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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
1997-4-25
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pubmed:abstractText |
Features characteristic to rheumatoid joint destruction, including synovial overgrowth and bone resorption, are experimentally produced by augmenting c-fos gene expression. We tested here if arthritic joint destruction was inhibited upon inactivation of the c-fos/AP-1 signal by administering short double-stranded AP-1 DNA oligonucleotides into mice with collagen-induced arthritis to compete for the binding of AP-1 in vivo at the promoter binding site. Arthritic joint destruction was inhibited in a sequence-specific and dose-dependent manner by oligonucleotides containing the AP-1 sequence. The oligonucleotides inhibited gene expression at the transcriptional level. Nucleotide sequences besides AP-1 also appeared to be important structurally for binding of AP-1 onto DNA and for the stability of oligonucleotides against nucleases. Immunohistochemical chase experiment administering biotinylated oligonucleotides into arthritic mice showed that AP-1 oligonucleotides reached the inflamed joint. Thus, activation of c-fos/AP-1 appears essentially important in arthritic joint destruction.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1373140,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1398148,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1411083,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1540182,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1570520,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1578135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1599482,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-1751545,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-2145197,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-2221014,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-2271017,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-2440339,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-2462278,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-2801316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-2840203,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-3034432,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-3226317,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-3263439,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-3290682,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-3492706,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-3898078,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-4004962,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-6838672,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-6960240,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-7590814,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-7687073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-7811235,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-7939732,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-8137552,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-8219207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-8226872,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-8323022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-8335341,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-8478846,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9077528-8612229
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-9738
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
99
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1210-6
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9077528-Animals,
pubmed-meshheading:9077528-Arthritis,
pubmed-meshheading:9077528-Collagen,
pubmed-meshheading:9077528-Injections, Intraperitoneal,
pubmed-meshheading:9077528-Knee Joint,
pubmed-meshheading:9077528-Male,
pubmed-meshheading:9077528-Mice,
pubmed-meshheading:9077528-Mice, Inbred DBA,
pubmed-meshheading:9077528-Oligonucleotides,
pubmed-meshheading:9077528-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:9077528-Transcription Factor AP-1,
pubmed-meshheading:9077528-Transfection
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pubmed:year |
1997
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pubmed:articleTitle |
Studies on the contribution of c-fos/AP-1 to arthritic joint destruction.
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pubmed:affiliation |
Kobe University School of Medicine, Faculty of Health Science, Sumaku, Japan.
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pubmed:publicationType |
Journal Article
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