| http://purl.uniprot.org/citations/26108185 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/26108185 | http://www.w3.org/2000/01/rdf-schema#comment | "Peroxisome proliferator-activated receptor-gamma (PPAR-γ), a stress-induced transcription factor, protects neurons against ischemic stroke insult by reducing oxidative stress. NADPH oxidase (NOX) activation, a major driving force in ROS generation in the setting of reoxygenation/reperfusion, constitutes an important pathogenetic mechanism of ischemic brain damage. In the present study, both transient in vitro oxygen-glucose deprivation and in vivo middle cerebral artery (MCA) occlusion-reperfusion experimental paradigms of ischemic neuronal death were used to investigate the interaction between PPAR-γ and NOX. With pharmacological (PPAR-γ antagonist GW9662), loss-of-function (PPAR-γ siRNA), and gain-of-function (Ad-PPAR-γ) approaches, we first demonstrated that 15-deoxy-∆(12,14)-PGJ2 (15d-PGJ2), via selectively attenuating p22phox expression, inhibited NOX activation and the subsequent ROS generation and neuronal death in a PPAR-γ-dependent manner. Secondly, results of promoter analyses and subcellular localization studies further revealed that PPAR-γ, via inhibiting hypoxia-induced NF-κB nuclear translocation, indirectly suppressed NF-κB-driven p22phox transcription. Noteworthily, postischemic p22phox siRNA treatment not only reduced infarct volumes but also improved functional outcome. In summary, we report a novel transrepression mechanism involving PPAR-γ downregulation of p22phox expression to suppress the subsequent NOX activation, ischemic neuronal death, and brain infarct. Identification of a PPAR-γ → NF-κB → p22phox neuroprotective signaling cascade opens a new avenue for protecting the brain against ischemic insult."xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.org/dc/terms/identifier | "doi:10.1007/s12035-015-9294-z"xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/author | "Hsu C.Y."xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/author | "Wu J.S."xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/author | "Cheung W.M."xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/author | "Lin T.N."xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/author | "Tsai H.D."xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/name | "Mol Neurobiol"xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/pages | "3626-3645"xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/title | "PPAR-gamma Ameliorates Neuronal Apoptosis and Ischemic Brain Injury via Suppressing NF-kappaB-Driven p22phox Transcription."xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://purl.uniprot.org/core/volume | "53"xsd:string |
| http://purl.uniprot.org/citations/26108185 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26108185 |
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| http://purl.uniprot.org/uniprot/#_A0N0D0-mappedCitation-26108185 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26108185 |
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| http://purl.uniprot.org/uniprot/#_P37238-mappedCitation-26108185 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26108185 |
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| http://purl.uniprot.org/uniprot/#_Q3TAM0-mappedCitation-26108185 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/26108185 |