PMID- 29466698
OWN - NLM
STAT- MEDLINE
DCOM- 20180709
LR  - 20211204
IS  - 0925-4439 (Print)
IS  - 0925-4439 (Linking)
VI  - 1864
IP  - 5 Pt A
DP  - 2018 May
TI  - ERK1/2/mTOR/Stat3 pathway-mediated autophagy alleviates traumatic brain 
      injury-induced acute lung injury.
PG  - 1663-1674
LID - S0925-4439(18)30068-1 [pii]
LID - 10.1016/j.bbadis.2018.02.011 [doi]
AB  - Acute lung injury (ALI) is one of several complications in patients with 
      traumatic brain injury (TBI). Autophagy is a primary homeostatic process that 
      promotes cell survival under stress. Accumulating evidence implicates autophagy 
      in the pathogenesis of ALI under various conditions. However, the role of 
      autophagy in TBI-induced ALI remains unknown. The aim of this study was to adjust 
      autophagy with pharmacological agents to determine its functional significance in 
      TBI-induced ALI. Rats were preconditioned with autophagy promoter rapamycin or 
      inhibitor 3-methyladenine before they were challenged with TBI. Extracellular 
      signal-regulated kinase 1/2 (ERK1/2) inhibitor U0126, mechanistic target of 
      rapamycin (mTOR) inhibitor rapamycin, and signal transducer and activator of 
      transcription 3 (Stat3) inhibitor S31-201 were used to test the role of 
      ERK1/2/mTOR/Stat3 signaling pathway in regulating autophagy. Autophagy is 
      activated in lung tissues after TBI. Enhancement of autophagy suppressed 
      apoptosis, inflammation and oxidative stress in lung tissues, which were 
      activated after TBI, whereas inhibition of autophagy aggravated these critical 
      pathological changes. Autophagy also improved TBI-induced impairment in pulmonary 
      barrier function, oxygenation function and static compliance. Furthermore, 
      TBI-induced autophagy was mediated by ERK1/2/mTOR/Stat3 pathway, which may serve 
      to reduce ALI and improve pulmonary barrier function, oxygenation function and 
      static compliance. These findings are important for the prevention and treatment 
      of TBI-induced ALI.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Xu, Xiupeng
AU  - Xu X
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Zhi, Tongle
AU  - Zhi T
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Chao, Honglu
AU  - Chao H
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Jiang, Kuan
AU  - Jiang K
AD  - Department of Neurosurgery, Yixing People's Hospital, Yixing, Jiangsu, China.
FAU - Liu, Yinlong
AU  - Liu Y
AD  - Department of Neurosurgery, Suzhou Municipal Hospital, Suzhou, Jiangsu, China.
FAU - Bao, Zhongyuan
AU  - Bao Z
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Fan, Liang
AU  - Fan L
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Wang, Dong
AU  - Wang D
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Li, Zheng
AU  - Li Z
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Liu, Ning
AU  - Liu N
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China.
FAU - Ji, Jing
AU  - Ji J
AD  - Department of Neurosurgery, the First Affiliated Hospital of Nanjing Medical 
      University, Nanjing, Jiangsu, China. Electronic address: jijing@njmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180218
PL  - Netherlands
TA  - Biochim Biophys Acta Mol Basis Dis
JT  - Biochimica et biophysica acta. Molecular basis of disease
JID - 101731730
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (Stat3 protein, rat)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
SB  - IM
EIN - Biochim Biophys Acta. 2018 Apr 12;:. PMID: 29656877
MH  - Acute Lung Injury/etiology/*metabolism/pathology
MH  - Animals
MH  - Apoptosis
MH  - *Autophagy
MH  - Brain Injuries, Traumatic/complications/*metabolism/pathology
MH  - Lung/metabolism/pathology
MH  - *MAP Kinase Signaling System
MH  - Male
MH  - Mitogen-Activated Protein Kinase 3/antagonists & inhibitors/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - STAT3 Transcription Factor/*metabolism
MH  - TOR Serine-Threonine Kinases/antagonists & inhibitors/*metabolism
OTO - NOTNLM
OT  - Acute lung injury
OT  - Apoptosis
OT  - Autophagy
OT  - Inflammation
OT  - Oxidative stress
OT  - Traumatic brain injury
EDAT- 2018/02/22 06:00
MHDA- 2018/07/10 06:00
CRDT- 2018/02/22 06:00
PHST- 2017/08/07 00:00 [received]
PHST- 2018/01/21 00:00 [revised]
PHST- 2018/02/15 00:00 [accepted]
PHST- 2018/02/22 06:00 [pubmed]
PHST- 2018/07/10 06:00 [medline]
PHST- 2018/02/22 06:00 [entrez]
AID - S0925-4439(18)30068-1 [pii]
AID - 10.1016/j.bbadis.2018.02.011 [doi]
PST - ppublish
SO  - Biochim Biophys Acta Mol Basis Dis. 2018 May;1864(5 Pt A):1663-1674. doi: 
      10.1016/j.bbadis.2018.02.011. Epub 2018 Feb 18.