下调和上调
液泡
自噬
氧化应激
焊剂(冶金)
自噬体
细胞生物学
化学
活性氧
生物
粒体自噬
溶酶体
程序性细胞死亡
线粒体
细胞凋亡
细胞内
衰老
神经退行性变
氧化磷酸化
未折叠蛋白反应
内质网
生物化学
细胞质
有机化学
基因
作者
Yan Wang,Ying Ma,Yongshuai Yao,Qing Liu,Yanting Pang,Meng Tang
标识
DOI:10.1016/j.envpol.2021.117295
摘要
Ambient particulate matter (APM) has been authenticated to exert hazards on human vascular endothelial cells, including abnormal autophagy. However, the potential reasons for autophagosome accumulation are still obscure. Since autophagy is a dynamic process, it is imperative to systemically consider the autophagic induction combined with its degradation to reflect realistic scenarios. Therefore, in the current study, different exposure durations were initially employed for the detection of autophagic marker proteins to assess the dynamic autophagic state preliminarily. Additionally, LC3 turn-over and autophagic flux assays were used to determine the specific cause of LC3II upregulation in EA.hy926 human vascular endothelial cells by a type of standard urban particulate matter, PM SRM1648a. As a result, PM SRM1648a stimulates excess autophagic vacuoles in EA. hy926 cells, in which the underlying causes are probably different at varying incubation endpoints. Intriguingly, LC3II upregulation was due to the intensifying autophagic initiation after 6 h of exposure, whereas as exposure period was extended to 24 h, overloaded autophagic vacuoles were attributed to the defective autophagy. Mechanistically, PM SRM1648a damages EA. hy926 cells by inducing lysosomal disequilibrium and resultant autophagic malfunction which are not directly mediated by oxidative stress. These data indicate that appropriate maintenance of lysosomal function and autophagic flux is probably a protective measure against APM-induced endothelial cell damage.
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