PMID- 27532878
OWN - NLM
STAT- MEDLINE
DCOM- 20180108
LR  - 20211204
IS  - 1473-558X (Electronic)
IS  - 0959-4965 (Linking)
VI  - 27
IP  - 14
DP  - 2016 Sep 28
TI  - Protective effects of transient receptor potential canonical channels on 
      oxygen-glucose deprivation-induced cell injury in neurons and PC12 cells.
PG  - 1072-80
LID - 10.1097/WNR.0000000000000659 [doi]
AB  - Hypoxic-ischemic encephalopathy (HIE) is a serious clinical problem, responsible 
      for many cases of motor impairment, cognitive deficits, and mortality. Transient 
      receptor potential canonical (TRPC) channels are nonselective cation channels 
      that play a role in many disorders, including trauma, pulmonary hypertension, and 
      excitotoxicity. However, the properties and underlying mechanisms of TRPC 
      channels in HIE are still controversial. Extracellular signal-regulated kinase 
      (ERK) and mammalian target of rapamycin (mTOR) are central signaling pathways 
      that transmit signals from extracellular to intracellular agents and mediate 
      prosurvival, proliferation, and motility proteins. The relationship between TRPC 
      channels, ERK, and mTOR is unclear. We used oxygen-glucose 
      deprivation/reoxygenation in primary cortical neurons and PC12 cells to mimic an 
      HIE episode. The potential effects and mechanisms of TRPC channels were examined. 
      MNC (M: MK-801; N: nimodipine; C: CNQX) were used to exclude the interference of 
      N-methyl-D-aspartate receptors, AMPK receptors, and calcium channels. We 
      administered TRPC inhibitor SKF96365 to the cells, and then measured cell 
      apoptosis and expression of ERK and mTOR signal pathways. At the same time, an 
      ERK inhibitor or an mTOR agonist was used to further ensure the relation between 
      TRPC channels and ERK, mTOR. Results showed that hypoxia-ischemia clearly induced 
      cell apoptosis, activated the ERK pathway, and suppressed the mTOR pathway. 
      Blocking of TRPC channels could enhance hypoxia-ischemia-induced apoptosis and 
      lead to increased p-ERK pathway activity and decreased p-mTOR pathway activity. 
      However, the ERK inhibitor or the mTOR agonist could reverse the effect of 
      SKF96365. This study suggests that TRPC channels may be an effective treatment 
      for HIE, regulating the ERK and mTOR pathways.
FAU - Wang, Yan
AU  - Wang Y
AD  - Institute of Neuroscience, Basic Medical College, Chongqing Medical University, 
      Chongqing, People's Republic of China.
FAU - Li, Yingbo
AU  - Li Y
FAU - Di, Chen
AU  - Di C
FAU - Liu, Tu
AU  - Liu T
FAU - Hou, Qianlin
AU  - Hou Q
FAU - Wang, Shali
AU  - Wang S
LA  - eng
PT  - Journal Article
PL  - England
TA  - Neuroreport
JT  - Neuroreport
JID - 9100935
RN  - 0 (Annexin A5)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Flavonoids)
RN  - 0 (Imidazoles)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Transient Receptor Potential Channels)
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 (Extracellular Signal-Regulated MAP Kinases)
RN  - I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole)
RN  - IY9XDZ35W2 (Glucose)
RN  - SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one)
SB  - IM
MH  - Animals
MH  - Annexin A5/metabolism
MH  - Apoptosis/drug effects/physiology
MH  - Calcium Channel Blockers/pharmacology
MH  - Cell Hypoxia/drug effects
MH  - Cells, Cultured
MH  - Cerebral Cortex/cytology
MH  - Dose-Response Relationship, Drug
MH  - Embryo, Mammalian
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Flavonoids/pharmacology
MH  - Glucose/*deficiency
MH  - Imidazoles/pharmacology
MH  - Neurons/drug effects/*metabolism
MH  - PC12 Cells
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Rats
MH  - Signal Transduction/drug effects/physiology
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Transient Receptor Potential Channels/*metabolism
EDAT- 2016/08/18 06:00
MHDA- 2018/01/09 06:00
CRDT- 2016/08/18 06:00
PHST- 2016/08/18 06:00 [entrez]
PHST- 2016/08/18 06:00 [pubmed]
PHST- 2018/01/09 06:00 [medline]
AID - 10.1097/WNR.0000000000000659 [doi]
PST - ppublish
SO  - Neuroreport. 2016 Sep 28;27(14):1072-80. doi: 10.1097/WNR.0000000000000659.