Abstract
Metals are vital toxic components of fine particulate matter (PM2.5). Cellular responses to exposure to PM2.5 or PM metal components remain unknown. Post-transcriptional profiling and subsequent cell- and individual-based assays implied that the metal ion-binding miR-4516/RPL37/autophagy pathway could play a critical role in cellular responses to PM2.5 and PM metal stresses. miR-4516 was up-regulated in A549 cells exposed to PM2.5 and in the serum of individuals living in a city with moderate air pollution. The expression levels of the miR-4516 target genes, namely, RPL37 and UBA52, were involved in ribosome function and inhibited by exposure to PM2.5 and PM metal components. Autophagy in A549 cells was induced by PM2.5 exposure as a response to decreased RPL37 expression. Moreover, enhanced miR-4516 expression was positively correlated with the augmentation of the internal burden of aluminum and lead in individuals living in a city with moderate air pollution. Hereby, the miR-4516/RPL37/autophagy pathway may represent a novel mechanism that mediates responses to PM metal components.
Highlights
Accumulated evidence from epidemiological studies supports the association between fine particulate matter (PM2.5) and increased risk of respiratory damages worldwide [1,2,3]
Posttranscriptional profiling and subsequent cell- and individual-based assays implied that the metal ion-binding miR-4516/RPL37/autophagy pathway could play a critical role in cellular responses to PM2.5 and PM metal stresses. miR-4516 was up-regulated in A549 cells exposed to PM2.5 and in the serum of individuals living in a city with moderate air pollution
The heatmap presented the induced and suppressed miRNAs of samples exposed to 500 μg/mL PM2.5 relative to the matched controls (Figure 1A). miR-4516 was the most modulated miRNA, with an fold change (FC) of 9.687 and false discovery rate (FDR) of 0.0136. miR-4516 expression in A549 cells and sera was confirmed by qRT-PCR analysis
Summary
Accumulated evidence from epidemiological studies supports the association between fine particulate matter (PM2.5) and increased risk of respiratory damages worldwide [1,2,3]. In addition to mass concentration, the chemical composition of PM2.5 could play a role in inducing harmful effects [8, 9] Both heavy and transition metals, such as lead (Pb), arsenic (As), zinc (Zn), aluminum (Al), titanium (Ti), manganese (Mn), copper (Cu), nickel (Ni), cadmium (Cd), and iron (Fe), are major toxic components of PM2.5 [7, 10,11,12,13]. These elements are associated with adverse health effects. Pb exposure was found to be positively correlated with serum levels of miR-222; microRNA (miRNA) expression www.impactjournals.com/oncotarget might represent a vital mechanism to mediate individual responses to PM metal components [18]
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