Rosuvastatin Can Block Pro‐Inflammatory Actions of Transgenic Human C‐Reactive Protein Without Reducing its Circulating Levels. Issue 2 (April 2014)
- Record Type:
- Journal Article
- Title:
- Rosuvastatin Can Block Pro‐Inflammatory Actions of Transgenic Human C‐Reactive Protein Without Reducing its Circulating Levels. Issue 2 (April 2014)
- Main Title:
- Rosuvastatin Can Block Pro‐Inflammatory Actions of Transgenic Human C‐Reactive Protein Without Reducing its Circulating Levels
- Authors:
- Šilhavý, Jan
Zídek, Václav
Landa, Vladimír
Šimáková, Miroslava
Mlejnek, Petr
Škop, Vojtěch
Oliyarnyk, Olena
Kazdová, Ludmila
Mancini, Massimiliano
Saar, Kathrin
Schulz, Herbert
Hübner, Norbert
Kurtz, Theodore W.
Pravenec, Michal - Abstract:
- <abstract abstract-type="main" id="cdr12061-abs-0001"> <title>Summary</title> <sec id="cdr12061-sec-0001" sec-type="section"> <title>Aims</title> <p>Statins have antiinflammatory effects and are known to decrease risk of cardiovascular events and to reduce serum levels of C‐reactive protein (CRP), a widely studied biomarker and potential mediator of inflammation and heart disease. However, it is unclear whether statins can block pro‐inflammatory effects of human CRP independent of their ability to reduce serum levels of human CRP. Here, we investigated whether rosuvastatin could block pro‐inflammatory effects of human CRP without reducing circulating levels of human CRP.</p> </sec> <sec id="cdr12061-sec-0002" sec-type="section"> <title>Methods and Results</title> <p>We studied the antiinflammatory effects of rosuvastatin in spontaneously hypertensive rats (SHR) transgenically expressing human CRP (CRP‐transgenic SHR) and in nontransgenic SHR lacking human CRP (nontransgenic SHR). The CRP‐transgenic SHR is characterized by increased serum levels of human CRP and inflammation. In the CRP‐transgenic strain, we found that rosuvastatin treatment decreased circulating levels of inflammatory response markers IL6 and TNF<italic>α</italic> without decreasing circulating levels of human CRP. In contrast, in the nontransgenic strain lacking human CRP, rosuvastatin treatment had little or no effect on IL6 and TNF<italic>α</italic> levels. Rosuvastatin also reduced cardiac inflammation<abstract abstract-type="main" id="cdr12061-abs-0001"> <title>Summary</title> <sec id="cdr12061-sec-0001" sec-type="section"> <title>Aims</title> <p>Statins have antiinflammatory effects and are known to decrease risk of cardiovascular events and to reduce serum levels of C‐reactive protein (CRP), a widely studied biomarker and potential mediator of inflammation and heart disease. However, it is unclear whether statins can block pro‐inflammatory effects of human CRP independent of their ability to reduce serum levels of human CRP. Here, we investigated whether rosuvastatin could block pro‐inflammatory effects of human CRP without reducing circulating levels of human CRP.</p> </sec> <sec id="cdr12061-sec-0002" sec-type="section"> <title>Methods and Results</title> <p>We studied the antiinflammatory effects of rosuvastatin in spontaneously hypertensive rats (SHR) transgenically expressing human CRP (CRP‐transgenic SHR) and in nontransgenic SHR lacking human CRP (nontransgenic SHR). The CRP‐transgenic SHR is characterized by increased serum levels of human CRP and inflammation. In the CRP‐transgenic strain, we found that rosuvastatin treatment decreased circulating levels of inflammatory response markers IL6 and TNF<italic>α</italic> without decreasing circulating levels of human CRP. In contrast, in the nontransgenic strain lacking human CRP, rosuvastatin treatment had little or no effect on IL6 and TNF<italic>α</italic> levels. Rosuvastatin also reduced cardiac inflammation and oxidative tissue damage, reduced epididymal fat mass, and improved adipose tissue lipolysis much more in the CRP‐transgenic strain than in the nontransgenic strain.</p> </sec> <sec id="cdr12061-sec-0003" sec-type="section"> <title>Conclusion</title> <p>Rosuvastatin can protect against pro‐inflammatory effects of human CRP in a manner that is not dependent on achieving a reduction in circulating levels of human CRP.</p> </sec> </abstract> … (more)
- Is Part Of:
- Cardiovascular therapeutics. Volume 32:Issue 2(2014:Apr.)
- Journal:
- Cardiovascular therapeutics
- Issue:
- Volume 32:Issue 2(2014:Apr.)
- Issue Display:
- Volume 32, Issue 2 (2014)
- Year:
- 2014
- Volume:
- 32
- Issue:
- 2
- Issue Sort Value:
- 2014-0032-0002-0000
- Page Start:
- 59
- Page End:
- 65
- Publication Date:
- 2014-04
- Subjects:
- Cardiovascular pharmacology -- Periodicals
Cardiovascular agents -- Periodicals
Cardiovascular system -- Diseases -- Chemotherapy -- Periodicals
Cardiovascular Agents -- Periodicals
Cardiovascular Diseases -- drug therapy -- Periodicals
Agents cardiovasculaires -- Périodiques
Appareil cardiovasculaire -- Maladies -- Chimiothérapie -- Périodiques
616.1005 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1755-5922 ↗
http://www.blackwell-synergy.com/loi/cath ↗
http://www.blackwellpublishing.com/journal.asp?ref=1755-5914&site=1 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/1755-5922.12061 ↗
- Languages:
- English
- ISSNs:
- 1755-5914
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3051.520500
British Library HMNTS - ELD Digital store - Ingest File:
- 3649.xml