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PM2.5 aggravates the lipid accumulation, mitochondrial damage and apoptosis in macrophage foam cells

Liu, Jiangyan, Liang, Shuang, Du, Zhou, Zhang, Jingyi, Sun, Baiyang, Zhao, Tong, Yang, Xiaozhe, Shi, Yanfeng, Duan, Junchao, Sun, Zhiwei
Environmental pollution 2019 v.249 pp. 482-490
apoptosis, atherosclerosis, caspase-3, caspase-9, cell viability, cytotoxicity, foam cells, foaming, low density lipoprotein, membrane potential, mitochondria, mitochondrial membrane, oxidation, particulates, protein content, risk factors, staining
Epidemiological evidence showed that the particulate matter exposure is associated with atherosclerotic plaque progression, which may be related to foam cell formation, but the mechanism is still unknown. The study was aimed to investigate the toxic effects and possible mechanism of PM2.5 on the formation of macrophage foam cells induced by oxidized low density lipoprotein (ox-LDL). Results showed that PM2.5 induced cytotoxicity by decreasing the cell viability and increasing the LDH level in macrophage foam cells. PM2.5 aggravated the lipid accumulation in ox-LDL-stimulated macrophage RAW264.7 within markedly increasing level of intracellular lipid by Oil red O staining. The level of ROS increased obivously after co-exposure to PM2.5 and ox-LDL than single exposure group. In addition, serious mitochondrial damage such as the mitochondrial swelling, cristae rupturing and disappearance were observed in macrophage foam cells. The loss of the mitochondrial membrane potential (MMP) further exacerbated the mitochondrial damage in PM2.5-induced macrophage foam cells. The apoptotic rate increased more severely via up-regulated protein level of Bax, Cyt C, Caspase-9, Caspase-3, and down-regulated that of Bcl-2, indicating that PM2.5 activated the mitochondrial-mediated apoptosis pathway. In summary, our results demonstrated that PM2.5 aggravated the lipid accumulation, mitochondrial damage and apoptosis in macrophage foam cells, suggesting that PM2.5 was a risk factor of atherosclerosis progression.