Coal-fired PM2.5 induces endothelial cell injury and the expression of atherosclerosis-related adhesion molecules: Involvement of the p38 and JNK signaling pathways

Abstract

It has been reported that PM2.5 causes endothelial cell injury and promotes atherosclerosis. However, the exact mechanism through which coal-fired PM2.5 induces endothelial cell injury, and the involvement of the p38 and JNK signaling pathways in this process remain unclear. In this study, EA.hy926 cells were exposed to coal-fired PM2.5 at concentrations of 25, 50, and 100 μg/mL, and the toxic effects were observed. The phosphorylation of the JNK and p38 signaling pathways was investigated through western blot analysis. Additionally, the expression of adhesion molecules (ICAM-1 and E-selectin) was assessed using ELISA and flow cytometry. Changes in cellular toxicity and adhesion molecules were evaluated after pretreatment with the p38 inhibitor SB203580 (10 μM) and the JNK inhibitor SP600125 (25 μM). We observed that exposure to coal-fired PM2.5 led to a decrease in cell survival rate and proliferation while promoting apoptosis. Exposure to coal-fired PM2.5 promoted the expression of ICAM-1 and E-selectin, as well as the phosphorylation of p38 and JNK in EA.hy926 cells. After using p38 and JNK inhibitors, there was an observed increase in cell survival rate and proliferation, accompanied by a decrease in apoptosis. The levels of ICAM-1 and E-selectin showed no significant changes with the addition of p38 and JNK inhibitors. Our results indicated that coal-fired PM2.5 caused cellular toxicity and increased the levels of ICAM-1 and E-selectin. The p38 and JNK signaling pathways might play a role in the reduction of cell viability, while the regulation of ICAM-1 and E-selectin might not be influenced by these pathways.