PMID- 25637490
OWN - NLM
STAT- MEDLINE
DCOM- 20151215
LR  - 20150313
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 290
DP  - 2015 Apr 2
TI  - Over-expressed EGR1 may exaggerate ischemic injury after experimental stroke by 
      decreasing BDNF expression.
PG  - 509-17
LID - S0306-4522(15)00075-5 [pii]
LID - 10.1016/j.neuroscience.2015.01.020 [doi]
AB  - PURPOSE: This study aimed to clarify whether ischemia-induced early growth 
      response 1 (EGR1) influenced the outcomes of experimental stroke by regulating 
      brain-derived neurotrophic factor (BDNF) expression. METHODS AND RESULTS: To 
      mimic ischemia, mice were subjected to middle cerebral artery occlusion, and 
      neurons challenged with oxygen-glucose deprivation. The expression of EGR1 was 
      increased immediately and reached the peak 24h after reperfusion. To increase and 
      to decrease EGR1 expressions, two types of recombinant lentiviruses were 
      constructed. EGR1 over-expression induced by recombinant lentiviruses expanded 
      infarct volumes and increased the numbers of terminal deoxynucleoitidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) and Fluoro-Jade C-positive 
      cells; while decreased EGR1 expression induced by recombinant lentiviruses 
      diminished infarct volumes and decreased the numbers of TUNEL- and Fluoro-Jade 
      C-positive cells. Both in vitro and in vivo, increasing EGR1 expression with 
      recombinant lentiviruses lead to decreased BDNF expressions; while silencing EGR1 
      expression with recombinant lentiviruses lead to increased BDNF expressions. 
      Results from electrophoretic mobility shift assay indicated that EGR1 influenced 
      the BDNF expression by binding to its promoter. CONCLUSION: Ischemia-induced EGR1 
      expression may exaggerate brain injury by reducing BDNF expression. Inhibiting 
      EGR1 may become a potential treatment for improving outcomes of ischemic stroke.
CI  - Copyright (c) 2015 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Yang, L
AU  - Yang L
AD  - Department of Neurology, Jinling Hospital, Southern Medical University, Nanjing, 
      Jiangsu, China.
FAU - Jiang, Y
AU  - Jiang Y
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Wen, Z
AU  - Wen Z
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Xu, X
AU  - Xu X
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Xu, X
AU  - Xu X
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Zhu, J
AU  - Zhu J
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Xie, X
AU  - Xie X
AD  - Department of Neurology, Jinling Hospital, Southern Medical University, Nanjing, 
      Jiangsu, China.
FAU - Xu, L
AU  - Xu L
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Xie, Y
AU  - Xie Y
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Liu, X
AU  - Liu X
AD  - Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 
      Nanjing, Jiangsu, China.
FAU - Xu, G
AU  - Xu G
AD  - Department of Neurology, Jinling Hospital, Southern Medical University, Nanjing, 
      Jiangsu, China; Department of Neurology, Jinling Hospital, Medical School of 
      Nanjing University, Nanjing, Jiangsu, China. Electronic address: 
      gelinxu@gmail.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150128
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (EGR1 protein, human)
RN  - 0 (Early Growth Response Protein 1)
RN  - 0 (Egr1 protein, mouse)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Brain/*metabolism/pathology
MH  - Brain Ischemia/*metabolism/pathology
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cell Hypoxia/physiology
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Early Growth Response Protein 1/genetics/*metabolism
MH  - Gene Transfer Techniques
MH  - Glucose/deficiency
MH  - Humans
MH  - Infarction, Middle Cerebral Artery
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Neurons/metabolism/pathology
MH  - Stroke/*metabolism/pathology
OTO - NOTNLM
OT  - BDNF
OT  - EGR1
OT  - infarct volume
OT  - ischemic stroke
EDAT- 2015/02/01 06:00
MHDA- 2015/12/17 06:00
CRDT- 2015/02/01 06:00
PHST- 2014/11/06 00:00 [received]
PHST- 2015/01/03 00:00 [revised]
PHST- 2015/01/18 00:00 [accepted]
PHST- 2015/02/01 06:00 [entrez]
PHST- 2015/02/01 06:00 [pubmed]
PHST- 2015/12/17 06:00 [medline]
AID - S0306-4522(15)00075-5 [pii]
AID - 10.1016/j.neuroscience.2015.01.020 [doi]
PST - ppublish
SO  - Neuroscience. 2015 Apr 2;290:509-17. doi: 10.1016/j.neuroscience.2015.01.020. 
      Epub 2015 Jan 28.