Skip Navigation

Cardiovascular Research 2002 55(2):329-340; doi:10.1016/S0008-6363(02)00413-3
© 2002 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Deten, A.
Right arrow Articles by Zimmer, H.-G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Deten, A.
Right arrow Articles by Zimmer, H.-G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

Cardiac cytokine expression is upregulated in the acute phase after myocardial infarction. Experimental studies in rats

Alexander Deten*, Hans Christian Volz, Wilfried Briest and Heinz-Gerd Zimmer

Carl-Ludwig-Institute of Physiology, University of Leipzig, Liebigstr. 27, D-04103 Leipzig, Germany

* Corresponding author. Tel.: +49-341-971-5500; fax: +49-341-971-5509 deta{at}medizin.uni-leipzig.de

Objective: The proinflammatory cytokines interleukin (IL)-1β and IL-6 are supposed to be involved in various cardiovascular diseases including reperfusion injury and cardiac hypertrophy. Methods and results: In the present study, we have examined the cytokine expression from 3 h up to 12 weeks after permanent coronary artery occlusion in rats. In the first 3–12 h, there was a strong induction in IL-1β and IL-6 mRNA expression in the infarct area (up to 50-fold) as well as in the non-infarcted myocardium (up to 15-fold). From day 3 onwards the cytokine expression was not significantly altered compared to sham-operated controls. In addition, the expression of C/AATT-enhancer binding protein-β was about fourfold elevated in the first hours after myocardial infarction, but not thereafter. Furthermore, the expression of gp130 and IL-6 receptor increased significantly in the infarct area. The elevation in cytokine expression preceded the increase in matrix-metalloproteinase-9 in the infarct area as well as the increase in ANP and collagen expression in the non-infarcted myocardium. Conclusions: We suggest that IL-6 and IL-1β act synergistically in promoting resorption of the necrotic tissue, matrix remodeling and wound healing. Furthermore, they may be involved in the early induction of fibrosis and compensatory cardiac hypertrophy of the non-infarcted myocardium, but seem not to play a key role in long-term cardiac remodeling in chronic heart failure after myocardial infarction.

KEYWORDS Infarction; Heart failure; Cytokines; Remodeling; Hypertrophy


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J CARDIOVASC PHARMACOL THERHome page
S. Chua, L.-T. Chang, C.-K. Sun, J.-J. Sheu, F.-Y. Lee, A. A. Youssef, C.-H. Yang, C.-J. Wu, and H.-K. Yip
Time Courses of Subcellular Signal Transduction and Cellular Apoptosis in Remote Viable Myocardium of Rat Left Ventricles Following Acute Myocardial Infarction: Role of Pharmacomodulation
Journal of Cardiovascular Pharmacology and Therapeutics, June 1, 2009; 14(2): 104 - 115.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.