Transcription profiling of human peripheral lymphocytes after exposure to cigarette smoke - super series
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Jinguo Chen
PROVIDER: E-GEOD-12587 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Little is known about alteration of the global gene expression by cigarette smoke (CS) and few biomarkers for smoking-related harm are available. We used Affymetrix HG-U133A GeneChips to measure the transcriptomes in eight cultured lymphocyte samples exposed to cigarette smoke condensate (CSC) in vitro . The in vitro exposure of lymphocytes to CSC significantly changed expression levels of 2,266 genes many of which biologically interacted. They included genes encoding for xenobiotic metabolism and oxidative stress-response (e.g. Nrf2 and AhR signaling pathways), inflammation/immune response (e.g. cytokines), apoptosis, cell cycle and tumorigenesis. However, the magnitude of expression responses for some genes showed high inter-individual variability. Experiment Overall Design: The goals of this study were to evaluate novel gene expression profiles and pathways affected by cigarette smoke condensate (CSC), and to identify potential biomarkers for cigarette smoke exposure and harm. To this end, we isolated the PBMC from eight light smokers, cultured the cells in vitro and exposed them to 2R4F CSC, then determined the gene expression profiles with Affymetrix microarray and analyzed alteration of global gene expression after exposure to CSC.
2009-09-15 | E-GEOD-12586 | biostudies-arrayexpress
Project description:Little is known about alteration of the global gene expression by cigarette smoke (CS) and few biomarkers for smoking-related harm are available. We used Affymetrix HG-U133A GeneChips to measure the transcriptomes in lymphocytes of 23 current healthy smokers. When heavy smokers were compared with light smokers, 311 genes demonstrated a significant difference in mRNA expression of their blood lymphocytes. Experiment Overall Design: The goals of this study were to evaluate novel gene expression profiles and pathways affected by cigarette smoking, and to identify potential biomarkers for cigarette smoke exposure and harm. To this end, we isolated the PBMC from 10 heavy and 13 light smokers, determined their gene expression profiles with Affymetrix microarray and analyzed their relationship with cigarette smoking.
2009-09-15 | E-GEOD-12585 | biostudies-arrayexpress
Project description:Cigarette smoking is a major cause of preventable morbidity and mortality. While quitting smoking is the best option, switching from cigarettes to non-combustible alternatives (NCAs) such as e-vapor products is a viable harm reduction approach for smokers who would otherwise continue to smoke. A key challenge for the clinical assessment of NCAs is that self-reported product use can be unreliable, compromising the proper evaluation of their risk reduction potential. In this cross-sectional study with 205 healthy volunteers, we combined comprehensive exposure characterization with in-depth multi-omics profiling to compare effects across four study groups: cigarette smokers (CS), e-vapor users (EV), former smokers (FS) and never smokers (NS). Multi-omics analyses included metabolomics, transcriptomics, DNA methylomics, proteomics, and lipidomics. Comparison of the molecular effects between CS and NS recapitulated several previous observations, such as increases in inflammatory markers in CS. Generally, FS and EV demonstrated intermediate molecular effects between the NS and CS groups. Stratification of the FS and EV by combustion exposure markers suggested that this positioning on the scale between CS and NS was partially driven by non-compliance / dual use. Overall, this study highlights the importance of in-depth exposure characterization before biological effect characterization for any NCA assessment study.
2024-02-22 | E-MTAB-12751 | biostudies-arrayexpress
Project description:Next generation product such as heat-not-burn type product and e-cigarette emit lower yields of chemical constituents than cigarette because combustion of tobacco leaves is not associated with their vapor generation. Therefore it is expected that the usage of these product bring beneficial impact on public health. However, risk-reduced potential as well as risk concerns in long-term use of these products has not yet been fully understood. In this study, we intended to estimate the risk reduced potential of our proprietary novel tobacco vapor product (NTV) by repeated exposure of in vitro 3D bronchial epithelial cells to NTV vapor in comparison with repeated exposure to cigarette smoke. In addition, to reflect the realistic situation of smokers, exposure switching from cigarette smoke to NTV vapor and cigarette smoke exposure cessation were conducted.
2020-03-31 | E-MTAB-8155 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease (COPD) is combination of progressive lung diseases. The diagnosis of COPD is generally based on the pulmonary function testing, however, difficulties underlie in prognosis of potential or early stage of COPD patients due to the complexity and heterogeneity of the pathogenesis. Transcriptomic technology is expected as one of the solution to resolve such complexities; therefore, we obtained transcriptomic data by in vitro testing with exposures of human 3D cultured bronchial epithelial tissues (MucilAir) to known inducible factors for early events of COPD to identify the potential descriptive marker genes. Fifteen potential biomarker genes were identified by transcriptomic analysis, and 10 out of 15 genes, as well as their coding proteins, have not been previously reported as biomarkers for chronic inflammatory lung diseases. The expression levels of these 15 genes with machine learning classification well distinguished between COPD and non-COPD patients with remarkable accuracy, suggesting these identified genes are potential descriptive marker genes for COPD.
2020-01-22 | E-MTAB-7992 | biostudies-arrayexpress
Project description:We conducted a study on variation in the human peripheral blood transcriptome using the PAXgeneTM Blood RNA System (PreAnalytix) and GeneChip Human Genome U133 plus 2.0 Array (Affymetrix). Data regarding the RNA integrity number (RIN) and complete blood count (CBC) for each healthy individual were collected and combined with gene expression profiles to characterize both biological and technological variation. The effect of RNA sample degradation on microarray performance in peripheral blood transcriptome analysis was also investigated.
