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Kwon, Hyug Moo
Immunometabolism and Cancer Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorder, Genomic instability

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Gene expression profiling in brain following acute systemic hypertonicity: novel genes possibly involved in osmoadaptation

Cited 9 times inthomson ciCited 10 times inthomson ci
Title
Gene expression profiling in brain following acute systemic hypertonicity: novel genes possibly involved in osmoadaptation
Author
Maallem, SaidWierinckx, AnneLachuer, JoelKwon, H. MooTappaz, Marcel L.
Issue Date
2008-05
Publisher
WILEY-BLACKWELL
Citation
JOURNAL OF NEUROCHEMISTRY, v.105, no.4, pp.1198 - 1211
Abstract
In brain osmoprotective genes known to be involved in cellular osmoadaptation to hypertonicity, as well as the related transcription factor tonicity-responsive enhancer binding protein (TonEBP) are only expressed in some cell subsets. In the search for other genes possibly involved in osmoadaptation of brain cells we have analyzed, through microarray, the transcriptional profile of forebrain from rats subjected to 45 min, 90 min, and 6 h systemic hypertonicity. Microarray data were validated by quantitative real-time PCR. Around 23 000 genes gave a reliable hybridization signal. The number of genes showing a higher expression increased from around 15 (45 min) up to nearly 200 (6 h). Among about 30 immediate early genes (IEGs) encoding transcription factors, only Atf3, Verge, and Klf4 showed a rapid increased expression. TonEBP-mRNA tissue level and TonEBP-mRNA labeling in neurons remained unchanged whereas TonEBP labeling was rapidly increased in neurons. Sodium-dependent neutral amino acid transporter-2 (SNAT2) encoded by gene Slc38a2 showed a delayed increased expression. The rapid tonicity-induced activation of Atf3, Verge, and Klf4 may regulate genes involved in osmoadaptation. Nfat5 encoding TonEBP is not an IEG and the early tonicity-induced expression of TonEBP in neurons may result from translational activation. Increased expression of sodium-dependent neutral amino-acid transporter 2 may lead to the cellular accumulation of amino acids for adaptation to hypertonicity.
URI
https://scholarworks.unist.ac.kr/handle/201301/4743
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=41949107014
DOI
10.1111/j.1471-4159.2008.05222.x
ISSN
0022-3042
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BIO_Journal Papers
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