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Next Generation Sequencing of Transcriptomes of PM2.5-exposed Mice

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE186404 | GEO | 2024/01/22

REPOSITORIES: GEO

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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.

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Next Generation Sequencing of Transcriptomes of PM2.5-exposed Mice

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