PMID- 25845384
OWN - NLM
STAT- MEDLINE
DCOM- 20160303
LR  - 20211203
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 12
IP  - 2
DP  - 2015 Aug
TI  - Particulate matter 2.5 induces autophagy via inhibition of the 
      phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin kinase signaling 
      pathway in human bronchial epithelial cells.
PG  - 1914-22
LID - 10.3892/mmr.2015.3577 [doi]
AB  - Particulate matter 2.5 (PM2.5) is a significant risk factor for asthma. A recent 
      study revealed that autophagy was associated with asthma pathogenesis. However, 
      the specific mechanisms underlying PM2.5-induced autophagy in asthma have 
      remained elusive. In the present study, PM2.5-induced autophagy was evaluated in 
      Beas-2B human bronchial epithelial cells and the potential molecular mechanisms 
      were investigated. Using electron microscopy, immunofluorescence staining and 
      immunoblot studies, it was confirmed that PM2.5 induced autophagy in Beas-2B 
      cells as a result of PM2.5-mediated inhibition of the phosphatidylinositol 
      3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway in Beas-2B 
      cells. LY294002, a PI3K inhibitor, reduced the accumulation of 
      microtubule-associated protein 1 light chain 3 II and attenuated the effect of 
      PM2.5. Phosphorylated (p-)p38, p-extracellular signal-regulated kinase and 
      p-c-Jun N-terminal kinase were dephosphorylated following exposure to PM2.5. The 
      roles of p53, reactive oxygen species scavenger tetramethylthiourea and autophagy 
      inhibitor 3-methyladenine in PM2.5-induced autophagy in Beas-2B cells were also 
      investigated. The results suggested that the PI3K/Akt/mTOR signaling pathway may 
      be a key contributor to PM2.5-induced autophagy in Beas-2B cells. The results of 
      the present study therefore provided an a insight into potential future clinical 
      applications targeting these signaling pathways, for the prevention and/or 
      treatment of PM2.5-induced lung diseases.
FAU - Liu, Tie
AU  - Liu T
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Wu, Bin
AU  - Wu B
AD  - Department of Respiratory Medicine, Affiliated Hospital of Guangdong Medical 
      College, Zhanjiang, Guangdong 524001, P.R. China.
FAU - Wang, Yahong
AU  - Wang Y
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - He, Huijuan
AU  - He H
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Lin, Ziying
AU  - Lin Z
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Tan, Jianxin
AU  - Tan J
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Yang, Lawei
AU  - Yang L
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Kamp, David W
AU  - Kamp DW
AD  - Department of Medicine, Division of Pulmonary and Critical Care Medicine, 
      Northwestern University Feinberg School of Medicine and Jesse Brown VA Medical 
      Center, Chicago, IL 60611, USA.
FAU - Zhou, Xu
AU  - Zhou X
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Tang, Jinfeng
AU  - Tang J
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Huang, Haili
AU  - Huang H
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Zhang, Liangqing
AU  - Zhang L
AD  - Department of Immunology and Tumor Research Institute, The First Affiliated 
      Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shanxi 710061, P.R. 
      China.
FAU - Bin, Liu
AU  - Bin L
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
FAU - Liu, Gang
AU  - Liu G
AD  - Clinical Research Center, Guangdong Medical College, Zhanjiang, Guangdong 524001, 
      P.R. China.
LA  - eng
GR  - P30 CA060553/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150331
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Air Pollutants)
RN  - 0 (Particulate Matter)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Air Pollutants/chemistry/*toxicity
MH  - Autophagy/*drug effects
MH  - Bronchi/cytology/drug effects/metabolism
MH  - Cell Line
MH  - Epithelial Cells/cytology/drug effects/metabolism
MH  - Humans
MH  - Lung Diseases/chemically induced/etiology
MH  - Particulate Matter/chemistry/*toxicity
MH  - Phosphatidylinositol 3-Kinase/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Respiratory Mucosa/*cytology/drug effects/metabolism
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/*metabolism
PMC - PMC6918810
EDAT- 2015/04/08 06:00
MHDA- 2016/03/05 06:00
PMCR- 2016/08/01
CRDT- 2015/04/08 06:00
PHST- 2014/05/14 00:00 [received]
PHST- 2015/02/11 00:00 [accepted]
PHST- 2015/04/08 06:00 [entrez]
PHST- 2015/04/08 06:00 [pubmed]
PHST- 2016/03/05 06:00 [medline]
PHST- 2016/08/01 00:00 [pmc-release]
AID - mmr-12-02-1914 [pii]
AID - 10.3892/mmr.2015.3577 [doi]
PST - ppublish
SO  - Mol Med Rep. 2015 Aug;12(2):1914-22. doi: 10.3892/mmr.2015.3577. Epub 2015 Mar 
      31.