PMID- 30699428
OWN - NLM
STAT- MEDLINE
DCOM- 20200916
LR  - 20200916
IS  - 1423-0216 (Electronic)
IS  - 1021-7401 (Linking)
VI  - 26
IP  - 1
DP  - 2019
TI  - Astrocyte-Conditioned Medium Protects Prefrontal Cortical Neurons from 
      Glutamate-Induced Cell Death by Inhibiting TNF-alpha Expression.
PG  - 33-42
LID - 10.1159/000495211 [doi]
AB  - OBJECTIVE: Both excitotoxicity and neurotrophin deficiency may contribute to the 
      etiology of depression and neurodegeneration. Astrocytes not only regulate 
      glutamate metabolism and clearance, they also produce neurotrophins in the brain. 
      However, the direct interaction between neurons and astrocytes remains unknown. 
      METHODS: This study evaluated the cellular mechanisms by which 
      astrocyte-conditioned medium (ACM) protects prefrontal cortical neurons from 
      glutamate-induced death by measuring cell viability and morphology as well as 
      mRNA and protein expression of brain-derived neurotrophic factor (BDNF), BDNF 
      receptors, glial cell line-derived neurotrophic factor (GDNF), and the 
      proinflammatory cytokine, tumor necrosis factor (TNF)-alpha. Neurons and astrocytes 
      were purified from the brains of neonatal 1-day-old Sprague-Dawley rats. ACM was 
      harvested after exposing astrocytes to culture medium containing 100 muM glutamate 
      for 48 h. RESULTS: Glutamate insult (100 muM for 6 h) significantly reduced 
      neuronal cell viability and increased the mRNA expression of BDNF. Glutamate (24 
      h) decreased neuronal viability and the expression of BDNF, but increased mRNA 
      expression of GFAP, p75 neurotrophin receptor (p75NTR), and TNF-alpha. ACM 
      pretreatment (2 h) reversed glutamate-decreased cell viability and increased 
      BDNF, but reduced the expression of GDNF, P75NTR, and TNF-alpha at the mRNA level. 
      Western blotting generally confirmed the mRNA expression following 24 glutamate 
      insults. Furthermore, the glutamate-induced decrease in the protein expression of 
      BDNF and full-length TrkB receptor and increase in pro-BDNF, truncated TrkB 
      isoform 1 receptor, p75NTR, GDNF, and TNF-alpha were significantly attenuated by ACM 
      pretreatment. CONCLUSIONS: The study demonstrates that ACM exerts neuroprotective 
      effects on cell viability, and this effect is most likely mediated through the 
      modulation of neurotrophin and TNF-alpha expression.
CI  - (c) 2019 S. Karger AG, Basel.
FAU - Song, Cai
AU  - Song C
AD  - Research Institute for Marine Drugs and Nutrition, Food Science and Technology, 
      Guangdong Ocean University, Zhanjiang, China, cai.song@dal.ca.
AD  - Graduate Institute of Biomedical Sciences, College of Medicine, China Medical 
      University, and Departments of Medical Research, China Medical University 
      Hospital, Taichung, Taiwan, cai.song@dal.ca.
FAU - Wu, Yih-Shyuan
AU  - Wu YS
AD  - Graduate Institute of Biomedical Sciences, College of Medicine, China Medical 
      University, and Departments of Medical Research, China Medical University 
      Hospital, Taichung, Taiwan.
FAU - Yang, Zhi-You
AU  - Yang ZY
AD  - Research Institute for Marine Drugs and Nutrition, Food Science and Technology, 
      Guangdong Ocean University, Zhanjiang, China.
FAU - Kalueff, Allan V
AU  - Kalueff AV
AD  - Research Institute for Marine Drugs and Nutrition, Food Science and Technology, 
      Guangdong Ocean University, Zhanjiang, China.
AD  - Institute of Translational Biomedicine, St. Petersburg State University, St. 
      Petersburg, Russian Federation.
AD  - Ural Federal University, Ekaterinburg, Russian Federation.
FAU - Tsao, Yin-Yin
AU  - Tsao YY
AD  - Graduate Institute of Biomedical Sciences, College of Medicine, China Medical 
      University, and Departments of Medical Research, China Medical University 
      Hospital, Taichung, Taiwan.
FAU - Dong, Yilong
AU  - Dong Y
AD  - School of Medicine, Yunnan University, Kunming, China.
FAU - Su, Kuan-Pin
AU  - Su KP
AD  - Graduate Institute of Biomedical Sciences, College of Medicine, China Medical 
      University, and Departments of Medical Research, China Medical University 
      Hospital, Taichung, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190130
PL  - Switzerland
TA  - Neuroimmunomodulation
JT  - Neuroimmunomodulation
JID - 9422763
RN  - 0 (Bdnf protein, rat)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Gdnf protein, rat)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Astrocytes/*metabolism
MH  - Brain-Derived Neurotrophic Factor/drug effects/genetics/metabolism
MH  - Cell Death/*drug effects
MH  - Cell Survival/drug effects
MH  - Culture Media, Conditioned
MH  - Glial Cell Line-Derived Neurotrophic Factor/drug effects/genetics/metabolism
MH  - Glutamic Acid/*pharmacology
MH  - Neurons/*drug effects/metabolism
MH  - Prefrontal Cortex/cytology
MH  - RNA, Messenger/*drug effects/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/drug effects/genetics/metabolism
MH  - Tumor Necrosis Factor-alpha/*drug effects/genetics/metabolism
OTO - NOTNLM
OT  - Astrocytes
OT  - Cell viability
OT  - Glutamate
OT  - Neurotrophic factors
OT  - Tumor necrosis factor-alpha
EDAT- 2019/01/31 06:00
MHDA- 2020/09/17 06:00
CRDT- 2019/01/31 06:00
PHST- 2018/10/02 00:00 [received]
PHST- 2018/11/08 00:00 [accepted]
PHST- 2019/01/31 06:00 [pubmed]
PHST- 2020/09/17 06:00 [medline]
PHST- 2019/01/31 06:00 [entrez]
AID - 000495211 [pii]
AID - 10.1159/000495211 [doi]
PST - ppublish
SO  - Neuroimmunomodulation. 2019;26(1):33-42. doi: 10.1159/000495211. Epub 2019 Jan 
      30.