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Impairment of insulin receptor substrate 1 signaling by insulin resistance inhibits neurite outgrowth and aggravates neuronal cell death

DC Field Value Language
dc.contributor.author김어수-
dc.contributor.author김철훈-
dc.contributor.author송주현-
dc.contributor.author송호택-
dc.contributor.author이종은-
dc.date.accessioned2016-02-04T11:23:24Z-
dc.date.available2016-02-04T11:23:24Z-
dc.date.issued2015-
dc.identifier.issn0306-4522-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/140317-
dc.description.abstractIn the central nervous system (CNS), insulin resistance (I/R) can cause defective neurite outgrowth and neuronal cell death, which can eventually lead to cognitive deficits. Recent research has focused on the relationship between I/R and the cognitive impairment caused by dementia, with the goal of developing treatments for dementia. Insulin signal transduction mediated by insulin receptor substrate (IRS-1) has been thoroughly studied in the CNS of patients with I/R. In the present study, we investigated whether the impairment of IRS-1-mediated insulin signaling contributes to neurite outgrowth and neuronal loss, both in mice fed a high-fat diet and in mouse neuroblastoma (Neuro2A) cells. To investigate the changes caused by the inhibition of IRS-1-mediated insulin signaling in the brain, we performed Cresyl Violet staining and immunochemical analysis. To investigate the changes caused by the inhibition of IRS-1-mediated insulin signaling in neuroblastoma cells, we performed Western blot analysis, reverse transcription-PCR, and immunochemical analysis. We show that the deactivation of IRS-1-mediated insulin signaling can inhibit neuronal outgrowth and aggravate neuronal cell death in the insulin-resistant CNS. Thus, IRS-1-mediated insulin signal transduction may be an important factor in the treatment of cognitive decline induced by I/R.-
dc.description.statementOfResponsibilityopen-
dc.format.extent26~38-
dc.relation.isPartOfNEUROSCIENCE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis*-
dc.subject.MESHBrain/metabolism*-
dc.subject.MESHBrain/pathology-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHDiet, High-Fat-
dc.subject.MESHForkhead Box Protein O3-
dc.subject.MESHForkhead Transcription Factors/metabolism-
dc.subject.MESHInsulin Receptor Substrate Proteins/metabolism*-
dc.subject.MESHInsulin Resistance*-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred ICR-
dc.subject.MESHNeurites/metabolism-
dc.subject.MESHNeurons/metabolism*-
dc.subject.MESHNeurons/pathology-
dc.subject.MESHOncogene Protein v-akt/metabolism-
dc.subject.MESHPhosphorylation-
dc.subject.MESHReactive Oxygen Species-
dc.subject.MESHSignal Transduction-
dc.titleImpairment of insulin receptor substrate 1 signaling by insulin resistance inhibits neurite outgrowth and aggravates neuronal cell death-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Radiology (영상의학)-
dc.contributor.googleauthorJ. Song-
dc.contributor.googleauthorS.M. Kang-
dc.contributor.googleauthorE. Kim-
dc.contributor.googleauthorC.-H. Kim-
dc.contributor.googleauthorH.-T. Song-
dc.contributor.googleauthorJ.E. Lee-
dc.identifier.doi10.1016/j.neuroscience.2015.05.072-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00686-
dc.contributor.localIdA01057-
dc.contributor.localIdA02063-
dc.contributor.localIdA02080-
dc.contributor.localIdA03146-
dc.relation.journalcodeJ02362-
dc.identifier.eissn1873-7544-
dc.identifier.pmid26047734-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0306452215005230-
dc.subject.keywordhigh-fat diet (HFD) animal model-
dc.subject.keywordinsulin receptor substrate 1 (IRS-1)-
dc.subject.keywordinsulin resistance-
dc.subject.keywordneurite outgrowth-
dc.subject.keywordneuronal cell death-
dc.contributor.alternativeNameKim, Eo Su-
dc.contributor.alternativeNameKim, Chul Hoon-
dc.contributor.alternativeNameSong, Ju Hyun-
dc.contributor.alternativeNameSong, Ho Taek-
dc.contributor.alternativeNameLee, Jong Eun-
dc.contributor.affiliatedAuthorKim, Eo Su-
dc.contributor.affiliatedAuthorKim, Chul Hoon-
dc.contributor.affiliatedAuthorSong, Ju Hyun-
dc.contributor.affiliatedAuthorSong, Ho Taek-
dc.contributor.affiliatedAuthorLee, Jong Eun-
dc.rights.accessRightsnot free-
dc.citation.volume301-
dc.citation.startPage26-
dc.citation.endPage38-
dc.identifier.bibliographicCitationNEUROSCIENCE, Vol.301 : 26-38, 2015-
dc.identifier.rimsid51553-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Psychiatry (정신과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Radiology (영상의학교실) > 1. Journal Papers

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