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Proteomic characteristics of PM2.5-induced differentially expressed proteins in k-ras-silenced HBE cells
Runbing Li1,2, Jiening Pu1,2, Ying Cai1,2
1School of Public Health, University of South China, Hengyang, China.
Abstract:
The human bronchial epithelial cells (HBE) and K-ras-silenced HBE cells were treated with fine particulate matter (PM2.5) samples from Taiyuan for 24 h. To screen the proteomic characteristics of PM2.5-induced differentially expressed proteins (DEPs), the Q Exactive mass spectrometer was used. Gene ontology (GO) analysis, Kyoto encyclopedia of genes and genomes (KEGG) analysis, functional prediction, protein-protein interaction (PPI) network analysis, and visualization of differential protein interactions were performed. 251 DEPs in K-ras silenced cells and 535 DEPs in normal HBE cells were identified, respectively. KEGG analysis showed that the differentially expressed proteins of PM2.5-treated cells were related to the biosynthesis of ribosomes, antibiotics, and amino acids. On the other hand, K-ras silenced cells were related to metabolic pathways, RNA transport, and DNA replication. Through the construction of a PPI network, the top 10 hub proteins were screened from the two cell groups, among which MRPL13, RPS20, and EIF1AX were of great significance. Our results indicated that the K-ras gene plays an important role in PM2.5-induced DEPs, and the findings provide a scientific basis for the further study of PM2.5 toxic mechanisms and biomarkers.
Insights
Fine particulate matter (PM2.5) exposure affects protein expression in human bronchial cells. Silencing K-ras alters these responses, highlighting K-ras
Area of Science:
- Environmental Health
- Proteomics
- Molecular Biology
Background:
- Fine particulate matter (PM2.5) poses significant health risks, particularly to the respiratory system.
- Understanding the molecular mechanisms of PM2.5 toxicity is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the proteomic changes in human bronchial epithelial (HBE) cells induced by PM2.5 exposure.
- To determine the role of K-ras in mediating these PM2.5-induced proteomic alterations.
Main Methods:
- Human bronchial epithelial cells (HBE) and K-ras-silenced HBE cells were exposed to Taiyuan PM2.5 samples.
- Quantitative proteomics using a Q Exactive mass spectrometer was employed to identify differentially expressed proteins (DEPs).
- Bioinformatic analyses including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) network analyses were performed.
Main Results:
- A total of 535 DEPs were identified in normal HBE cells and 251 DEPs in K-ras-silenced HBE cells following PM2.5 exposure.
- KEGG analysis revealed that PM2.5-induced DEPs in normal HBE cells were associated with ribosome biosynthesis, antibiotic biosynthesis, and amino acid biosynthesis.
- In K-ras-silenced cells, DEPs were linked to metabolic pathways, RNA transport, and DNA replication, with MRPL13, RPS20, and EIF1AX identified as significant hub proteins.
Conclusions:
- The K-ras gene significantly influences the proteomic response to PM2.5 exposure in HBE cells.
- These findings provide a foundation for further research into the toxicological mechanisms and potential biomarkers of PM2.5.
