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

AMPK is required for PM_2.5-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

Medicine, Pulmonary Division

Research output: Contribution to journal › Article › peer-review

50 Scopus citations

Abstract

The aim is to investigate the molecular mechanisms underlying the PM_2.5-induced autophagy in human lung cancer epithelial cells (A549). The effects of the PM_2.5 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 PM_2.5 exposure; the role of autophagy in PM_2.5-induced apoptosis was examined using 3-methyladenine and rapamycin. PM_2.5 induced morphological and biochemical markers of autophagy in A549. Phosphorylation of AMPK and dephosphorylation of mTOR were observed following PM_2.5 treatment, and AMPK inhibitor blocked LC3B-II expression. In addition, we demonstrated that PM_2.5-induced autophagy confers a pro-survival role in host defense.

Original language	English (US)
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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Cite this

@article{52d3cf1545ce4899b755b2447ef38edf,

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

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.",

keywords = "A549, Autophagy, COPD, Oxidative stress, PM",

author = "Yahong Wang and Ziying Lin and Haili Huang and Huijuan He and Lawei Yang and Ting Chen and Teng Yang and Nina Ren and Yun Jiang and Wenya Xu and Kamp, {David W.} and Tie Liu and Gang Liu",

year = "2015",

month = jan,

day = "30",

language = "English (US)",

volume = "8",

pages = "58--72",

journal = "International Journal of Clinical and Experimental Medicine",

issn = "1940-5901",

publisher = "e-Century Publishing Corporation",

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}

TY - JOUR

T1 - AMPK is required for PM2.5-induced autophagy in human lung epithelial A549 cells

AU - Wang, Yahong

AU - Lin, Ziying

AU - Huang, Haili

AU - He, Huijuan

AU - Yang, Lawei

AU - Chen, Ting

AU - Yang, Teng

AU - Ren, Nina

AU - Jiang, Yun

AU - Xu, Wenya

AU - Kamp, David W.

AU - Liu, Tie

AU - Liu, Gang

PY - 2015/1/30

Y1 - 2015/1/30

N2 - 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.

AB - 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.

KW - A549

KW - Autophagy

KW - COPD

KW - Oxidative stress

KW - PM

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