| C-reactive protein promotes cardiac fibrosis and inflammation in angiotensin II-induced hypertensive cardiac disease. | |
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MedLine Citation:
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PMID: 20157054 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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 alpha-smooth muscle actin) and inflammation (interleukin 1beta and tumor necrosis factor-alpha). 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-beta1 and overactivation of both transforming growth factor-beta/Smad and nuclear factor-kappaB 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 alpha-smooth muscle actin, as well as proinflammation cytokines (interleukin 1beta and tumor necrosis factor-alpha), 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-beta/Smad and nuclear factor-kappaB signaling pathways may be the mechanisms by which CRP promotes cardiac fibrosis and inflammation under high Ang II conditions. |
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Authors:
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Rongxin Zhang; Yuan Yuan Zhang; Xiao R Huang; Yin Wu; Arthur C K Chung; Ed Xuekui Wu; Alexander J Szalai; Benjamin C Y Wong; Chu-Pak Lau; Hui Y Lan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-02-15 |
Journal Detail:
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Title: Hypertension Volume: 55 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-18 Completed Date: 2010-04-09 Revised Date: 2010-06-18 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 953-60 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Hong Kong, Hong Kong Special Administrative Region, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Angiotensin II / pharmacology* Animals Blood Pressure / drug effects, genetics C-Reactive Protein / genetics, metabolism* Cells, Cultured Enzyme-Linked Immunosorbent Assay Fibrosis / metabolism, pathology* Heart / drug effects, physiopathology Heart Rate / drug effects Humans Hypertension / metabolism, pathology*, physiopathology Immunohistochemistry Inflammation / genetics, metabolism, pathology Interleukin-1beta / metabolism Mice Myocardium / metabolism, pathology* Receptor, Angiotensin, Type 1 / metabolism Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Smad Proteins / metabolism Tumor Necrosis Factor-alpha / metabolism Up-Regulation Ventricular Remodeling / genetics* |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-1beta; 0/Receptor, Angiotensin, Type 1; 0/Smad Proteins; 0/Tumor Necrosis Factor-alpha; 11128-99-7/Angiotensin II; 9007-41-4/C-Reactive Protein |
| Comments/Corrections | |
Comment In:
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Hypertension. 2010 Jul;56(1):e15; author reply e16
[PMID:
20479326
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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