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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

Authors
 J Song  ;  SM Kang  ;  E Kim  ;  C-H Kim  ;  H-T Song  ;  JE Lee 
Citation
 CELL DEATH & DISEASE, Vol.6 : 1844, 2015 
Journal Title
 CELL DEATH & DISEASE 
Issue Date
2015
MeSH
Animals ; Cell Differentiation ; Cell Proliferation ; Cell Survival ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Cyclin-Dependent Kinase Inhibitor p21/genetics* ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Diet, High-Fat/adverse effects ; Gene Expression Regulation ; Glucose/toxicity* ; Humans ; Hyperglycemia/etiology ; Hyperglycemia/genetics* ; Hyperglycemia/metabolism ; Hyperglycemia/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neural Stem Cells ; Neurogenesis/drug effects ; Neurogenesis/genetics ; Primary Cell Culture ; Receptors, Adiponectin/genetics* ; Receptors, Adiponectin/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics* ; Receptors, Cytoplasmic and Nuclear/metabolism ; Signal Transduction ; Synapses/drug effects ; Synapses/metabolism ; Synapses/pathology ; Tumor Suppressor Protein p53/genetics* ; Tumor Suppressor Protein p53/metabolism
Abstract
In 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
Files in This Item:
T201502910.pdf Download
DOI
10.1038/cddis.2015.220
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
Yonsei Authors
Kim, Eosu(김어수) ORCID logo https://orcid.org/0000-0001-9472-9465
Kim, Chul Hoon(김철훈) ORCID logo https://orcid.org/0000-0002-7360-429X
Song, Ju Hyun(송주현)
Song, Ho Taek(송호택) ORCID logo https://orcid.org/0000-0002-6655-2575
Lee, Jong Eun(이종은) ORCID logo https://orcid.org/0000-0001-6203-7413
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/140792
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