Eicosapentaenoic acid (EPA) can modulate expression of cytoprotective and inflammatory proteins in pulmonary endothelial cells (ECs) when exposed to air pollution particulate matter, according to research presented at the National Lipid Association’s 2022 Scientific Sessions, from June 2nd through 5th, in Scottsdale, AZ.
Investigators assessed the ability of EPA to modulate expression of inflammatory proteins and related pathways, including neutrophil degranulation, in pulmonary ECs after exposure to air pollution particulate matter of different sizes.
The pulmonary ECs were pre-treated with EPA (40 µM) for 2 hours in 2% fetal bovine serum (FBS)-containing medium and challenged with urban particulate matter (50 µg/mL) for 2 hours, and proteomic analysis was conducted.
The researchers performed a bicinchoninic acid assay to quantify the total protein in each sample. Each multiplexed sample was then fractionated to increase the overall protein coverage using high pH reversed phase fractionation. Proteins with a fold change >1.0 and P <.05 for the relevant comparisons were considered significant and further analyzed.
EPA significantly modulated the expression of 205 and 347 proteins relative to fine and urban particulate matter, respectively. Neutrophil degranulation was in pathways modulated by both particulate matter, in which fine and urban particulate matter modulated 36 and 13 proteins, respectively. A total of 8 proteins were common to fine and urban particulate matter, including 1.5-fold and 1.3-fold increases in C-X-C motif chemokine 6, respectively.
EPA treatment modulated 22 and 35 proteins associated with neutrophil degranulation compared with fine and urban particulate matter, respectively. Relative to fine particulate matter, EPA increased expression of heat shock protein 90-β and decreased expression of interleukin enhancer-binding factor 2. EPA also decreased expression of C-X-C motif chemokine 6 and increased expression of glutathione S-transferase P, compared with urban particulate matter.
“EPA favorably modulated expression of various cytoprotective as well as inflammatory proteins in pulmonary ECs during exposure to multiple air pollution particulate matter,” stated the researchers. “These findings support a potential cardiovascular benefit for EPA under inflammatory conditions caused by air pollution particulate matter.”
Disclosure: This study was conducted with financial support from Amarin Pharma Inc, Bridgewater, NJ, and Elucida Research.
Sherratt SCR, Libby P, Bhatt DL, Mason RP. Eicosapentaenoic acid (EPA) modulates expression of inflammatory proteins in pulmonary endothelial cells following exposure to air pollution particle matter. Presented at: National Lipid Association (NLA) Scientific Sessions 2022; June 2-5; Scottsdale, AZ. Abstract #37.
This article originally appeared on The Cardiology Advisor