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Major role of the PI3K/Akt pathway in ischemic tolerance induced by sublethal oxygen-glucose deprivation in cortical neurons in vitro.
MedLine Citation:
PMID:  21725824     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Ischemic preconditioning can provide protection to neurons from subsequent lethal ischemia. The molecular mechanisms of neuronal ischemic tolerance, however, are still not well-known. The present study, therefore, examined the role of MAPK and PI3K/Akt pathways in ischemic tolerance induced by preconditioning with sublethal oxygen-glucose deprivation (OGD) in cultured rat cortical neurons. Ischemic tolerance was simulated by preconditioning of the neurons with sublethal 1-h OGD imposed 12 h before lethal 3-h OGD. The time-course studies of relative phosphorylation and expression levels of ERK1/2, JNK and p38 MAPK showed lack of their involvement in ischemic tolerance. However, there were significant increases in Akt phosphorylation levels during the reperfusion period following preconditioned lethal OGD. In addition, Bcl-2 associated death promoter (Bad) and GSK-3β were also found to be inactivated during that reperfusion period. Finally, treatment with an inhibitor of PI3K, wortmannin, applied from 15 min before and during lethal OGD abolished not only the preconditioning-induced neuroprotection but also the Akt activation. Concomitant with blockade of the Akt activation, PI3K inhibition also resulted in activation of Bad and GSK-3β. The results suggest that ischemic tolerance induced by sublethal OGD preconditioning is primarily mediated through activation of the PI3K/Akt pathway, but not the MAPK pathway, in rat cortical neurons.
Authors:
Mohammad Iqbal Hossain Bhuiyan; Seo Yun Jung; Hyoung Ja Kim; Yong Sup Lee; Changbae Jin
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Publication Detail:
Type:  Journal Article     Date:  2011-07-02
Journal Detail:
Title:  Archives of pharmacal research     Volume:  34     ISSN:  0253-6269     ISO Abbreviation:  Arch. Pharm. Res.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-07-04     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8000036     Medline TA:  Arch Pharm Res     Country:  Korea (South)    
Other Details:
Languages:  eng     Pagination:  1023-34     Citation Subset:  IM    
Affiliation:
Integrated Omics Center, Life/Health Division, Korea Institute of Science and Technology (KIST), P.O. Box 131, Cheongryang, Seoul, 130-650, Korea, cbjin@kist.re.kr.
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