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Adiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study

DC FieldValueLanguage
dc.contributor.author김어수-
dc.contributor.author김철훈-
dc.contributor.author송주현-
dc.contributor.author송호택-
dc.contributor.author이종은-
dc.date.accessioned2016-02-04T11:36:17Z-
dc.date.available2016-02-04T11:36:17Z-
dc.date.issued2015-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/140792-
dc.description.abstractIn the central nervous system (CNS), hyperglycemia leads to neuronal damage and cognitive decline. Recent research has focused on revealing alterations in the brain in hyperglycemia and finding therapeutic solutions for alleviating the hyperglycemia-induced cognitive dysfunction. Adiponectin is a protein hormone with a major regulatory role in diabetes and obesity; however, its role in the CNS has not been studied yet. Although the presence of adiponectin receptors has been reported in the CNS, adiponectin receptor-mediated signaling in the CNS has not been investigated. In the present study, we investigated adiponectin receptor (AdipoR)-mediated signaling in vivo using a high-fat diet and in vitro using neural stem cells (NSCs). We showed that AdipoR1 protects cell damage and synaptic dysfunction in the mouse brain in hyperglycemia. At high glucose concentrations in vitro, AdipoR1 regulated the survival of NSCs through the p53/p21 pathway and the proliferation- and differentiation-related factors of NSCs via tailless (TLX). Hence, we suggest that further investigations are necessary to understand the cerebral AdipoR1-mediated signaling in hyperglycemic conditions, because the modulation of AdipoR1 might alleviate hyperglycemia-induced neuropathogenesis-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.relation.isPartOfCELL DEATH & DISEASE-
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.MESHCell Differentiation-
dc.subject.MESHCell Proliferation-
dc.subject.MESHCell Survival-
dc.subject.MESHCerebral Cortex/drug effects-
dc.subject.MESHCerebral Cortex/metabolism-
dc.subject.MESHCerebral Cortex/pathology-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21/genetics*-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21/metabolism-
dc.subject.MESHDiet, High-Fat/adverse effects-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHGlucose/toxicity*-
dc.subject.MESHHumans-
dc.subject.MESHHyperglycemia/etiology-
dc.subject.MESHHyperglycemia/genetics*-
dc.subject.MESHHyperglycemia/metabolism-
dc.subject.MESHHyperglycemia/pathology-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHNeural Stem Cells-
dc.subject.MESHNeurogenesis/drug effects-
dc.subject.MESHNeurogenesis/genetics-
dc.subject.MESHPrimary Cell Culture-
dc.subject.MESHReceptors, Adiponectin/genetics*-
dc.subject.MESHReceptors, Adiponectin/metabolism-
dc.subject.MESHReceptors, Cytoplasmic and Nuclear/genetics*-
dc.subject.MESHReceptors, Cytoplasmic and Nuclear/metabolism-
dc.subject.MESHSignal Transduction-
dc.subject.MESHSynapses/drug effects-
dc.subject.MESHSynapses/metabolism-
dc.subject.MESHSynapses/pathology-
dc.subject.MESHTumor Suppressor Protein p53/genetics*-
dc.subject.MESHTumor Suppressor Protein p53/metabolism-
dc.titleAdiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Psychiatry (정신과학)-
dc.contributor.googleauthorJ Song-
dc.contributor.googleauthorSM Kang-
dc.contributor.googleauthorE Kim-
dc.contributor.googleauthorC-H Kim-
dc.contributor.googleauthorH-T Song-
dc.contributor.googleauthorJE Lee-
dc.identifier.doi10.1038/cddis.2015.220-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00686-
dc.contributor.localIdA01057-
dc.contributor.localIdA02063-
dc.contributor.localIdA02080-
dc.contributor.localIdA03146-
dc.relation.journalcodeJ00482-
dc.identifier.eissn2041-4889-
dc.identifier.pmid26247729-
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.accessRightsfree-
dc.citation.volume6-
dc.citation.startPage1844-
dc.identifier.bibliographicCitationCELL DEATH & DISEASE, Vol.6 : 1844, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Psychiatry (정신과학교실) > 1. Journal Papers
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 Radiology (영상의학교실) > 1. Journal Papers

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