Microbiome in PM2.5
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1130117 | ENA |
REPOSITORIES: ENA
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2025-04-17 | GSE283083 | GEO
Project description:Purpose: The goal of this study is to investigate the effects of fine particulate matter (PM2.5) exposure on mouse olfactory bulb using next generation sequencing (NGS). Methods: After 28 days of 3 mg/kg/3 day and 10 mg/kg/3 day PM2.5 exposure, olfactory bulb mRNA profiles of 8-week-old wild-type (WT) male C57BL/6 mice were generated by deep sequencing, in 3-4 repeats, using Illumina NovaSeq 6000. For each sample, clean reads were obtained that mapped to mm10 using HISAT2 (hierarchical indexing for spliced alignment of transcripts) v2.0.477. Results: Our study revealed that PM2.5 treatment caused significant effects on the gene expression profilling of mouse olfactory bulb. Overall, the sequencing identified 34,745 transcripts, and two kinds of treatments obtained 60 and 138 differently expressed genes (DEGs) respectively, with a criteria of fold change >2 and q-value <0.5. Most biological events that DEGs involved were inflammation relevant. Conclusions: Our study revealed that PM2.5 treatment caused significant effects on the gene expression profiling of mouse olfactory bulb.
2024-01-22 | GSE186404 | 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: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:Yangyinqingfei Decoction (YYQFD), a traditional Chinese prescription, is well known in the treatment of diphtheria and lung-related diseases in clinic. However, the underlying mechanism how to treat lung-related diseases remains unclear. In the present study, the intervention effect of YYQFD on PM2.5-induced lung injury mice and its potential mechanism were investigated by metabolomics and proteomic techniques. The results showed that YYQFD could significantly improve pulmonary functions, relieve lung injury, as well as reduce IL-6, TNF-α and MDA, and increase SOD levels in serum and BALF of PM2.5-induced lung injury mice. Furthermore, the protein-metabolite joint analysis presented that YYQFD regulated the pathways of arachidonic acid metabolism, linoleic acid metabolism, and biosynthesis of unsaturated fatty acids with significantly down-regulating arachidonic acid, 20-HETE, prostaglandin E2, lecithin, linoleic acid, α-linolenic acid, eicosatetraenoic acid, and γ-linolenic acid, and up-regulating PTGES2, GPX2 and CBR3 protein expressions in lung tissue. A regulatory metabolic network map was further constructed, which provide us a better understanding about the role of YYQFD on PM2.5-induced lung injury mice and new insight into YYQFD application for the treatment of lung-related diseases.
2022-12-22 | PXD037163 | Pride
Project description:Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical com position, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5 in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1(PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In partic ular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regu latory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu win ter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5;and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contrib utes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.
2022-10-30 | GSE216512 | GEO
Project description:To unravel changes in gene expression due to exposure to PM2.5, we performed bulk RNA-seq analyses of zebrafish larvae exposed to PM2.5 and controls. Among others, PM2.5 increased oxoglutarate alpha-ketoglutarate receptor 1a, nitric oxide synthase, arachidonate 5-lipoxygenase b, immunity-related GTPase family e1, sulfotransferase family 5A, and macrophage expressed 1. NADPH oxidase organizer 1a and NADPH oxidase 1 were upregulated due to PM2.5 exposure. Furthermore, protein tyrosine/serine/threonine phosphatase activity was decreased after exposure to PM2.5. GESA analysis showed that genes involved in proteasome complex formation, inflammatory and immune response, leucocyte-mediated cytotoxicity, peptidase activator activity protein folding, and apoptotic signaling were upregulated after exposure to PM2.5. These results indicate that PM2.5 exposure caused the activation of immune-inflammatory and oxidative stress pathways and lipid and metabolic dysregulation.
2025-05-05 | GSE285038 | GEO