Source:http://linkedlifedata.com/resource/pubmed/id/19228263
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11-12
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| pubmed:dateCreated |
2010-4-16
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| pubmed:abstractText |
B-type natriuretic peptide (BNP) is a cardiac hormone, which plays a major role in body fluid and cardiovascular homeostasis. Produced by cardiac ventricles, its expression is highly regulated by various mediators. Canine cardiac fibroblasts have been identified as a source of BNP. Cardiac fibroblasts are key regulators of myocardial structure and function. We treated cultured human adult cardiac fibroblasts (HACF) with 2000 U/ml tumour necrosis factor-alpha (TNF-alpha), 200 U/ml interleukin-1alpha (IL-1alpha) or 50 ng/ml transforming growth factor-beta (TGF-beta) in the presence or absence of 500 nM fluvastatin. N-terminal pro-BNP (Nt-proBNP) concentration was determined by a competitive enzyme immunoassay. RealTime polymerase chain reaction (real-time PCR) was performed to investigate changes in BNP mRNA expression. Nt-proBNP peptide was present in the conditioned media of HACF and incubation with fluvastatin significantly reduced Nt-proBNP peptide levels. Treatment of HACF with TNF-alpha, IL-1alpha or TGF-beta significantly increased Nt-proBNP levels compared with untreated cells. This effect was completely abolished in the presence of fluvastatin. Real-time PCR analysis confirmed these changes at the level of mRNA expression. Our data suggest that cardiac fibroblasts are a potential source of BNP in the human heart. Pro-inflammatory cytokines, associated with ventricular dysfunction and cardiac fibrosis, seem to be major inducers of BNP production in cardiac fibroblasts. This effect can be reverted by a statin. Based on our data, we speculate that elevated plasma BNP levels might not only reflect increased myocardial stretch but also inflammatory and remodelling processes. A possible benefit of statin-induced reduction in BNP production requires further studies.
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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/Fatty Acids, Monounsaturated,
http://linkedlifedata.com/resource/pubmed/chemical/Indoles,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-11,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Leukemia Inhibitory Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Natriuretic Peptide, Brain,
http://linkedlifedata.com/resource/pubmed/chemical/Oncostatin M,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/fluvastatin,
http://linkedlifedata.com/resource/pubmed/chemical/pro-brain natriuretic peptide (1-76)
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| pubmed:status |
MEDLINE
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| pubmed:issn |
1582-4934
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
13
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
4415-21
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| pubmed:meshHeading |
pubmed-meshheading:19228263-Adult,
pubmed-meshheading:19228263-Fatty Acids, Monounsaturated,
pubmed-meshheading:19228263-Fibroblasts,
pubmed-meshheading:19228263-Humans,
pubmed-meshheading:19228263-Indoles,
pubmed-meshheading:19228263-Interleukin-11,
pubmed-meshheading:19228263-Interleukin-1alpha,
pubmed-meshheading:19228263-Interleukin-6,
pubmed-meshheading:19228263-Leukemia Inhibitory Factor,
pubmed-meshheading:19228263-Myocardium,
pubmed-meshheading:19228263-Myocytes, Cardiac,
pubmed-meshheading:19228263-Natriuretic Peptide, Brain,
pubmed-meshheading:19228263-Oncostatin M,
pubmed-meshheading:19228263-Peptide Fragments,
pubmed-meshheading:19228263-RNA, Messenger,
pubmed-meshheading:19228263-Transforming Growth Factor beta,
pubmed-meshheading:19228263-Tumor Necrosis Factor-alpha,
pubmed-meshheading:19228263-Up-Regulation
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| pubmed:articleTitle |
Human cardiac fibroblasts express B-type natriuretic peptide: fluvastatin ameliorates its up-regulation by interleukin-1alpha, tumour necrosis factor-alpha and transforming growth factor-beta.
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| pubmed:affiliation |
Department of Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna, Austria.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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