Article: C-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease
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- Publisher Website: 10.1161/HYPERTENSIONAHA.109.140608
- Scopus: eid_2-s2.0-77950504894
- PMID: 20157054
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| Title | C-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease |
|---|---|
| Authors | Zhang, R Zhang, YY Huang, XR2 Wu, Y1 Chung, ACK2 Wu, EX1 Szalai, AJ3 Wong, BCY Lau, CP Lan, HY2 |
| Keywords | Angiotensin II Cardiac fibrosis CRP Hypertension Inflammation TGF-Β/Smads |
| Issue Date | 2010 |
| Publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/ |
| Citation | Hypertension, 2010, v. 55 n. 4, p. 953-960 [How to Cite?] DOI: http://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608 |
| Abstract | C-reactive protein (CRP) is a risk factor or biomarker for Cardiovascular diseases, including hypertension. The present study investigated the functional importance of human CRP in hypertensive Cardiac remodeling by a chronic infusion of angiotensin II (Ang II) into mice that express human CRP. Compared with the wild-type mice, although Ang II infusion Caused an equally high systolic blood pressure, levels of human CRP were further elevated, and Cardiac remodeling was markedly exacerbated in mice that express human CRP, resulting in a signifiCant reduction in the left ventricular ejection fraction and fractional shortening and an increase in Cardiac fibrosis (collagen I and III and α-smooth muscle actin) and inflammation (interleukin 1β and tumor necrosis factor-α). The enhancement in Cardiac remodeling in mice that express human CRP was associated with further upregulation of the Ang II type I receptor and transforming growth factor-β1 and overactivation of both transforming growth factor-β/Smad and nuclear factor-κB signaling pathways. Furthermore, in vitro studies in Cardiac fibroblasts revealed that CRP alone was able to signifiCantly induce expression of the Ang II type I receptor, collagen I/III, and α-smooth muscle actin, as well as proinflammation cytokines (interleukin 1β and tumor necrosis factor-α), which was further enhanced by addition of Ang II. In conclusion, CRP is not only a biomarker but also a mediator in Ang II-mediated Cardiac remodeling. Enhanced upregulation of the Ang II type I receptor and activation of the transforming growth factor-β/Smad and nuclear factor-κB signaling pathways may be the mechanisms by which CRP promotes Cardiac fibrosis and inflammation under high Ang II conditions. © 2010 American Heart Association, Inc. |
| ISSN | 0194-911X 2011 Impact Factor: 6.207 2011 SCImago Journal Rankings: 0.623 |
| DOI | http://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608 |
| References | References in Scopus |
| dc.contributor.author | Zhang, R | ||||||
|---|---|---|---|---|---|---|---|
| dc.contributor.author | Zhang, YY | ||||||
| dc.contributor.author | Huang, XR | ||||||
| dc.contributor.author | Wu, Y | ||||||
| dc.contributor.author | Chung, ACK | ||||||
| dc.contributor.author | Wu, EX | ||||||
| dc.contributor.author | Szalai, AJ | ||||||
| dc.contributor.author | Wong, BCY | ||||||
| dc.contributor.author | Lau, CP | ||||||
| dc.contributor.author | Lan, HY | ||||||
| dc.date.accessioned | 2010-12-23T08:33:34Z | ||||||
| dc.date.available | 2010-12-23T08:33:34Z | ||||||
| dc.date.issued | 2010 | ||||||
| dc.description.abstract | C-reactive protein (CRP) is a risk factor or biomarker for Cardiovascular diseases, including hypertension. The present study investigated the functional importance of human CRP in hypertensive Cardiac remodeling by a chronic infusion of angiotensin II (Ang II) into mice that express human CRP. Compared with the wild-type mice, although Ang II infusion Caused an equally high systolic blood pressure, levels of human CRP were further elevated, and Cardiac remodeling was markedly exacerbated in mice that express human CRP, resulting in a signifiCant reduction in the left ventricular ejection fraction and fractional shortening and an increase in Cardiac fibrosis (collagen I and III and α-smooth muscle actin) and inflammation (interleukin 1β and tumor necrosis factor-α). The enhancement in Cardiac remodeling in mice that express human CRP was associated with further upregulation of the Ang II type I receptor and transforming growth factor-β1 and overactivation of both transforming growth factor-β/Smad and nuclear factor-κB signaling pathways. Furthermore, in vitro studies in Cardiac fibroblasts revealed that CRP alone was able to signifiCantly induce expression of the Ang II type I receptor, collagen I/III, and α-smooth muscle actin, as well as proinflammation cytokines (interleukin 1β and tumor necrosis factor-α), which was further enhanced by addition of Ang II. In conclusion, CRP is not only a biomarker but also a mediator in Ang II-mediated Cardiac remodeling. Enhanced upregulation of the Ang II type I receptor and activation of the transforming growth factor-β/Smad and nuclear factor-κB signaling pathways may be the mechanisms by which CRP promotes Cardiac fibrosis and inflammation under high Ang II conditions. © 2010 American Heart Association, Inc. | ||||||
| dc.description.nature | Link_to_subscribed_fulltext | ||||||
| dc.identifier.citation | Hypertension, 2010, v. 55 n. 4, p. 953-960 [How to Cite?] DOI: http://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608 | ||||||
| dc.identifier.doi | http://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608 | ||||||
| dc.identifier.epage | 960 | ||||||
| dc.identifier.hkuros | 177196 | ||||||
| dc.identifier.isi | WOS:000275701600025
Funding Information: This work has been supported by grants from the Research Grant Council of Hong Kong (RGC GRF 767508 and 768409) and the Sun Chieh Yeh Heart Foundation. | ||||||
| dc.identifier.issn | 0194-911X 2011 Impact Factor: 6.207 2011 SCImago Journal Rankings: 0.623 | ||||||
| dc.identifier.issue | 4 | ||||||
| dc.identifier.openurl | | ||||||
| dc.identifier.pmid | 20157054 | ||||||
| dc.identifier.scopus | eid_2-s2.0-77950504894 | ||||||
| dc.identifier.spage | 953 | ||||||
| dc.identifier.uri | http://hdl.handle.net/10722/129201 | ||||||
| dc.identifier.volume | 55 | ||||||
| dc.language | eng | ||||||
| dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/ | ||||||
| dc.publisher.place | United States | ||||||
| dc.relation.ispartof | Hypertension | ||||||
| dc.relation.references | References in Scopus | ||||||
| dc.rights | This is a non-final version of an article published in final form in (provide complete journal citation) | ||||||
| dc.subject.mesh | Angiotensin II - pharmacology | ||||||
| dc.subject.mesh | C-Reactive Protein - genetics - metabolism | ||||||
| dc.subject.mesh | Fibrosis - metabolism - pathology | ||||||
| dc.subject.mesh | Hypertension - metabolism - pathology - physiopathology | ||||||
| dc.subject.mesh | Myocardium - metabolism - pathology | ||||||
| dc.subject | Angiotensin II | ||||||
| dc.subject | Cardiac fibrosis | ||||||
| dc.subject | CRP | ||||||
| dc.subject | Hypertension | ||||||
| dc.subject | Inflammation | ||||||
| dc.subject | TGF-Β/Smads | ||||||
| dc.title | C-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease | ||||||
| dc.type | Article |
Author Affiliations
- The University of Hong Kong
- Prince of Wales Hospital Hong Kong
- University of Alabama