Abstract
The aim is to investigate the molecular mechanisms underlying the PM2.5-induced autophagy in human lung cancer epithelial cells (A549). The effects of the PM2.5 on morphological and biochemical markers of autophagy in A549 were analyzed by electron microscopy, GFP-LC3 puncta was observed by confocal fluorescence microscope. The effects of phosphorylation of AMPK, mTOR, AKT, ERK, JNK, and p53 on LC3II in A549 were observed following PM2.5 exposure; the role of autophagy in PM2.5-induced apoptosis was examined using 3-methyladenine and rapamycin. PM2.5 induced morphological and biochemical markers of autophagy in A549. Phosphorylation of AMPK and dephosphorylation of mTOR were observed following PM2.5 treatment, and AMPK inhibitor blocked LC3B-II expression. In addition, we demonstrated that PM2.5-induced autophagy confers a pro-survival role in host defense.
Original language | English (US) |
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Pages (from-to) | 58-72 |
Number of pages | 15 |
Journal | International Journal of Clinical and Experimental Medicine |
Volume | 8 |
Issue number | 1 |
State | Published - Jan 30 2015 |
Keywords
- A549
- Autophagy
- COPD
- Oxidative stress
- PM
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology