p38 MAPK Participates in the Mediation of GLT-1 Up-regulation During the Induction of Brain Ischemic Tolerance by Cerebral Ischemic Preconditioning

Our previous study has proved that the up-regulation of glial glutamate transporter 1 (GLT-1) played an important role in the acquisition of brain ischemic tolerance after cerebral ischemic preconditioning (CIP) in rats. However, little is known about the mechanism involved in the up-regulation of G...

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Published in:Molecular neurobiology 2017-01, Vol.54 (1), p.58-71
Main Authors: Zhang, Min, Gong, Jian-Xue, Wang, Jia-Lei, Jiang, Meng-Yang, Li, Li, Hu, Yu-Yan, Qi, Jie, Zhang, Ling-Yan, Zhao, Hang, Cui, Xin, Xian, Xiao-Hui, Li, Wen-Bin
Format: Article
Language:English
Subjects:
Animals
Biomedical and Life Sciences
Biomedicine
Brain
Brain Ischemia - metabolism
Brain Ischemia - pathology
Cell Biology
Excitatory Amino Acid Transporter 2 - biosynthesis
Hippocampus - metabolism
Hippocampus - pathology
Ischemia
Ischemic Preconditioning - methods
Male
Neurobiology
Neurology
Neurosciences
p38 Mitogen-Activated Protein Kinases - metabolism
Rats
Rats, Wistar
Rodents
Studies
Up-Regulation - physiology
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Summary:Our previous study has proved that the up-regulation of glial glutamate transporter 1 (GLT-1) played an important role in the acquisition of brain ischemic tolerance after cerebral ischemic preconditioning (CIP) in rats. However, little is known about the mechanism involved in the up-regulation of GLT-1 in the process. The present study investigates whether p38 MAPK, ERK1/2, and/or JNK participates in the up-regulation of GLT-1 during the induction of brain ischemic tolerance by CIP. It was found that CIP significantly enhanced the expression of p-p38 MAPK without altering p-ERK1/2 and p-JNK expression in the CA1 hippocampus. Inhibition of p38 MAPK function by its selective inhibitor SB203580 or knockdown p38 MAPK expression by its antisense oligodeoxynucleotides (AS-ODNs) suppressed the induction of brain ischemic tolerance. Furthermore, p38 MAPK was activated earlier than the up-regulation of GLT-1 in the CA1 hippocampus after CIP. Meanwhile, the expression of p-p38 MAPK by astrocytes was increased, and p38 MAPK AS-ODNs dose-dependently inhibited the up-regulation of GLT-1 after CIP. Taken together, it could be concluded that p38 MAPK participates in the mediation of GLT-1 up-regulation during the induction of brain ischemic tolerance after CIP.
ISSN:0893-7648
1559-1182
DOI:10.1007/s12035-015-9652-x