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Airborne nanoparticles (PM 0.1 ) induce autophagic cell death of human neuronal cells
Author(s) -
Jeon YuMi,
Lee MiYoung
Publication year - 2016
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.3324
Subject(s) - autophagy , viability assay , neurodegeneration , reactive oxygen species , programmed cell death , oxidative stress , microbiology and biotechnology , comet assay , chemistry , sh sy5y , dna damage , downregulation and upregulation , hsp70 , cell , heat shock protein , apoptosis , biology , biochemistry , cell culture , dna , medicine , neuroblastoma , genetics , disease , pathology , gene
Airborne nanoparticles PM 0.1 (<100 nm in diameter) were collected and their chemical composition was determined. Al was by far the most abundant metal in the PM 0.1 followed by Zn, Cr, Mn, Cu, Pb and Ni. Exposure to PM 0.1 resulted in a cell viability decrease in human neuronal cells SH‐SY5Y in a concentration‐dependent manner. Upon treatment with N‐acetylcysteine, however, cell viability was significantly recovered, suggesting the involvement of reactive oxygen species (ROS). Cellular DNA damage by PM 0.1 was also detected by the Comet assay. PM 0.1 ‐induced autophagic cell death was explained by an increase in the expression of microtubule‐associated protein light chain 3A‐ІІ (LC3A‐ІІ) and autophagy‐related protein Atg 3 and Atg 7. Analysis of 2‐DE gels revealed that six proteins were upregulated, whereas eight proteins were downregulated by PM 0.1 exposure. Neuroinflammation‐related lithostathine and cyclophilin A complexed with dipeptide Gly‐Pro, autophagy‐related heat shock protein gp96 and neurodegeneration‐related triosephosphate isomerase were significantly changed upon exposure to PM 0.1 . These results, taken together, suggest that PM 0.1 ‐induced oxidative stress via ROS generation plays a key role in autophagic cell death and differential protein expressions in SH‐SY5Y cells. This might provide a plausible explanation for the underlying mechanisms of PM 0.1 toxicity in neuronal cells and even the pathogenesis of diseases associated with its exposure. Copyright © 2016 John Wiley & Sons, Ltd.