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Mitochondrial dysfunction in endothelial cells induced by airborne fine particulate matter (<2.5 μm)
Author(s) -
Miao Xiaoyan,
Li Wenke,
Niu Bingyu,
Li Jiangshuai,
Sun Jingjie,
Qin Mengnan,
Zhou Zhixiang
Publication year - 2019
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3828
Subject(s) - mfn2 , mitochondrion , fis1 , mitochondrial fission , mitochondrial fusion , mitochondrial permeability transition pore , microbiology and biotechnology , mitochondrial apoptosis induced channel , chemistry , membrane potential , mitochondrial toxicity , dnm1l , apoptosis , biology , mitochondrial dna , inner mitochondrial membrane , programmed cell death , biochemistry , gene
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.