Abstract
To investigate the effect of stimulation of human bronchial epithelial cells (HBECs) by arterial traffic ambient PM2.5 (TAPM2.5) and wood smoke PM2.5 (WSPM2.5) on the expression of long non-coding RNAs (lncRNAs) in order to find new therapeutic targets for treatment of chronic obstructive pulmonary disease (COPD). HBECs were exposed to TAPM2.5 and WSPM2.5 at a series of concentrations. The microarray analysis was used to detect the lncRNA and mRNA expression profiles. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and gene ontology (GO) enrichment were conducted to analyze the differentially expressed lncRNAs and mRNAs. Quantitative real-time PCR (qRT-PCR) was performed to confirm the differential expression of lncRNAs. Western blot was performed to study the expression of autophagy and apoptosis-associated proteins. Flow cytometry was used to detect the apoptotic cells. The results indicated that fine particulate matter (PM2.5)-induced cell damage of HBECs occurred in a dose-dependent manner. The microarray analysis indicated that treatment with TAPM2.5 and WSPM2.5 led to the alteration of lncRNA and mRNA expression profiles. LncRNA maternally expressed gene 3 (MEG3) was significantly up-regulated in HBECs after PM2.5 treatment. The results of Western blot showed that PM2.5 induced cell apoptosis and autophagy by up-regulating apoptosis-associated gene, caspase-3, and down-regulating autophagy-associated markers, Bcl-2 and LC3 expression. In addition, we demonstrated that TAPM2.5 and WSPM2.5 accelerated apoptosis of human bronchial (HBE) cells, silencing of MEG3 suppressed apoptosis and autophagy of HBE cells. These findings suggested that the lncRNA MEG3 mediates PM2.5-induced cell apoptosis and autophagy, and probably through regulating the expression of p53.
Highlights
Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death and constitutes 6% of all global deaths [1]
We found that exposure of TAPM2.5 and WSPM2.5 induced the alteration of long non-coding RNA (lncRNA) expression profiles, and caused cell apoptosis and autophagy
DMSO compared with TAPM2.5-100, DMSO compared with TAPM2.5-300, DMSO compared with TAPM2.5-1000, DMSO compared with WSPM2.5-1000, DMSO compared with WSPM2.5-3000, and DMSO compared with WSPM2.5-10000
Summary
Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death and constitutes 6% of all global deaths [1]. Fine particulate matter (PM2.5) with an aerodynamic equivalent diameter of less than or equal to 2.5 μm are the atmospheric particles and important component of air pollution. It constitutes heavy metal particles, acidic oxides, organic pollutants, bacteria, fungi, and viruses [4,5,6]. Long-term exposure to traffic and PM2.5 at relatively low levels was associated with lower FEV1 and FVC and an accelerated rate of decline in lung function [10]. It was observed that acute exposure to elevated PM2.5 concentration is associated with acute exacerbation, hospitalization, and mortality due to COPD [11,12]
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