PMID- 32715876
OWN - NLM
STAT- MEDLINE
DCOM- 20210514
LR  - 20211204
IS  - 1473-2300 (Electronic)
IS  - 0300-0605 (Print)
IS  - 0300-0605 (Linking)
VI  - 48
IP  - 7
DP  - 2020 Jul
TI  - The PI3K/AKT/mTOR pathway regulates autophagy to induce apoptosis of alveolar 
      epithelial cells in chronic obstructive pulmonary disease caused by PM2.5 
      particulate matter.
PG  - 300060520927919
LID - 10.1177/0300060520927919 [doi]
LID - 0300060520927919
AB  - OBJECTIVE: Many lung diseases are associated with changes in autophagic activity. 
      The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target 
      of rapamycin (mTOR) signaling pathway plays a key regulatory role in autophagy. 
      Our aim was to explore the function of PI3K/AKT/mTOR pathway on autophagy in 
      chronic obstructive pulmonary disease (COPD) caused by particulate matter with a 
      diameter <2.5 microm (PM2.5). METHODS: Male C57BL/6 mice were randomly divided into 
      sham, model, and PI3K inhibitor groups. Mice were exposed to PM2.5 for 4 weeks to 
      establish an in vivo COPD model. Alveolar epithelial cells were stimulated with 
      PM2.5 to establish an in vitro COPD model. RESULTS: In mice with COPD induced by 
      PM2.5, the PI3K inhibitor PF-04979064 suppressed protein expression of PI3K, 
      p-AKT, and p-mTOR to increase apoptosis of alveolar epithelial cells and reduce 
      autophagy. Short interfering PI3K suppressed the PI3K/AKT/mTOR pathway to induce 
      apoptosis and reduce autophagy of alveolar epithelial cells in an in vitro model 
      of COPD. Activation of PI3K induced the PI3K/AKT/mTOR pathway to reduce apoptosis 
      of alveolar epithelial cells in the in vitro model of COPD by promoting 
      autophagy. CONCLUSIONS: These data demonstrate that PI3K/AKT/mTOR pathway 
      regulates autophagy to induce apoptosis of alveolar epithelial cells in COPD.
FAU - Zhang, Fang
AU  - Zhang F
AUID- ORCID: 0000-0002-2615-2251
AD  - Department of Respiration, Gansu Province People Hospital, Lanzhou City, Gansu 
      Province, China.
FAU - Ma, Hui
AU  - Ma H
AD  - Department of Respiratory, Gansu Province People Hospital, Lanzhou City, Gansu 
      Province, China.
FAU - Wang, Zhong Lan
AU  - Wang ZL
AD  - Department of Respiratory Diseases, Gansu Province People Hospital, Lanzhou City, 
      Gansu Province, China.
FAU - Li, Wei Hua
AU  - Li WH
AD  - Department of Central Laboratory, Gansu Province People Hospital, Lanzhou City, 
      Gansu Province, China.
FAU - Liu, Hua
AU  - Liu H
AD  - Department of Respiration, Gansu Province People Hospital, Lanzhou City, Gansu 
      Province, China.
FAU - Zhao, Yan Xia
AU  - Zhao YX
AD  - Department of Respiration, Gansu Province People Hospital, Lanzhou City, Gansu 
      Province, China.
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Int Med Res
JT  - The Journal of international medical research
JID - 0346411
RN  - 0 (Particulate Matter)
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  - Alveolar Epithelial Cells
MH  - Animals
MH  - Apoptosis
MH  - Autophagy
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Particulate Matter/toxicity
MH  - Phosphatidylinositol 3-Kinase
MH  - Phosphatidylinositol 3-Kinases/genetics
MH  - *Proto-Oncogene Proteins c-akt/genetics
MH  - *Pulmonary Disease, Chronic Obstructive
MH  - TOR Serine-Threonine Kinases/genetics
PMC - PMC7385846
OTO - NOTNLM
OT  - Chronic obstructive pulmonary disease
OT  - PI3K/AKT/mTOR pathway
OT  - alveolar epithelial cells
OT  - autophagy
OT  - lung disease
OT  - particulate matter
EDAT- 2020/07/28 06:00
MHDA- 2021/05/15 06:00
PMCR- 2020/07/27
CRDT- 2020/07/28 06:00
PHST- 2020/07/28 06:00 [entrez]
PHST- 2020/07/28 06:00 [pubmed]
PHST- 2021/05/15 06:00 [medline]
PHST- 2020/07/27 00:00 [pmc-release]
AID - 10.1177_0300060520927919 [pii]
AID - 10.1177/0300060520927919 [doi]
PST - ppublish
SO  - J Int Med Res. 2020 Jul;48(7):300060520927919. doi: 10.1177/0300060520927919.