Perfil transcriptómico de células epiteliales corneales humanas expuestas a PM2.5: Identificación de genes y vías de...

High levels of PM2.5 air pollution pose serious health risks, especially in rapidly urbanizing areas. While its effects on organs such as the heart and lungs are well documented, its effects on the cornea remain less well understood. Emerging evidence links PM2.5 exposure to corneal damage through processes such as autophagy, inflammation, and oxidative stress; however, the precise molecular pathways remain largely unknown.

This study aimed to identify key genes and signaling pathways in PM2.5-exposed human corneal epithelial cells (HCECs) using RNA sequencing and bioinformatics analysis.

Human corneal epithelial cells were cultured and exposed to 25 μg/mL PM2.5 for 24 h. High-throughput sequencing was performed after total RNA extraction and library construction for mRNA and microRNA (miRNA). Clean reads were mapped to the reference genome after filtering out low-quality reads. The Differential Expression Sequencing 2 (DESeq2) R package was used to identify differentially expressed (DE) mRNAs and miRNAs with a fold change ≥2 or ≤0.5 and a false discovery rate (FDR) ≤ 0.001.. Bioinformatics analyses included hierarchical clustering, protein-protein interaction network construction, target gene prediction, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment.

The analysis identified 45 DE mRNAs, including 14 upregulated and 31 downregulated transcripts, along with 16 upregulated miRNAs. A gene interaction network was constructed comprising nine mRNAs (6 upregulated and 3 downregulated), while a combined miRNA-mRNA network included 14 miRNAs and 21 mRNAs, forming 73 interaction pairs. Functional enrichment analysis of these genes revealed 30 significantly enriched GO terms, as well as 27 KEGG signaling pathways.

This study constructed regulatory networks and identified genes DE in the corneal response to PM2.5 exposure, particularly those involved in autophagy, inflammatory responses, and oxidative stress-related pathways. These results lay the groundwork for further research into the effects of PM2.5 on ocular surface health and provide insights into the molecular mechanisms underlying PM2.5-induced damage to human corneal epithelial cells, potentially guiding the development of targeted diagnostics or therapies to mitigate ocular surface injury caused by PM2.5.