2011-01-01 | E-MEXP-2917 | biostudies-arrayexpress
Project description:Combined pulmonary fibrosis and emphysema (CPFE) is characterized by upper-lobe emphysema combined with lower-lobe fibrosis and a high prevalence of pulmonary hypertension. The aim of this study was to measure and analyze gene expression profiles in the lungs of CPFE patients. The results showed that the expression profiles of the fibrotic and emphysematous lesions were remarkably different in terms of function. Genes related to immune system, structural constituents of cytoskeleton, and cellular adhesion were overexpressed in fibrotic lesions, while genes associated with cellular fraction, cell membrane structures, vascular growth and biology, second-messenger-mediated signaling, and lung development (all processes that contribute to the destruction and repair of cells, vessels, and lung) were overexpressed in emphysematous lesions. The differences in gene expression were detected in fibrotic and emphysematous lesions in CPFE patients. We propose that the development of coexisted fibrotic and emphysematous lesions in CPFE is implemented by these different patterns of gene expressions. Lung tissue specimens from fibrous lesions and emphysematous lesions of 3 patients with combined pulmonary fibrosis and emphysema (CPFE) were obtained for RNA extraction and hybridization on Affymetrix microarrays. We hypothesized that coexisted fibrosis and emphysema in CPFE are programmed by differential gene expressions in the corresponding lesions in the lungs of smokers susceptible to CPFE. Given the importance of genetic susceptibility in understanding the etiology and pathogenesis of CPFE, we examined tissues from patients with CPFE to systemically identify genes significantly expressed in lung tissues with fibrotic lesions as well as genes significantly expressed in tissues with emphysematous lesions.
2012-06-26 | E-GEOD-38934 | biostudies-arrayexpress
Project description:Introduction Aminoacyl tRNA-synthetases are ubiquitously expressed enzymes that attach amino acids to their cognate tRNA molecule. Mutations in several of the aminoacyl tRNA-syntheases are described to cause peripheral neuropathy, i.e. AARS1, GARS1, HARS1, YARS1 and WARS1. The Alanyl-tRNA Synthetase (AARS) is encoded by the AARS1. Bi-allelic mutations have been described responsible for epileptic encephalopathy with persistent myelination defect, while mutation in a single allele cause Charcot-Marie-Tooth disease type 2 (CMT2). Do date it is uncertain how a single AARS1 mutation cause tissue specific neuropathy. Methods The AARS1 was sequenced by next-generation sequencing in probands. Family members were examined by Sanger sequencing. Blood samples from affected and healthy controls were used for quantitative RNA analysis, biochemical analysis of alanine, and proteomics. Results Three Norwegian CMT2 families carried the same novel heterozygous AARS1 variant (NM_001605.2:c.976C>T p.(Arg326Trp)). The three families consisted of in total 17 genetically examined family members, of which 11 individuals carried the AARS1 variant and six unaffected individuals did not carry the variant. All individuals carrying the AARS1 variant presented with a mild to moderately severe CMT2 phenotype with adult onset, except a man age 91 years (reported by his son). Label-free quantitative proteomic analysis of four affected individuals pointed towards an effect on the immune system, comprising proteins known to represent components of systemic response to chronic injury and inflammation. Interestingly, a wide-spread impact on mitochondrial dysfunction was identified. Specifically, the oxidative phosphorylation complexes I, IV and V were highly downregulated. Conclusion Three Norwegian CMT2 families with an AARS1 variant, suggests mitochondrial dysfunction in AARS1 neuropathy.
2022-10-14 | PXD023842 | Pride
Project description:Lung cancer is the most common cause of death from cancer worldwide, largely due to frequent late diagnosis. Thus, there is the urgent need to develop new approaches to improve theearly detection of lung cancer, which would greatly affect patient survival. The quantitative protein expression profiles of microvesicles isolated from sera from 46 lung cancer patients and 41 high-risk non-cancer subjects were obtained using a mass spectrometry method based on library matching. We identified 33 differentially expressed proteins that allow discriminating the two groups. Based on serum protein expression profiles, we built a machine learning algorithm , which highlighted a decrease in the levels of Arysulfatase A (ARSA) as the most discriminating factor found in tumors. Our study identified a signature able to discriminate with high specificity and selectivity early lung cancer patients from high-risk healthy subjects. Among the differentially expressed proteins, ARSA emerged as the most promising biomarker for lung cancer early diagnosis.
2023-02-13 | PXD034221 | Pride
Project description:Smoking is a major risk factor for Urothelial carcinoma (UC). However the complex mechanisms, how smoking promotes carcinogenesis and tumour progression, remain obscure. A microarray based approached was therefore performed to detect the smoking derived gene expression alteration in non-malignant and malignant urothelial tissues from patients with superficial or invasive UC. Smoking enhanced cell migration and response to tissue damages. In non-malignant tissues smoking induced immune response and altered the cytoskeleton. In urothelial carcinoma, smoking altered extracellular and chromosome structures. Smoking affected tissues from patients with invasive carcinomamore strongly, up-regulating particularly growth factors and oncogenes in non-malignant tissue of patients with invasive but not with superficial carcinoma. In former smokers, comparable changes were seen in tissues form patients with invasive disease while they were minor or reversed in tissue of patients with superficial disease. Best but not complete tissue repair was suggestedfor non-malignant tissue from patients with superficial tumours. we used microarray techniques to define gene expression profile which may explain the contribution of smoking to urothelial carcinoma. Gene expression profiling using GeneChip HG-U133A Plus 2.0 (Affymetrix) was performed on non-malignant and carcinogenic urothelium from six patients with superficial and six with invasive urothelial carcinoma, each group including two current, former, and non-smokers.
2013-03-20 | E-GEOD-21142 | biostudies-arrayexpress