AMPK is required for PM2.5-induced autophagy in human lung epithelial A549 cells

Yahong Wang, Ziying Lin, Haili Huang, Huijuan He, Lawei Yang, Ting Chen, Teng Yang, Nina Ren, Yun Jiang, Wenya Xu, David W. Kamp, Tie Liu, Gang Liu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


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 languageEnglish (US)
Pages (from-to)58-72
Number of pages15
JournalInternational Journal of Clinical and Experimental Medicine
Issue number1
StatePublished - Jan 30 2015


  • A549
  • Autophagy
  • COPD
  • Oxidative stress
  • PM

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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