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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2004-4-30
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pubmed:abstractText |
Previous studies demonstrated that angiotensin II (Ang II)-induced hypertrophy of smooth muscle cells (SMCs) was associated with increased transcription of SM alpha-actin gene. The aim of the present study was to determine whether myocardin, a SMC-selective cofactor of serum response factor (SRF), contributed to Ang II-induced increases in SM alpha-actin transcription. Results showed that Ang II increased myocardin mRNA expression as well as SM alpha-actin mRNA expression via the Ang II type 1 receptor in cultured rat aortic SMCs. Cotransfection studies revealed that CArG elements were required for Ang II-induced transcription of SM alpha-actin gene, and a dominant-negative form of myocardin or a short interfering RNA (siRNA) specific for myocardin decreased Ang II-induced SM alpha-actin transcription. Prx1, a homeodomain protein whose expression was increased by Ang II, also increased SM alpha-actin gene transcription in part via CArG elements, and siRNA specific for Prx1 markedly decreased basal and Ang II-induced SM alpha-actin transcription. Electrophoretic mobility shift assay showed that myocardin and Ang II, respectively, increased formation of a SMC-specific CArG-SRF-myocardin higher order complex. However, Ang II had no effect on binding between myocardin and SRF as determined by a mammalian two-hybrid assay, suggesting that Ang II-induced increases in formation of CArG-SRF-myocardin complex was the result of increased SRF binding to CArG elements and increased myocardin expression. Taken together, these results support a model in which Ang II-induced increases in expression of SM alpha-actin are mediated through Prx1-dependent increases in SRF binding to CArG elements and subsequent recruitment of myocardin.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Prrx1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Serum Response Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/myocardin
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1524-4571
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
30
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pubmed:volume |
94
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1075-82
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15016729-Actins,
pubmed-meshheading:15016729-Angiotensin II,
pubmed-meshheading:15016729-Animals,
pubmed-meshheading:15016729-Aorta,
pubmed-meshheading:15016729-Cells, Cultured,
pubmed-meshheading:15016729-Gene Expression Regulation,
pubmed-meshheading:15016729-Genes, Reporter,
pubmed-meshheading:15016729-Homeodomain Proteins,
pubmed-meshheading:15016729-Hypertrophy,
pubmed-meshheading:15016729-Mice,
pubmed-meshheading:15016729-Muscle, Smooth, Vascular,
pubmed-meshheading:15016729-Mutagenesis, Site-Directed,
pubmed-meshheading:15016729-Nuclear Proteins,
pubmed-meshheading:15016729-RNA, Messenger,
pubmed-meshheading:15016729-RNA, Small Interfering,
pubmed-meshheading:15016729-Rats,
pubmed-meshheading:15016729-Receptor, Angiotensin, Type 1,
pubmed-meshheading:15016729-Recombinant Fusion Proteins,
pubmed-meshheading:15016729-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:15016729-Serum Response Factor,
pubmed-meshheading:15016729-Trans-Activators,
pubmed-meshheading:15016729-Transcription, Genetic,
pubmed-meshheading:15016729-Two-Hybrid System Techniques
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pubmed:year |
2004
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pubmed:articleTitle |
Myocardin and Prx1 contribute to angiotensin II-induced expression of smooth muscle alpha-actin.
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pubmed:affiliation |
Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, Va 22908, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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