Document Detail

Transcription factor decoys for activator protein-1 (AP-1) inhibit oxidative stress-induced proliferation and matrix metalloproteinases in rat cardiac fibroblasts.
MedLine Citation:
PMID:  19100954     Owner:  NLM     Status:  MEDLINE    
Activator protein-1 (AP-1), which is a transcription factor, is implicated in the transcriptional regulation of a wide range of genes that participate in cell proliferation and extracellular matrix production. This investigation was performed to test the hypothesis that transfection of cardiac fibroblasts (CFs) with sufficient amounts of decoy oligodeoxynucleotides (ODNs) containing the AP-1-binding site would result in binding to the transfactor AP-1, which would thereby prevent CF proliferation and matrix metalloproteinase (MMP) expression. CFs from Sprague-Dawley rat hearts were cultured and exposed to different concentrations of xanthine + xanthine oxidase (XXO) and AP-1 decoy ODNs. MMP expression was assayed after oxidative stress and transfection with AP-1 decoy ODNs by real-time quantitative polymerase chain reaction and Western blot. Cell growth was determined by the cell count. XXO significantly increased the DNA-binding activity of AP-1 in a dose-dependent manner. We found that transfection with AP-1 decoy ODNs strongly inhibited XXO-induced CF proliferation and MMP gene expression in vitro. Taken together, our data demonstrate that AP-1 is a key transcription factor that mediates CF proliferation and MMP synthesis under oxidative stress. Transfection with AP-1 decoy ODNs may be a novel strategy to inhibit CF proliferation and MMP synthesis.
Shuanglun Xie; Ruqiong Nie; Jingfeng Wang; Fei Li; Woliang Yuan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-12-06
Journal Detail:
Title:  Translational research : the journal of laboratory and clinical medicine     Volume:  153     ISSN:  1931-5244     ISO Abbreviation:  Transl Res     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-22     Completed Date:  2009-03-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101280339     Medline TA:  Transl Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  17-23     Citation Subset:  AIM; IM    
Department of Cardiology, The Second Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510120 China.
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MeSH Terms
Animals, Newborn
Cell Proliferation
Cell Survival / drug effects
Cells, Cultured
Dose-Response Relationship, Drug
Gene Expression Regulation, Enzymologic
Gene Therapy / methods*
Matrix Metalloproteinase 13 / genetics*
Matrix Metalloproteinase 9 / genetics*
Myocytes, Cardiac / metabolism*
Oligodeoxyribonucleotides / genetics*
Oxidative Stress / genetics
Transcription Factor AP-1 / genetics*,  metabolism
Xanthine / pharmacology
Xanthine Oxidase / pharmacology
Reg. No./Substance:
0/Oligodeoxyribonucleotides; 0/Transcription Factor AP-1; 69-89-6/Xanthine; EC Oxidase; EC 3.4.24.-/Matrix Metalloproteinase 13; EC Metalloproteinase 9

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