Anti-inflammatory Effect of Glucagon Like Peptide-1 Receptor Agonist, Exendin-4, through Modulation of IB1/JIP1 Expression and JNK Signaling in Stroke
DC Field | Value | Language |
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dc.contributor.author | Kim, Soojin | - |
dc.contributor.author | Jeong, Jaewon | - |
dc.contributor.author | Jung, Hye-Seon | - |
dc.contributor.author | Kim, Bokyung | - |
dc.contributor.author | Kim, Ye-Eun | - |
dc.contributor.author | Lim, Da-Sol | - |
dc.contributor.author | Kim, So-Dam | - |
dc.contributor.author | Song, Yun Seon | - |
dc.date.available | 2021-02-22T11:12:35Z | - |
dc.date.issued | 2017-08 | - |
dc.identifier.issn | 1226-2560 | - |
dc.identifier.issn | 2093-8144 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8217 | - |
dc.description.abstract | Glucagon like peptide-1 (GLP-1) stimulates glucose-dependent insulin secretion. Dipeptidyl peptidase-4 (DPP-4) inhibitors, which block inactivation of GLP-1, are currently in clinical use for type 2 diabetes mellitus. Recently, GLP-1 has also been reported to have neuroprotective effects in cases of cerebral ischemia. We therefore investigated the neuroprotective effects of GLP-1 receptor (GLP-1R) agonist, exendin-4 (ex-4), after cerebral ischemia-reperfusion injury. Transient middle cerebral artery occlusion (tMCAO) was induced in rats by intracerebroventricular (i.c.v.) administration of ex-4 or ex9-39. Oxygen-glucose deprivation was also induced in primary neurons, bEnd.3 cells, and BV-2. Ischemia-reperfusion injury reduced expression of GLP-1R. Additionally, higher oxidative stress in SOD2 KO mice decreased expression of GLP-1R. Downregulation of GLP-1R by ischemic injury was 70% restored by GLP-1R agonist, ex-4, which resulted in significant reduction of infarct volume. Levels of intracellular cyclic AMP, a second messenger of GLP-1R, were also increased by 2.7-fold as a result of high GLP-1R expression. Moreover, our results showed that ex-4 attenuated pro-inflammatory cyclooxygenase-2 (COX-2) and prostaglandin E-2 after MCAO.C-Jun NH2 terminal kinase (JNK) signaling, which stimulates activation of COX-2, was 36% inhibited by i.c.v. injection of ex-4 at 24 h. Islet-brain 1 (IB1), a scaffold regulator of JNK, was 1.7-fold increased by ex-4. GLP-1R activation by ex-4 resulted in reduction of COX-2 through increasing IB1 expression, resulting in anti-inflammatory neuroprotection during stroke. Our study suggests that the anti-inflammatory action of GLP-1 could be used as a new strategy for the treatment of neuroinflammation after stroke accompanied by hyperglycemia. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | KOREAN SOC BRAIN & NEURAL SCIENCE, KOREAN SOC NEURODEGENERATIVE DISEASE | - |
dc.title | Anti-inflammatory Effect of Glucagon Like Peptide-1 Receptor Agonist, Exendin-4, through Modulation of IB1/JIP1 Expression and JNK Signaling in Stroke | - |
dc.type | Article | - |
dc.publisher.location | 대한민국 | - |
dc.identifier.doi | 10.5607/en.2017.26.4.227 | - |
dc.identifier.scopusid | 2-s2.0-85029304725 | - |
dc.identifier.wosid | 000424431900006 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL NEUROBIOLOGY, v.26, no.4, pp 227 - 239 | - |
dc.citation.title | EXPERIMENTAL NEUROBIOLOGY | - |
dc.citation.volume | 26 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 227 | - |
dc.citation.endPage | 239 | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART002258881 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.subject.keywordPlus | SUPEROXIDE DISMUTASE ACTIVITY | - |
dc.subject.keywordPlus | AMYLOID PRECURSOR PROTEIN | - |
dc.subject.keywordPlus | INSULIN-SECRETING CELLS | - |
dc.subject.keywordPlus | FOCAL CEREBRAL-ISCHEMIA | - |
dc.subject.keywordPlus | CORTICAL-NEURONS | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | TRANSGENIC MICE | - |
dc.subject.keywordPlus | BRAIN-DAMAGE | - |
dc.subject.keywordPlus | BETA-CELLS | - |
dc.subject.keywordPlus | KINASE JNK | - |
dc.subject.keywordAuthor | Neuroinflammation | - |
dc.subject.keywordAuthor | Cerebral ischemia | - |
dc.subject.keywordAuthor | Glucagon like peptide-1 receptor | - |
dc.subject.keywordAuthor | Exendine-4 | - |
dc.subject.keywordAuthor | Islet-brain 1 | - |
dc.subject.keywordAuthor | c-Jun NH2 terminal kinase | - |
dc.identifier.url | http://www.en-journal.org/journal/view.html?doi=10.5607/en.2017.26.4.227 | - |
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