Skip Navigation


European Heart Journal Advance Access originally published online on March 9, 2005
European Heart Journal 2005 26(7):728-739; doi:10.1093/eurheartj/ehi168
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary data
Right arrow All Versions of this Article:
26/7/728    most recent
ehi168v1
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 Related articles in EHJ
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Grün, K.
Right arrow Articles by Leipner, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Grün, K.
Right arrow Articles by Leipner, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions{at}oupjournals.org

Elevated expression of PDGF-C in coxsackievirus B3-induced chronic myocarditis

Katja Grün1, Boyka Markova2, Frank-D. Böhmer2, Alexander Berndt3, Hartwig Kosmehl4 and Carola Leipner1,*

1Institute of Virology and Antiviral Therapy, Klinikum, Friedrich Schiller University Jena, Hans-Knöll-Strasse 2, D-07745 Jena, Germany
2Institute of Molecular Cell Biology, Klinikum, Friedrich Schiller University Jena, Drackendorfer Strasse 1, D-07747 Jena, Germany
3Institute of Pathology, Klinikum, Friedrich Schiller University Jena, Ziegelmühlenweg 1, D-07743 Jena, Germany
4HELIOS Klinikum Erfurt GmbH, Institute of Pathology, Nordhäuser Strasse 74, D-099089 Erfurt, Germany

Received 5 February 2004; revised 14 December 2004; accepted 13 January 2005; online publish-ahead-of-print 9 March 2005.

* Corresponding author. Tel: +49 3641 657358; fax: +49 3641 657202. E-mail address: carola.leipner{at}uni-jena.de

See page 642 for the editorial comment on this article (doi:10.1093/eurheartj/ehi201)

Aims Coxsackievirus B3 (CVB3) is a frequent cause of human chronic myocarditis and subsequent fibrosis, leading to dilated cardiomyopathy. The molecular processes underlying the development of fibrosis are poorly understood. Enhanced levels of platelet-derived growth factors (PDGFs), especially PDGF-C, have recently been linked with the development of different forms of fibrosis. Therefore, the expression of PDGF was analysed in hearts of CVB3-infected major histocompatability complex class II knockout mice. The latter were recently established as mouse model mimicking the chronic inflammation and fibrosis characteristic for this disease.

Methods and results Expression of PDGF was analysed by reverse transcription–polymerase chain reaction, in situ hybridization, and immunohistochemistry. Hearts of C57BL/6 mice served as controls because infection of these animals leads to acute cardiac inflammation, but the hearts heal without signs of chronic inflammation. In uninfected hearts, basal expression of PDGF, notably PDGF-C, was detectable throughout the heart. The chronic inflammatory process was associated with elevated and sustained expression of all tested PDGF isoforms. Immunostaining and in situ hybridization analysis localized enhanced PDGF levels to areas with highest virus load and inflammatory infiltrations, adjacent to fibrotic areas.

Conclusion PDGF may participate in fibrosis development in CVB3-induced myocarditis. Therefore, PDGF signalling may be considered a target for therapeutic interference.

Key Words: Chronic myocarditis • Coxsackievirus B3 (CVB3) • Platelet derived growth factor (PDGF) isoforms • PDGF-C • Major histocompatibility complex (MHC) class II knockout mouse


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

Related articles in EHJ:

Linkage between elevated PDGF-C expression and myocardial fibrogenesis in coxsackievirus B3-induced chronic myocarditis
Decheng Yang and Dexin Qiu
EHJ 2005 26: 642-643. [Extract] [FREE Full Text]  



This article has been cited by other articles:


Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
R. Tuuminen, A. I. Nykanen, R. Krebs, J. Soronen, K. Pajusola, M. A.I. Keranen, P. K. Koskinen, K. Alitalo, and K. B. Lemstrom
PDGF-A, -C, and -D but not PDGF-B Increase TGF-{beta}1 and Chronic Rejection in Rat Cardiac Allografts
Arterioscler Thromb Vasc Biol, May 1, 2009; 29(5): 691 - 698.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
C. Leipner, K. Grun, A. Muller, E. Buchdunger, L. Borsi, H. Kosmehl, A. Berndt, T. Janik, A. Uecker, M. Kiehntopf, et al.
Imatinib mesylate attenuates fibrosis in coxsackievirus b3-induced chronic myocarditis
Cardiovasc Res, July 1, 2008; 79(1): 118 - 126.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
F. Eitner, E. Bucher, C. van Roeyen, U. Kunter, S. Rong, C. Seikrit, L. Villa, P. Boor, L. Fredriksson, G. Backstrom, et al.
PDGF-C Is a Proinflammatory Cytokine that Mediates Renal Interstitial Fibrosis
J. Am. Soc. Nephrol., February 1, 2008; 19(2): 281 - 289.
[Full Text] [PDF]

Home page
 Eur Heart JHome page
D. Yang and D. Qiu
Linkage between elevated PDGF-C expression and myocardial fibrogenesis in coxsackievirus B3-induced chronic myocarditis
Eur. Heart J., April 1, 2005; 26(7): 642 - 643.
[Full Text] [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.