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rdf:type |
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lifeskim:mentions |
umls-concept:C0003009,
umls-concept:C0010453,
umls-concept:C0021289,
umls-concept:C0033634,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0086982,
umls-concept:C0205263,
umls-concept:C0225828,
umls-concept:C0521447,
umls-concept:C1879547
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pubmed:issue |
10
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pubmed:dateCreated |
2000-11-6
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pubmed:abstractText |
Rat neonatal ventricular cardiomyocytes (RNVM) possess G protein-coupled AT(1)receptors for angiotensin II (AngII) that activate multiple intracellular pathways. To elucidate potential signaling mechanisms involved, we focussed on the nuclear transcription factor-kappa B (NF- kappa B) in RNVM culture. Using specific antibody to NF- kappa Bp65, immunolocalization of NF- kappa B was cytoplasmic in unstimulated cardiomyocytes, whereas NF- kappa B was translocated into the RNVM nucleus in response to AngII. This translocation was inhibited in the presence of calphostin C, a specific inhibitor of protein kinase C (PKC). Western blot analysis showed an increase of NF- kappa B in AngII-stimulated cardiomyocyte nuclear extracts as compared to controls. Biomolecular interaction analysis (BIA analysis) of NF- kappa B activation showed that only AngII-nuclear extracts bound to NF- kappa B consensus sequence with a high degree of affinity. This DNA-binding capacity was completely lost in calphostin C-treated cells. At transcriptional level in RNVM, AngII mediates the upregulation of matrix gelatinase (MMP-9), which is totally inhibited by calphostin C treatment. In conclusion, cardiomyocyte nuclear NF- kappa B translocation in response to Ang II via PKC pathway activates cardiomyocyte-specific transcription of MMP-9 and may activate transcription from responsive genes which are involved in cardiac hypertrophy process and/or cardiac remodeling.
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-2828
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2000 Academic Press.
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pubmed:issnType |
Print
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pubmed:volume |
32
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1767-78
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11013121-Angiotensin II,
pubmed-meshheading:11013121-Animals,
pubmed-meshheading:11013121-Animals, Newborn,
pubmed-meshheading:11013121-Blotting, Western,
pubmed-meshheading:11013121-Cell Nucleus,
pubmed-meshheading:11013121-Cells, Cultured,
pubmed-meshheading:11013121-DNA,
pubmed-meshheading:11013121-Enzyme Activation,
pubmed-meshheading:11013121-Enzyme Inhibitors,
pubmed-meshheading:11013121-Immunohistochemistry,
pubmed-meshheading:11013121-Matrix Metalloproteinase 9,
pubmed-meshheading:11013121-Microscopy, Confocal,
pubmed-meshheading:11013121-Muscles,
pubmed-meshheading:11013121-NF-kappa B,
pubmed-meshheading:11013121-Naphthalenes,
pubmed-meshheading:11013121-Protein Kinase C,
pubmed-meshheading:11013121-Rats,
pubmed-meshheading:11013121-Rats, Wistar,
pubmed-meshheading:11013121-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11013121-Signal Transduction,
pubmed-meshheading:11013121-Surface Plasmon Resonance,
pubmed-meshheading:11013121-Time Factors,
pubmed-meshheading:11013121-Transcription, Genetic,
pubmed-meshheading:11013121-Transcription Factor RelA,
pubmed-meshheading:11013121-Up-Regulation
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pubmed:year |
2000
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pubmed:articleTitle |
Angiotensin II induces nuclear factor- kappa B activation in cultured neonatal rat cardiomyocytes through protein kinase C signaling pathway.
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pubmed:affiliation |
INSERM Unité U492, Faculté de Médecine, 8 rue du Général Sarrail, Créteil, 94010, France. rouet@im3.inserm.fr
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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