PMID- 28729914
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220330
IS  - 2081-3856 (Print)
IS  - 2081-6936 (Electronic)
IS  - 2081-6936 (Linking)
VI  - 8
DP  - 2017
TI  - Effects of mTOR on Neurological Deficits after Transient Global Ischemia.
PG  - 21-26
LID - 10.1515/tnsci-2017-0005 [doi]
AB  - Mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase and 
      activation of its signal pathway plays an important role in regulating protein 
      growth and synthesis as well as cell proliferation and survival. In the present 
      study, we examined the contribution of mTOR and its downstream products to brain 
      injuries and neurological deficiencies after cardiac arrest (CA) 
      induced-transient global ischemia. CA was induced by asphyxia followed by 
      cardiopulmonary resuscitation (CPR) in rats. Our results showed that expression 
      of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1) and p70 
      ribosomal S6 protein kinase 1 (S6K1) pathways were amplified in CA rats compared 
      to their controls. Blocking mTOR using rapamycin attenuated upregulation of 
      pro-inflammatory cytokines (namely IL-1beta, IL-6 and TNF-alpha), and Caspase-3, 
      indicating cell apoptosis and also promoting the levels of vascular endothelial 
      growth factor (VEGF) and its subtype receptor VEGFR-2 in the hippocampus. 
      Moreover, the effects of rapamycin were linked to improvement of neurological 
      deficits and increased brain water content observed in CA rats. In conclusion, 
      activation of mTOR signal is engaged in pathophysiological process during 
      CA-induced transient global ischemia and blocking mTOR pathway plays a beneficial 
      role in regulating injured neuronal tissues and neurological deficits via PIC, 
      apoptotic Caspase-3 and VEGF mechanisms. Targeting one or more of these specific 
      mTOR pathways and its downstream signaling molecules may present new 
      opportunities for neural dysfunction and vulnerability related to transient 
      global ischemia.
FAU - Xing, Jihong
AU  - Xing J
AD  - Department of Emergency Medicine, The First Hospital of Jilin University, 
      Changchun, Jilin 130021, China.
FAU - Lu, Jian
AU  - Lu J
AD  - Department of Abdominal Surgery, Jilin Province Carcinoma Hospital, Changchun, 
      Jilin 130021, China.
LA  - eng
PT  - Journal Article
DEP - 20170430
PL  - Germany
TA  - Transl Neurosci
JT  - Translational neuroscience
JID - 101550327
PMC - PMC5443888
OTO - NOTNLM
OT  - Caspase-3
OT  - cardiac arrest
OT  - cardiopulmonary resuscitation
OT  - cytokines
OT  - hippocampus
OT  - mTOR
OT  - rapamycin
COIS- Conflict of interests None
EDAT- 2017/07/22 06:00
MHDA- 2017/07/22 06:01
PMCR- 2017/04/30
CRDT- 2017/07/22 06:00
PHST- 2017/03/02 00:00 [received]
PHST- 2017/04/03 00:00 [accepted]
PHST- 2017/07/22 06:00 [entrez]
PHST- 2017/07/22 06:00 [pubmed]
PHST- 2017/07/22 06:01 [medline]
PHST- 2017/04/30 00:00 [pmc-release]
AID - tnsci-2017-0005 [pii]
AID - 10.1515/tnsci-2017-0005 [doi]
PST - epublish
SO  - Transl Neurosci. 2017 Apr 30;8:21-26. doi: 10.1515/tnsci-2017-0005. eCollection 
      2017.