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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1995-6-16
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pubmed:abstractText |
Increasing evidence suggests that angiotensin II may act as a growth factor for several muscle cell types. Angiotensin II stimulation activates many immediate early response genes like c-Fos, c-Jun, c-Myc and Egr-1 in both vascular smooth muscle cells and cardiomyocytes, independently of whether a hyperplastic or hypertrophic response is taking place. In this study we report that angiotensin II significantly stimulates AP1-driven transcription in mouse skeletal muscle cells C2C12 stably transfected with a TRE-tk-CAT plasmid in a dose-dependent manner (peak stimulation at 10(-5) M of angiotensin II). Moreover, angiotensin II increases the binding of the AP1 complex to its DNA target in both quiescent C2C12 myoblasts and in differentiated C2C12 myotubes. Most of the TRE-bound complexes in both unstimulated and angiotensin II-treated cells consist of c-jun/c-fos heterodimers. Using a set of different protein kinase inhibitors, including HA1004, H7, tyrphostin, genistein and staurosporine, we could demonstrate that the angiotensin II-induced AP1 binding increase is not mediated by the cAMP-dependent pathway and that protein kinase C and tyrosine kinases are involved. Treatment of C2C12 cells with H2O2 induces a dose-dependent increase in c-jun/c-fos heterodimer binding, specifically reverted by the cysteine derivative and glutathione precursor N-acetyl-L-cysteine (NAC). The observation that the induction by angiotensin II of both the AP1 DNA binding activity and DNA synthesis in quiescent C2C12 myoblasts is abolished by NAC strongly suggests a role for reactive oxygen intermediates (ROIs) in the intracellular transduction of angiotensin II signals for immediate early gene induction and for cell proliferation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Oligodeoxyribonucleotides,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-fos,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0077-8923
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
27
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pubmed:volume |
752
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
394-405
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:7755283-Angiotensin II,
pubmed-meshheading:7755283-Animals,
pubmed-meshheading:7755283-Antioxidants,
pubmed-meshheading:7755283-Base Sequence,
pubmed-meshheading:7755283-Cell Differentiation,
pubmed-meshheading:7755283-Cell Line,
pubmed-meshheading:7755283-Gene Expression,
pubmed-meshheading:7755283-Genes, Immediate-Early,
pubmed-meshheading:7755283-Heart,
pubmed-meshheading:7755283-Mice,
pubmed-meshheading:7755283-Molecular Sequence Data,
pubmed-meshheading:7755283-Muscle, Skeletal,
pubmed-meshheading:7755283-Muscle, Smooth, Vascular,
pubmed-meshheading:7755283-Myocardium,
pubmed-meshheading:7755283-Oligodeoxyribonucleotides,
pubmed-meshheading:7755283-Protein Kinase Inhibitors,
pubmed-meshheading:7755283-Protein Kinases,
pubmed-meshheading:7755283-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:7755283-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:7755283-Reactive Oxygen Species,
pubmed-meshheading:7755283-Recombinant Fusion Proteins,
pubmed-meshheading:7755283-Signal Transduction,
pubmed-meshheading:7755283-Transcription Factor AP-1,
pubmed-meshheading:7755283-Transfection
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pubmed:year |
1995
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pubmed:articleTitle |
Reactive oxygen intermediates (ROIs) are involved in the intracellular transduction of angiotensin II signal in C2C12 cells.
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pubmed:affiliation |
Fondazione Andrea Cesalpino, University of Rome La Sapienza, Italy.
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pubmed:publicationType |
Journal Article,
Review
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