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Article: C-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease

TitleC-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease
Authors
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/
Citation
Hypertension, 2010, v. 55 n. 4, p. 953-960 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/129201
ISSN
2013 Impact Factor: 7.632
2013 SCImago Journal Rankings: 3.702
ISI Accession Number ID
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.

References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Ren_HK
dc.contributor.authorZhang, YYen_HK
dc.contributor.authorHuang, XRen_HK
dc.contributor.authorWu, Yen_HK
dc.contributor.authorChung, ACKen_HK
dc.contributor.authorWu, EXen_HK
dc.contributor.authorSzalai, AJen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorLan, HYen_HK
dc.date.accessioned2010-12-23T08:33:34Z-
dc.date.available2010-12-23T08:33:34Z-
dc.date.issued2010en_HK
dc.identifier.citationHypertension, 2010, v. 55 n. 4, p. 953-960en_HK
dc.identifier.issn0194-911Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/129201-
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.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/en_HK
dc.relation.ispartofHypertensionen_HK
dc.rightsThis is a non-final version of an article published in final form in (provide complete journal citation)-
dc.subjectAngiotensin IIen_HK
dc.subjectCardiac fibrosisen_HK
dc.subjectCRPen_HK
dc.subjectHypertensionen_HK
dc.subjectInflammationen_HK
dc.subjectTGF-Β/Smadsen_HK
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.titleC-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0194-911X&volume=55&issue=4&spage=953&epage=960&date=2010&atitle=C-reactive+protein+promotes+cardiac+fibrosis+and+inflammation+in+angiotensin+II-induced+hypertensive+cardiac+disease-
dc.identifier.emailWu, EX:ewu1@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWu, EX=rp00193en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1161/HYPERTENSIONAHA.109.140608en_HK
dc.identifier.pmid20157054-
dc.identifier.scopuseid_2-s2.0-77950504894en_HK
dc.identifier.hkuros177196en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950504894&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume55en_HK
dc.identifier.issue4en_HK
dc.identifier.spage953en_HK
dc.identifier.epage960en_HK
dc.identifier.isiWOS:000275701600025-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhang, R=9842860900en_HK
dc.identifier.scopusauthoridZhang, YY=8631539600en_HK
dc.identifier.scopusauthoridHuang, XR=7410248090en_HK
dc.identifier.scopusauthoridWu, Y=8940205500en_HK
dc.identifier.scopusauthoridChung, ACK=7103291604en_HK
dc.identifier.scopusauthoridWu, EX=7202128034en_HK
dc.identifier.scopusauthoridSzalai, AJ=7003664600en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridLan, HY=35783008500en_HK

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