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Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

ABSTRACT: Lung myeloid dendritic cells isolated from emphysema but not healthy subjects induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung myeloid dendritic cells from healthy or emphysema subjects. These genes may play crucial roles in directing Th1 and Th17 cells differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26296 | GEO | 2011/01/01

SECONDARY ACCESSION(S): PRJNA135059

REPOSITORIES: GEO

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Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

Project description:Lung myeloid dendritic cells isolated from emphysema but not healthy subjects induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung myeloid dendritic cells from healthy or emphysema subjects. These genes may play crucial roles in directing Th1 and Th17 cells differentiation. Total mRNA was extracted from lung myeloid dendritic cells isolated from lungs of three healthy controls and three emphysema patients.

2011-01-01 | E-GEOD-26296 | biostudies-arrayexpress

Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

Project description:Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses. Lung APCs were isolated from PBS (reference groups) or nCB exposed wildtype or Mir22-/- mice, total four groups. There were three replicates in each group.

2015-09-05 | E-GEOD-72734 | biostudies-arrayexpress

Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

2015-09-05 | GSE72734 | GEO

Homo sapiens

Project description:Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

| PRJNA135059 | ENA

Single-cell RNAseq of the human normal and emphysema lung

Project description:To study emphysema, we conduct single-cell RNAseq of the human healthy and emphysema lung using 10X genomics scRNAseq technique.

2023-02-13 | GSE196638 | GEO

Epigenetic stabilization of DC and DC precursor classical activation by TNFalpha drives protective T-cell polarization

Project description:We report that TNFalpha mediated dendritic cell priming via alterations in histone 3 lysine 4 trimethylation (H3K4me3) sustains lasting protective Th1/Th17 responses during invasive Cryptococcus neoformans pulmonary infection. Cryptococcus neoformans pulmonary infection results in increased global lung dendritic cell H3K4me3 over naive lung dendritic cells. Blockage of TNFalpha during Cryptococcus neoformans pulmonary infection results in decreased H3K4me3 at sites crucial to protective Th1/Th17 responses.

2018-08-15 | GSE118543 | GEO

Emphysema Lung Tissue Gene Expression Profiling

Project description:Gene expression profiling of lung tissue from undiseased (NML), 'usual' emphysema (EML), and Alpha-1 Antitrypsin Deficiency-related emphysema (ADL). Keywords = Emphysema Keywords = COPD Keywords = Alpha-1 Antitrypsin Deficiency Keywords: ordered

2004-06-01 | GSE1122 | GEO

Transcription profiling of human lung tissue from severe emphysema versus normal or mild emphysema human patients

Project description:Comparison of severely emphysematous tissue removed at lung volume reduction surgery to that of normal or mildly emphysematous lung tissue resected from smokers with nodules suspicious for lung cancer. Data obtained from the 18 patients with severe emphysema and 12 patients with mild/no emphysema. Research may provide insights into the pathogenetic mechanisms involved in chronic obstructive pulmonary disease (COPD).

2007-08-13 | E-GEOD-1650 | biostudies-arrayexpress

Expression Profiling Identifies Genes Involved in Emphysema

Project description:Chronic obstructive pulmonary disease (COPD) is a major public health problem. The aim of this study was to identify genes involved in emphysema severity in COPD patients. Gene expression profiling was performed on total RNA extracted from non-tumor lung tissue from 30 smokers with emphysema. Class comparison analysis based on gas transfer measurement was performed to identify differentially expressed genes. Genes were then selected for technical validation by quantitative reverse transcriptase-PCR (qRT-PCR) if also represented on microarray platforms used in previously published emphysema studies. Genes technically validated advanced to tests of biological replication by qRT-PCR using an independent test set of 62 lung samples. Class comparison identified 98 differentially expressed genes (p<0.01). Fifty-one of those genes had been previously evaluated in differentiation between normal and severe emphysema lung. qRT-PCR confirmed the direction of change in expression in 29 of the 51 genes and 11 of those validated, remaining significant at p<0.05. Biological replication in an independent cohort confirmed the altered expression of eight genes, with seven genes differentially expressed by greater than 1.3 fold, identifying these as candidate determinants of emphysema severity. Gene expression profiling of lung from emphysema patients identified seven candidate genes associated with emphysema severity including COL6A3, SERPINF1, ZNHIT6, NEDD4, CDKN2A, NRN1 and GSTM3.

2009-09-21 | GSE17770 | GEO

Project description:Increased small airway resistance and decreased lung elasticity contribute to the airflow limitation in chronic obstructive pulmonary disease (COPD). The lesion that corresponds to loss of lung elasticity is emphysema; the small airway obstruction is due to inflammatory narrowing and obliteration. Despite their convergence in altered physiology, different mechanisms contribute to these processes. The relationships between gene expression and these specific phenotypes may be more revealing than comparison with lung function. We measured the ratio of alveolar surface area to lung volume (SA/V) in lung tissue from 43 smokers. Two samples from 21 subjects, in which SA/V differed by > 49 cm2/mL were profiled to select genes whose expression correlated with SA/V. The level of expression of 181 transcripts was related to SA/V ( p< 0.05). The relationship between expression of these transcripts and SA/V was tested in the 22 remaining subjects as a replication. Thirty of the 181 genes remained significantly associated with SA/V (P<0.05) and the direction of association was the same in 164/181. Pathway and network analysis revealed enrichment of genes involved in protein ubiquitination, and western blotting showed altered expression of genes involved in protein ubiquitination in obstructed individuals. These data implicate modified protein ubiquitination and degradation as a potentially important pathway in the pathogenesis of emphysema. Raw data not available for this study

2014-11-07 | GSE63073 | GEO

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