Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/163910
Title: Aldose reductase is implicated in high glucose-induced oxidative stress in mouse embryonic neural stem cells
Authors: Fu, Jiang 
Tay, SSW 
Ling, EA 
Dheen, ST 
Keywords: Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
Neurosciences
Neurosciences & Neurology
aldose reductase
apoptosis
cell viability
fidarestat
Glut1
neural stem cells
oxidative stress
proliferation
DIABETIC COMPLICATIONS
INDUCED APOPTOSIS
GENE-EXPRESSION
POLYOL PATHWAY
IN-VITRO
TRANSPORTER EXPRESSION
INHIBITOR FIDARESTAT
RETINAL PERICYTES
TISSUE SITES
RAT EMBRYO
Issue Date: 1-Nov-2007
Publisher: BLACKWELL PUBLISHING
Citation: Fu, Jiang, Tay, SSW, Ling, EA, Dheen, ST (2007-11-01). Aldose reductase is implicated in high glucose-induced oxidative stress in mouse embryonic neural stem cells. JOURNAL OF NEUROCHEMISTRY 103 (4) : 1654-1665. ScholarBank@NUS Repository.
Abstract: Oxidative stress caused by hyperglycemia is one of the key factors responsible for maternal diabetes-induced congenital malformations, including neural tube defects in embryos. However, mechanisms by which maternal diabetes induces oxidative stress during neurulation are not clear. The present study was aimed to investigate whether high glucose induces oxidative stress in neural stem cells (NSCs), which compose the neural tube during development. We also investigated the mechanism by which high glucose disturbs the growth and survival of NSCs in vitro. NSCs were exposed to physiological d-glucose concentration (PG, 5 mmol/L), PG with l-glucose (25 mmol/L), or high d-glucose concentration (HG, 30 or 45 mmol/l). HG induced reactive oxygen species production and mRNA expression of aldose reductase (AR), which catalyzes the glucose reduction through polyol pathway, in NSCs. Expression of glucose transporter 1 (Glut1) mRNA and protein which regulates glucose uptake in NSCs was increased at early stage (24 h) and became down-regulated at late stage (72 h) of exposure to HG. Inhibition of AR by fidarestat, an AR inhibitor, decreased the oxidative stress, restored the cell viability and proliferation, and reduced apoptotic cell death in NSCs exposed to HG. Moreover, inhibition of AR attenuated the down-regulation of Glut1 expression in NSCs exposed to HG for 72 h. These results suggest that the activation of polyol pathway plays a role in the induction of oxidative stress which alters Glut1 expression and cell cycle in NSCs exposed to HG, thereby resulting in abnormal patterning of the neural tube in embryos of diabetic pregnancy. © 2007 The Authors.
Source Title: JOURNAL OF NEUROCHEMISTRY
URI: https://scholarbank.nus.edu.sg/handle/10635/163910
ISSN: 00223042
14714159
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