利用生物信息学分析鉴定长期暴露于生物质燃烧产生的颗粒物（PM）后 BEAS-2B 细胞中差异表达的基因和通路。

Identification of differentially expressed genes and pathways in BEAS-2B cells upon long-term exposure to particulate matter (PM) from biomass combustion using bioinformatics analysis.

机构信息

Dongguan Maternal and Child Health Care Hospital.

出版信息

Environ Health Prev Med. 2023;28:51. doi: 10.1265/ehpm.22-00272.

DOI:10.1265/ehpm.22-00272

PMID:37722877

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10519835/

Abstract

BACKGROUND

Long-term exposure to PM from burning domestic substances has been linked to an increased risk of lung disease, but the underlying mechanisms are unclear. This study is to explore the hub genes and pathways involved in PM toxicity in human bronchial epithelial BEAS-2B cells.

METHODS

The GSE158954 dataset is downloaded from the GEO database. Differentially expressed genes (DEGs) were screened using the limma package in RStudio (version 4.2.1). In addition, DEGs analysis was performed by Gene Ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. A protein-protein interaction (PPI) network was constructed, MCODE plug-in and the cytoHubba plug-in in Cytoscape software was used to identify the hub genes. Finally, CytoHubba and DEGs were used to integrate the hub genes, and preliminary validation was performed by comparing the toxicology genomics database (CTD). Differential immune cell infiltration was investigated using the CIBERSORT algorithm.

RESULTS

A total of 135 DEGs were identified, of which 57 were up-regulated and 78 were down-regulated. Functional enrichment analyses in the GO and KEGG indicated the potential involvement of DEGs was mainly enriched in the regulation of endopeptidase activity and influenza A. Gene Set Enrichment Analysis revealed that Chemical Carcinogenesis - DNA adducts were remarkably enriched in PM groups. 53 nodes and 198 edges composed the PPI network. Besides, 5 direct-acting genes were filtered at the intersection of cytohubba plug-in, MCODE plug-in and CTD database. There is a decreasing trend of dendritic cells resting after BEAS-2B cells long-term exposure to PM.

CONCLUSIONS

The identified DEGs, modules, pathways, and hub genes provide clues and shed light on the potential molecular mechanisms of BEAS-2B cells upon long-term exposure to PM.

摘要

背景

长期接触燃烧的国内物质产生的 PM 与肺部疾病风险增加有关，但潜在机制尚不清楚。本研究旨在探索人支气管上皮 BEAS-2B 细胞中 PM 毒性涉及的枢纽基因和途径。

方法

从 GEO 数据库下载 GSE158954 数据集。使用 RStudio（版本 4.2.1）中的 limma 包筛选差异表达基因（DEGs）。此外，通过基因本体论（GO）功能分析和京都基因与基因组百科全书（KEGG）途径分析进行 DEGs 分析。构建蛋白质-蛋白质相互作用（PPI）网络，使用 Cytoscape 软件中的 MCODE 插件和 cytoHubba 插件识别枢纽基因。最后，使用 CytoHubba 和 DEGs 整合枢纽基因，并通过比较毒理学基因组学数据库（CTD）进行初步验证。使用 CIBERSORT 算法研究差异免疫细胞浸润。

结果

共鉴定出 135 个 DEGs，其中 57 个上调，78 个下调。GO 和 KEGG 中的功能富集分析表明，DEGs 的潜在参与主要富集在肠肽酶活性和流感 A 的调节中。基因集富集分析表明，化学致癌作用 - DNA 加合物在 PM 组中明显富集。PPI 网络由 53 个节点和 198 个边组成。此外，在 cytohubba 插件、MCODE 插件和 CTD 数据库的交集处筛选出 5 个直接作用基因。长期暴露于 PM 后，BEAS-2B 细胞中的树突状细胞休息呈下降趋势。