Document Detail

Knock-down of postsynaptic density protein 95 expression by antisense oligonucleotides protects against apoptosis-like cell death induced by oxygen-glucose deprivation in vitro.
MedLine Citation:
PMID:  22233891     Owner:  NLM     Status:  In-Data-Review    
Objective Postsynaptic density protein 95 (PSD-95) plays important roles in the regulation of glutamate signaling, such as that of N-methyl-D-aspartate receptors (NMDARs). In this study, the functional roles of PSD-95 in tyrosine phosphorylation of NMDAR subunit 2A (NR2A) and in apoptosis-like cell death induced by oxygen-glucose deprivation (OGD) in cultured rat cortical neurons were investigated. Methods We used immunoprecipitation and immunoblotting to detect PSD-95 protein level, tyrosine phosphorylation level of NR2A, and the interaction between PSD-95 and NR2A or Src. Apoptosis-like cells were observed by 4,6-diamidino-2-phenylindole staining. Results Tyrosine phosphorylation of NR2A and apoptosis-like cell death were increased after recovery following 60-min OGD. The increases were attenuated by pretreatment with antisense oligonucleotides against PSD-95 before OGD, but not by missense oligonucleotides or vehicle. PSD-95 antisense oligonucleotides also inhibited the increased interaction between PSD-95 and NR2A or Src, while NR2A expression did not change under this condition. Conclusion PSD-95 may be involved in regulating NR2A tyrosine phosphorylation by Src kinase. Inhibition of PSD-95 expression can be neuroprotective against apoptosis-like cell death after recovery from OGD.
Jing-Zhi Yan; Yong Liu; Yan-Yan Zong; Guang-Yi Zhang
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Neuroscience bulletin     Volume:  28     ISSN:  1995-8218     ISO Abbreviation:  Neurosci Bull     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101256850     Medline TA:  Neurosci Bull     Country:  China    
Other Details:
Languages:  eng     Pagination:  69-76     Citation Subset:  IM    
Jiangsu Key Laboratory of Brain Disease Bioinformation, Research Center for Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002 China; E-mail:
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