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- W3023805943 endingPage "122608" @default.
- W3023805943 startingPage "122608" @default.
- W3023805943 abstract "Abstract Epidemiological studies revealed a sharp increase in respiratory diseases attributed to PM2.5. However, the underlying mechanisms remain unclear. Evidence suggested mitochondrion as a sensitive target upon the stimulus of PM2.5, and the centrality in the pathological processes and clinical characterization of lung diseases. To investigate cell fate and related mechanisms caused by PM2.5, we exposed human lung epithelial cells (BEAS-2B) to PM2.5 (0-100 μg/mL). Consequently, PM2.5 components were found in cytoplasm, and morphological and functional alterations in mitochondria occurred, as evidenced by loss of cristae, vacuolization and even the outer mitochondrial membrane rupture, mitochondrial membrane potential collapse, enhanced reactive oxygen species (ROS)/mtROS level, calcium overload, suppressed cellular respiration and ATP production in PM2.5-treated cells. Further, disturbed dynamics toward fission was clearly observed in PM2.5-treated mitochondria, associated with DRP1 mitochondrial translocation and phosphorylation. Besides, PM2.5 induced mitochondria-mediated apoptosis. More importantly, mechanistic results revealed ROS- and DRP1-mediated mitochondrial fission in a reciprocal way, and DRP1 inhibitor (Mdivi-1) significantly alleviated the pro-apoptotic effect of PM2.5 through reversing the activated mitochondrial apoptotic pathway. In summary, our results firstly revealed PM2.5 induced apoptosis in lung epithelial cells through a ROS-DRP1-mitochodrial fission axis-mediated mitochondrial apoptotic pathway, ultimately contributing to the onset and development of pulmonary diseases." @default.
- W3023805943 created "2020-05-13" @default.
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- W3023805943 date "2020-10-01" @default.
- W3023805943 modified "2023-10-17" @default.
- W3023805943 title "PM2.5 triggered apoptosis in lung epithelial cells through the mitochondrial apoptotic way mediated by a ROS-DRP1-mitochondrial fission axis" @default.
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- W3023805943 doi "https://doi.org/10.1016/j.jhazmat.2020.122608" @default.
- W3023805943 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32387827" @default.
- W3023805943 hasPublicationYear "2020" @default.
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