e.g., TIMP1 (up-regulation) and APOA1 (down-regulation)) and novel proteins such as C6orf58 and BPIFB1 (LPLUNC1) (both up-regulated in the COPD group compared with the healthy smokers). In summary, our study demonstrates that sputum proteomics/transcriptomics can capture the complex and reversible physiological response to cigarette smoke exposure, which appears to be only slightly modulated in early-stage COPD patients. The study has been registered on ClinicalTrials.gov with identifier NCT01780298.
2015-08-28 | PXD001977 | Pride
Project description:Chronic obstructive pulmonary disease (COPD) is one of the most prevalent lung diseases, and involves persistent airflow limitation and incorporates both emphysema and chronic bronchitis. Cigarette smoking has been identified as the main risk factor for disease development and progression. In a basic model of COPD, the disease is initiated when the physiologic response mechanisms to cigarette smoke exposure are overwhelmed; for example, because of long-term exposure effects or other aging-related changes. In this parallel-group case-controlled clinical study we asked to what extent the different transitions in a chronic-exposure-to-disease model are reflected in the proteome and cellular transcriptome of induced sputum samples from the lung. For this, we selected 60 age- and gender-matched individuals for each of four study groups: current healthy smokers, current-smoker COPD patients, former smokers, and never smokers (a total of 240 individuals). Induced sputum was collected, the cell-free supernatant was analyzed by quantitative proteomics (isobaric-tag based), and the cellular mRNA fraction was analyzed by microarray-based expression profiling. The sputum proteome of current smokers (healthy or COPD patients) clearly reflected the common physiological responses to smoke exposure, including alterations in mucin/trefoil proteins (e.g., MUC5AC and TFF1/3up-regulation), peptidase regulators (e.g., TIMP1 up-regulation), and a prominent xenobiotic/oxidative stress response (e.g., NQO1 and ALDH3A1 up-regulation). The latter response also was observed in the sputum transcriptome, which additionally demonstrated an immune-related polarization change (toward a M2 signature). The (long-term) former smoker group showed nearly complete reversal of the observable biological effects. Thirteen differentially abundant proteins between the COPD and healthy smoker groups were identified. These abundant proteins included previously reported COPD-associated proteins (e.g., TIMP1 (up-regulation) and APOA1 (down-regulation)) and novel proteins such as C6orf58 and BPIFB1 (LPLUNC1) (both up-regulated in the COPD group compared with the healthy smokers). In summary, our study demonstrates that sputum proteomics/transcriptomics can capture the complex and reversible physiological response to cigarette smoke exposure, which appears to be only slightly modulated in early-stage COPD patients. The study has been registered on ClinicalTrials.gov with identifier NCT01780298.
2016-10-21 | MSV000080275 | MassIVE
Project description:The Arraystar Human LncRNA Array v2.0 was designed for researchers who were interested in profiling both LncRNAs and protein-coding RNAs in human genome. 33,045 LncRNAs were collected from the authoritative data sources including RefSeq, UCSC knowngenes, Ensembl and many related literatures. This experiment is to profile lncRNAs and protein-coding RNAs using Arraystar Human LncRNA Array v2.0. Identification of coding RNAs and lncRNAs that are diffrentially expressed in colorectal cancer by comparing sample A-E (normal colorectal cells) vs sample F-J (colorectal tumor cells) and c-MYC-regulating lncRNAs by comparing sample 1-3 (triplicate of HCT116 cells treated with control siRNA) vs sample 4-6 (triplicate of HCT116 cells treated with siRNA targeting MYC) and sample 7-9 (triplicate of RKO cells treated with control siRNA) vs sample 10-12 (triplicate of RKO cells treated with siRNA targeting MYC) .
2013-09-20 | E-GEOD-39846 | biostudies-arrayexpress
Project description:Background: CD8 cells seem to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, relatively little is known about their phenotype and function. Aims: To define the transcriptome of pulmonary CD8 cells in COPD and compare to paired circulating CD8 cells and smoker control pulmonary CD8 cells. COPD was defined according to the Global initiative for chronic Obstructive Lung Disease guidelines. Severity of disease was defined according to the patients lung function. In particular the forced evpiratroy volume in 1 second (FEV1).
2013-08-01 | E-MTAB-1688 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease (COPD) is one of the most prevalent lung diseases, and involves persistent airflow limitation and incorporates both emphysema and chronic bronchitis. Cigarette smoking has been identified as the main risk factor for disease development and progression. In a basic model of COPD, the disease is initiated when the physiologic response mechanisms to cigarette smoke exposure are overwhelmed; for example, because of long-term exposure effects or other aging-related changes. In this parallel-group case-controlled clinical study we asked to what extent the different transitions in a chronic-exposure-to-disease model are reflected in the proteome and cellular transcriptome of induced sputum samples from the lung. For this, we selected 60 age- and gender-matched individuals for each of four study groups: current healthy smokers, current-smoker COPD patients, former smokers, and never smokers (a total of 240 individuals). Induced sputum was collected, the cell-free supernatant was analyzed by quantitative proteomics (isobaric-tag based), and the cellular mRNA fraction was analyzed by microarray-based expression profiling. The sputum proteome of current smokers (healthy or COPD patients) clearly reflected the common physiological responses to smoke exposure, including alterations in mucin/trefoil proteins (e.g., MUC5AC and TFF1/3up-regulation), peptidase regulators (e.g., TIMP1 up-regulation), and a prominent xenobiotic/oxidative stress response (e.g., NQO1 and ALDH3A1 up-regulation). The latter response also was observed in the sputum transcriptome, which additionally demonstrated an immune-related polarization change (toward a M2 signature). The (long-term) former smoker group showed nearly complete reversal of the observable biological effects. Thirteen differentially abundant proteins between the COPD and healthy smoker groups were identified. These abundant proteins included previously reported COPD-associated proteins (e.g., TIMP1 (up-regulation) and APOA1 (down-regulation)) and novel proteins such as C6orf58 and BPIFB1 (LPLUNC1) (both up-regulated in the COPD group compared with the healthy smokers). In summary, our study demonstrates that sputum proteomics/transcriptomics can capture the complex and reversible physiological response to cigarette smoke exposure, which appears to be only slightly modulated in early-stage COPD patients. The study has been registered on ClinicalTrials.gov with identifier NCT01780298.
2015-08-28 | E-MTAB-3604 | biostudies-arrayexpress