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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2009-5-18
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pubmed:abstractText |
We have recently shown a significant reduction in cytokine-induced transcription of type I collagen and fibronectin in systemic sclerosis (SSc) skin fibroblasts upon treatment with trichostatin A (TSA). Moreover, in a mouse model of fibrosis, TSA prevented the dermal accumulation of extracellular matrix. The purpose of this study was to analyze the silencing of histone deacetylase 7 (HDAC-7) as a possible mechanism by which TSA exerts its antifibrotic function.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Connective Tissue Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Matrix Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/HDAC7 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Hdac7 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylases,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxamic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/trichostatin A
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0004-3591
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pubmed:author |
pubmed-author:BrentanoFabiaF,
pubmed-author:DistlerJörg H WJH,
pubmed-author:DistlerOliverO,
pubmed-author:GayRenate ERE,
pubmed-author:GaySteffenS,
pubmed-author:HemmatazadHosseinH,
pubmed-author:HuberLars CLC,
pubmed-author:JüngelAstridA,
pubmed-author:MaurerBrittaB,
pubmed-author:MichelBeat ABA,
pubmed-author:PileckyteMargaritaM,
pubmed-author:RodriguesHanna MaciejewskaHM
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pubmed:issnType |
Print
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pubmed:volume |
60
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1519-29
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pubmed:dateRevised |
2009-12-11
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pubmed:meshHeading |
pubmed-meshheading:19404935-Blotting, Western,
pubmed-meshheading:19404935-Cells, Cultured,
pubmed-meshheading:19404935-Collagen Type I,
pubmed-meshheading:19404935-Collagen Type III,
pubmed-meshheading:19404935-Connective Tissue Growth Factor,
pubmed-meshheading:19404935-Enzyme Inhibitors,
pubmed-meshheading:19404935-Extracellular Matrix Proteins,
pubmed-meshheading:19404935-Fibroblasts,
pubmed-meshheading:19404935-Histone Deacetylase Inhibitors,
pubmed-meshheading:19404935-Histone Deacetylases,
pubmed-meshheading:19404935-Humans,
pubmed-meshheading:19404935-Hydroxamic Acids,
pubmed-meshheading:19404935-Intercellular Adhesion Molecule-1,
pubmed-meshheading:19404935-Polymerase Chain Reaction,
pubmed-meshheading:19404935-Scleroderma, Systemic,
pubmed-meshheading:19404935-Skin,
pubmed-meshheading:19404935-Transforming Growth Factor beta
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pubmed:year |
2009
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pubmed:articleTitle |
Histone deacetylase 7, a potential target for the antifibrotic treatment of systemic sclerosis.
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pubmed:affiliation |
Center of Experimental Rheumatology, University Hospital Zurich, Zurich, Switzerland. hossein.hemmatazad@usz.ch
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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