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Article: C-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease
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TitleC-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease
 
AuthorsZhang, R
Zhang, YY
Huang, XR2
Wu, Y1
Chung, ACK2
Wu, EX1
Szalai, AJ3
Wong, BCY
Lau, CP
Lan, HY2
 
KeywordsAngiotensin II
Cardiac fibrosis
CRP
Hypertension
Inflammation
TGF-Β/Smads
 
Issue Date2010
 
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
 
CitationHypertension, 2010, v. 55 n. 4, p. 953-960 [How to Cite?]
DOI: http://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608
 
AbstractC-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.
 
ISSN0194-911X
2013 Impact Factor: 7.632
2013 SCImago Journal Rankings: 3.702
 
DOIhttp://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608
 
ISI Accession Number IDWOS:000275701600025
Funding AgencyGrant Number
Research Grant Council of Hong Kong (RGC)GRF 767508
GRF 768409
Sun Chieh Yeh Heart Foundation
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhang, R
 
dc.contributor.authorZhang, YY
 
dc.contributor.authorHuang, XR
 
dc.contributor.authorWu, Y
 
dc.contributor.authorChung, ACK
 
dc.contributor.authorWu, EX
 
dc.contributor.authorSzalai, AJ
 
dc.contributor.authorWong, BCY
 
dc.contributor.authorLau, CP
 
dc.contributor.authorLan, HY
 
dc.date.accessioned2010-12-23T08:33:34Z
 
dc.date.available2010-12-23T08:33:34Z
 
dc.date.issued2010
 
dc.description.abstractC-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.naturelink_to_subscribed_fulltext
 
dc.identifier.citationHypertension, 2010, v. 55 n. 4, p. 953-960 [How to Cite?]
DOI: http://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608
 
dc.identifier.doihttp://dx.doi.org/10.1161/HYPERTENSIONAHA.109.140608
 
dc.identifier.epage960
 
dc.identifier.hkuros177196
 
dc.identifier.isiWOS:000275701600025
Funding AgencyGrant Number
Research Grant Council of Hong Kong (RGC)GRF 767508
GRF 768409
Sun Chieh Yeh Heart Foundation
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.issn0194-911X
2013 Impact Factor: 7.632
2013 SCImago Journal Rankings: 3.702
 
dc.identifier.issue4
 
dc.identifier.openurl
 
dc.identifier.pmid20157054
 
dc.identifier.scopuseid_2-s2.0-77950504894
 
dc.identifier.spage953
 
dc.identifier.urihttp://hdl.handle.net/10722/129201
 
dc.identifier.volume55
 
dc.languageeng
 
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofHypertension
 
dc.relation.referencesReferences in Scopus
 
dc.rightsThis is a non-final version of an article published in final form in (provide complete journal citation)
 
dc.subject.meshAngiotensin II - pharmacology
 
dc.subject.meshC-Reactive Protein - genetics - metabolism
 
dc.subject.meshFibrosis - metabolism - pathology
 
dc.subject.meshHypertension - metabolism - pathology - physiopathology
 
dc.subject.meshMyocardium - metabolism - pathology
 
dc.subjectAngiotensin II
 
dc.subjectCardiac fibrosis
 
dc.subjectCRP
 
dc.subjectHypertension
 
dc.subjectInflammation
 
dc.subjectTGF-Β/Smads
 
dc.titleC-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong
  2. Prince of Wales Hospital Hong Kong
  3. University of Alabama