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Sp1 mediates repression of the resistin gene by PPARgamma agonists in 3T3-L1 adipocytes

Cited 20 time in Web of Science Cited 22 time in Scopus
Authors
Chung, S S; Choi, H H; Cho, Y M; Lee, H K; Park, K S
Issue Date
2006-08-01
Publisher
Elsevier
Citation
Biochem Biophys Res Commun. 2006 Sep 15;348(1):253-8. Epub 2006 Jul 18.
Keywords
3T3-L1 CellsAdipocytes/metabolismBinding SitesGene Expression Regulation/drug effectsGlycosylationInsulin ResistanceMicePPAR gamma/agonists/*genetics/metabolismPlicamycin/analogs & derivatives/pharmacologyPromoter Regions, GeneticProtein BindingResistin/biosynthesis/*geneticsSignal Transduction/drug effects/geneticsSp1 Transcription Factor/*genetics/metabolismThiazolidinediones/pharmacology
Abstract
Resistin is an adipokine related to obesity and insulin resistance. Expression of the resistin gene is repressed by the treatment of peroxisome proliferator-activated receptor gamma (PPARgamma) agonists, thiazolidinediones (TZDs). In this study, we investigated the mechanism by which TZDs inhibit the resistin gene expression. Resistin gene expression was decreased by TZD in fully differentiated 3T3-L1 adipocytes, which was abolished after treatment of cycloheximide (a protein synthesis inhibitor). TZD could not repress the expression of the resistin gene in the presence of mithramycin A (an Sp1 binding inhibitor). Sp1 binding site of the resistin promoter (-122/-114bp) was necessary for the repression. Further investigation of the effect of TZDs on the modification of Sp1 showed that the level of O-glycosylation of Sp1 was decreased in this process. These results suggest that PPARgamma activation represses the expression of the resistin gene by modulating Sp1 activity.
ISSN
0006-291X (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16876120

http://hdl.handle.net/10371/38223
DOI
https://doi.org/10.1016/j.bbrc.2006.07.048
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College of Medicine/School of Medicine (의과대학/대학원)Molecular and Genomic Medicine (분자유전체의학전공)Journal Papers (저널논문_분자유전체의학전공)
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