Document Detail


Neuroprotection Induced In Vitro by Ischemic Preconditioning and Postconditioning: Modulation of Apoptosis and PI3K-Akt Pathways.
MedLine Citation:
PMID:  20953735     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Preconditioning and postconditioning are mild ischemic exposures before or after severe injurious ischemia, respectively, that elicit endogenous neuroprotective responses. Molecular mechanisms of neuroprotection through preconditioning and postconditioning are not completely understood. Here we optimized the in vitro oxygen and glucose deprivation (OGD) models of preconditioning and postconditioning in primary cortical neuron cultures that allow the studies of the corresponding molecular mechanisms of neuroprotection. We found that the cortical cells preconditioned with a single 45-min OGD treatment administered 24 h prior to injurious 2 h OGD were robustly protected after both 3 h and 16 h of reperfusion. For the postconditioning treatment, we found that three cycles of 15 min OGD followed by 15 min reperfusion, applied immediately after injurious 2 h OGD and prior to complete reperfusion, resulted in effective neuroprotection at both 3 h and 16 h of reperfusion. Using real-time RT-PCR arrays focused on genes of the apoptosis and PI3K-Akt pathways, we found that injurious OGD mainly induced apoptosis-related and repressed PI3K-Akt pathway-related genes after either 3 h or 16 h of reperfusion. Preconditioning treatment resulted in the activation of both pro-survival and anti-apoptotic pathways after 3 h of reperfusion and mainly anti-apoptotic pathway after 16 h of reperfusion. In contrast, the activation of PI3K-Akt pathway mainly contributed to the neuroprotective effect by the postconditioning treatment after 3 h of reperfusion, but differential gene expression likely contributed minimally, if at all, to the neuroprotection observed after 16 h of reperfusion. Among the novel markers of neuroprotection, Nol3 gene upregulation was observed after 3 h of reperfusion following either preconditioning or postconditioning treatments and after 16 h of reperfusion following preconditioning treatment.
Authors:
Shiv S Prasad; Marsha Russell; Margeryta Nowakowska
Related Documents :
10514095 - Participation of prostate apoptosis response-4 in degeneration of dopaminergic neurons ...
9522365 - Insulin-like growth factor-i analogue prevents apoptosis mediated through an interleuki...
9259455 - Apoptotic, injury-induced cell death in cultured mouse murine motor neurons.
9743565 - Evidence for synaptic apoptosis.
12548325 - Novel dermatologic uses of the immune response modifier imiquimod 5% cream.
10706075 - Proliferation of dendritic cell progenitors in long term culture is not dependent on gr...
Publication Detail:
Type:  Journal Article     Date:  2010-10-15
Journal Detail:
Title:  Journal of molecular neuroscience : MN     Volume:  43     ISSN:  1559-1166     ISO Abbreviation:  J. Mol. Neurosci.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-21     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9002991     Medline TA:  J Mol Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  428-42     Citation Subset:  IM    
Affiliation:
Genomics Division, Biologics and Genetic Therapies Directorate, Health Canada, 251 Sir Frederick Banting Driveway, A/L 2201E, Ottawa, ON, K1A 0K9, Canada, Shiv.Prasad@hc-sc.gc.ca.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Complex Catabolic Effects of Central Alpha-MSH Infusion in Rats of Altered Nutritional States: Diffe...
Next Document:  Relationship between striatal dopamine transporter availability and sleep quality in healthy adults.