Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA316200 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In order to assess the alteration of lncRNA expression in 16HBE cell treated with PM2.5 samples, we determined the lncRNA expression profiles in 16HBE cell treated with PBS (control group) and PM2.5 samples (low dose 125 μg/mL and high dose 500 μg/mL) using lncRNA Microarray.
2016-03-25 | GSE79570 | GEO
Project description:In order to assess the alteration of lncRNA expression in 16HBE cell treated with PM2.5 samples, we determined the lncRNA expression profiles in 16HBE cell treated with PBS (control group) and PM2.5 samples (low dose 125 μg/mL and high dose 500 μg/mL) using lncRNA Microarray. 16HBE Cells were treated with PM2.5 suspension at concentration of 125 μg/mL and 500 μg/mL, and PBS was used in the control group for 48 h. Then, total RNAs were extracted for lncRNA chip preparation and analysis.
2016-03-25 | E-GEOD-79570 | biostudies-arrayexpress
Project description:The purpose of this study is to investigate whether the expression profile of long chain non coding RNA (lncRNA) in different concentrations of PM2.5 after treatment of normal human bronchial cells is changed. The total RNAs were extracted from 16HBE cells after exposure to either PM2.5, at concentration of 50 μg/mL and 100μg/mL, or PBS (control group) for 48h. lncRNA-sequencing, detection and analysis was performed. Fold change ≥ 2 and p ≤ 0.05 were used as a cutoff values to determine significant differential expression Further, cluster analyses were performed to classify lncRNAs based on their distinguishable expression in different samples.
2018-04-13 | GSE113071 | GEO
Project description:Genome-wide analysis of lncRNA expression profiles in COPD rat model exposed by cigarette smoking (CS) and fine particulate matter (PM2.5). Goal was to explore the differences and similarities lncRNAs expression in rats model of COPD exposed by CS and PM2.5.
2021-06-21 | GSE178513 | GEO
Project description:To investigate the effect of PM2.5 on sebocyte, we treated PM2.5 on SZ95 seboccyte and perfomed transcriptome analysis. We examined the role of PM2.5 via identification of differentially expressed genes, functional enrichment and canonical pathway analysis, upstream regulator analysis, and disease and bio-logical function analysis through mRNA sequencing. Xenobiotic and lipid metabolism, inflam-mation, oxidative stress, and cell barrier damage-related pathways were enriched; additionally, PM2.5 altered steroid hormone biosynthesis and retinol metabolism-related pathways.
2022-10-19 | GSE213620 | GEO
Project description:mRNAs and LncRNA microarray of HBE cell exposed to Al2O3 NPs, PM2.5, DEP
| PRJNA577662 | ENA
Project description:Exposure to particulate matter (PM) is consistently associated with increased morbidity and mortality attributable in part to respiratory illnesses. The alveolar macrophage (AM) is one of the cell types in the lung constantly exposed to and activated by ambient pollutants. Upon contact with environmental particulate pollutants, AM produces reactive oxygen species (ROS) and antioxidant enzymes, but the scope of this oxidative stress response induced by PM remains poorly defined. In this study, we used microarray analysis to determine the gene expression profile in human alveolar macrophages upon exposure to PM and sought to gain more insight into the global response of pro- and anti-oxidant enzymes to PM exposure. Human AM were obtained by bronchoscopy from normal individuals. They were then incubated with Chapel Hill PM2.5 (1 ïg/ml) or vehicle for 4 hours (n = 6 independent samples each). mRNAs were extracted, amplified and hybridized to Agilent Human 1A microarray. Differentially expressed genes were identified by Statistical Analysis for Microarrays (SAM) with a FDR of 10% and a P ⤠0.05. Significant genes were also mapped with Gene Ontology (GO) based on their molecular function. We found 34 and 41 up- and down-regulated genes respectively. Of these, 22 genes (~30%) were involved in metal binding and 14 genes were linked to oxidative stress, including 5 metallothionein-1 (MT1) isoform genes. In lung cells, addition of MT-1F in the medium attenuated PM2.5-induced H2O2 production while knockdown of MT1F gene expression increased H2O2 and IL-6 release induced by PM2.5. Our microarray experiments provided a global view of gene expression after in vitro PM2.5 exposure in human AM. The expression profile was most notable for differential expression of genes related to metal binding and oxidative stress, especially upregulation of MT1 isoform genes. Our findings suggest that metals associated with PM, e.g., zinc, copper, and arsenic, induce MT-1 and may be the primary mediators for PM-induced oxidative stress. Keywords: in vitro exposure, PM2.5 particle treatment, human alveolar macrophages Total RNA was isolated from alveolar macrophages from 6 subjects were treated in vitro with PM2.5 particles or vehicle control for 4 hrs. All particle-treated samples were co-hybridized with the common reference sample (pool of all 6 vehicle-treated samples) twice with Cy3 and Cy5 dyes flipped (12 hybridizations). Three samples were also co-hybridized with its own individual control (vehicle-treatment for the same subject) with Cy3 and Cy5 dyes flipped (6 additional hybridizations).
2008-05-01 | E-GEOD-10394 | biostudies-arrayexpress
Project description:RNAseq analysis of PM2.5 treated mouse cardiomyocyte cell line
| PRJNA873040 | ENA
Project description:To determine the epigenetic mechanism by which PM2.5 deteriorated synaptic transmission and spatial learning and memory, we determined miRNA expression in hippocampi of mice in absent or present of PM2.5 exposure using GenoExplorer microRNA microarray analysis.
2017-01-24 | GSE93967 | GEO
Project description:To identify miRNAs involved in ST-induced cell transformation, we used microarray chips containing 856 miRNA probes to define miRNA expression profiles in 16HBE,16HBER and 16HBERST cells.
2011-04-01 | GSE26166 | GEO