Transcriptomic analysis of key genes and pathways in human bronchial epithelial cells BEAS-2B exposed to urban particula
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RESEARCH ARTICLE
Transcriptomic analysis of key genes and pathways in human bronchial epithelial cells BEAS-2B exposed to urban particulate matter Mengchan Zhu 1,2 & Jian Wang 1 & Cuicui Chen 1 & Yuanlin Song 1 & Jue Pan 2 Received: 23 April 2020 / Accepted: 20 October 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Urban particulate matter (PM), a great danger to public health, is associated with increasing risk of pulmonary diseases. However, the involved key genes and signaling pathways mediating the cellular responses to urban PM are largely unknown. In this study, human bronchial epithelial cells BEAS-2B was exposed to Standard reference material (SRM) 1649b, followed by RNAsequencing (RNA-seq) and a combination of different bioinformatics analysis. A total of 201 genes (111 upregulated and 90 downregulated) were identified as the differentially expressed genes (DEGs). Moreover, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) unveiled several significant genes and pathways involved in PM-induced lung toxicity. Protein-protein interaction (PPI) network was performed with the Search Tool for the Retrieval of Interacting Genes (STRING), and the hub gene modules were recognized by Molecular Complex Detection (MCODE), a plug-in of Cytoscape. Moreover, Connectivity Map (CMap) analysis found six candidate small molecular compounds to reverse PM-altered gene expression, including aminohippuric acid, captopril, cinoxacin, fasudil, pargyline, and altizide. Finally, the expressions of part vital genes related to inflammation (IL-1β, CXCL2, CXCL5, CXCL8), ferroptosis (HMOX1, GCLM), and autophagy (BECN1, MAPK1LC3B) were in accordance with the RNA-seq data, with a concentrationdependent manner. This study may be helpful in revealing the complex molecular mechanisms underlying PM-induced lung toxicity and provide some new therapeutic targets for PM-related pulmonary diseases. Keywords Urban PM . RNA-seq . Inflammation . Ferroptosis . Autophagy . Small molecular compounds
Introduction
Mengchan Zhu and Jian Wang contributed equally to this work. Responsible Editor: Mohamed M. Abdel-Daim Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/s11356-02011347-1. * Yuanlin Song [email protected] * Jue Pan [email protected] 1
Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China
2
Department of Infectious Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China
Air pollution, one of the great killers leading to 6.4 million deaths in 2015 (GBD 2015 Risk Factors Collaborators 2016), has been a prime challenge and health hazard all around the world, especially in urban area. Particulate matter (PM), an important constituent of air pollutants, is proved to be associated with a variety of adverse health impacts on humans (Chen and Hoek 2020; Orellano et al.
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