| pubmed-article:20145658 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C0056695 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C0475224 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C1415299 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:20145658 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:20145658 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:20145658 | pubmed:dateCreated | 2010-8-3 | lld:pubmed |
| pubmed-article:20145658 | pubmed:abstractText | Previous exposure to a nonlethal ischemic insult protects the brain against subsequent harmful ischemia. N-methyl-D-aspartate (NMDA) receptors are a highly studied target of neuroprotection after ischemia. Recently, NMDA receptor subtypes were implicated in neuronal survival and death. We focused on the contribution of NR2A and cyclic-AMP response element (CRE)-binding protein (CREB) signaling to ischemic tolerance using primary cortical neurons. Ischemia in vitro was modeled by oxygen-glucose deprivation (OGD). Ischemic tolerance was induced by applying 45-mins OGD 24 h before 180-mins OGD. Sublethal OGD also induced cross-tolerance against lethal glutamate and hydrogen peroxide. After sublethal OGD, expression of phosphorylated CREB and CRE transcriptional activity were significantly increased. When CRE activity was inhibited by CREB-S133A, a mutant CREB, ischemic tolerance was abolished. Inhibiting NR2A using NVP-AAM077 attenuated preconditioning-induced neuroprotection and correlated with decreased CRE activity levels. Activating NR2A using bicuculline and 4-aminopiridine induced resistance to lethal ischemia accompanied by elevated CRE activity levels, and this effect was abolished by NVP-AAM077. Elevated brain-derived neurotrophic factor (BDNF) transcriptional activities were observed after sublethal OGD and administration of bicuculline and 4-aminopiridine. NR2A-containing NMDA receptors and CREB signaling have important functions in the induction of ischemic tolerance. This may provide potential novel therapeutic strategies to treat ischemic stroke. | lld:pubmed |
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| pubmed-article:20145658 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20145658 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20145658 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20145658 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20145658 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:20145658 | pubmed:issn | 1559-7016 | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:KitagawaKazuo... | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:YagitaYoshiki... | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:SakodaSaburoS | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:SasakiTsutomu... | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:Omura-Matsuok... | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:SugiyamaYukio... | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:TerasakiYasuk... | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:OkazakiShuhei... | lld:pubmed |
| pubmed-article:20145658 | pubmed:author | pubmed-author:OyamaNaokiN | lld:pubmed |
| pubmed-article:20145658 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20145658 | pubmed:volume | 30 | lld:pubmed |
| pubmed-article:20145658 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20145658 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20145658 | pubmed:pagination | 1441-9 | lld:pubmed |
| pubmed-article:20145658 | pubmed:dateRevised | 2011-8-3 | lld:pubmed |
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| pubmed-article:20145658 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20145658 | pubmed:articleTitle | Activation of NR2A receptors induces ischemic tolerance through CREB signaling. | lld:pubmed |
| pubmed-article:20145658 | pubmed:affiliation | Department of Neurology, Osaka University Graduate School of Medicine, Osaka, Japan. yterasak@medone.med.osaka-u.ac.jp | lld:pubmed |
| pubmed-article:20145658 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20145658 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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