Mitochondrial dysfunction in endothelial cells induced by airborne fine particulate matter (<2.5 μm)

Exposure to ambient fine particulate matter (<2.5 μm; PM_2.5 ) increases the risk of the physiopathology of vascular diseases. However, the underlying mechanism, particularly the mitochondrial damage mechanism, of PM_2.5 -induced vascular dysfunction is still unclear. In this study, we examined PM_2.5 -induced alterations of mitochondrial morphology, and further demonstrated the adverse effects on mitochondrial dynamics and function in vascular endothelial cells. Consequently, cultured EA.hy926 cells were subjected to PM_2.5 collected from Beijing. A Cell Counting Assay Kit-8 demonstrated that PM_2.5 exposure decreased the proliferation of EA.hy926 cells in a dose-dependent manner. The exposure caused an increment of abnormal mitochondria coupled with the decrease of fusion protein MFN2 and the increase of fission protein FIS1, suggesting that PM_2.5 inhibits mitochondrial fusion. Further analyses revealed PM_2.5 decreased the mitochondrial membrane potential (ΔΨm) and increased the mitochondrial permeability transport pore opening, eventually resulting in impairments in adenosine triphosphate synthesis. Therefore, it is clearly shown that PM_2.5 triggered endothelial toxicity through mitochondria as the target, including the damage of mitochondrial homeostasis.