Skip Navigation

Cardiovascular Research 2000 45(2):410-417; doi:10.1016/S0008-6363(99)00351-X
© 2000 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 Schlüter, K.-D.
Right arrow Articles by Piper, H. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schlüter, K.-D.
Right arrow Articles by Piper, H. M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2000, European Society of Cardiology

Central role for ornithine decarboxylase in β-adrenoceptor mediated hypertrophy

Klaus-Dieter Schlütera,*, Karen Frischkopfa, Markus Fleschb, Stephan Rosenkranzb, Gerhild Taimora and Hans Michael Pipera

aPhysiologisches Institut, Justus-Liebig-Universität, Aulweg 129, D-35392 Giessen, Germany
bKlinik III für Innere Medizin der Universität zu Köln, Cologne, Germany

* Corresponding author. Tel.: +49-641-994-7234; fax: +49-641-994-7239 Klaus-Dieter.Schlueter{at}physiologie.med.uni-giessen.de

Objective: TGF-β stimulation of cardiac myocytes induces a hypertrophic responsiveness to β-adrenoceptor stimulation. This study investigates whether this β-adrenoceptor mediated effect depends on induction of ornithine decarboxylase (ODC). Methods: Isolated adult ventricular cardiomyocytes from rats were used as an experimental model. Cells were either cultured in 20% (v/v) FCS to activate autocrine released TGF-β or used without pre-treatment. The hypertrophic response was characterized by an increased 14C-phenylalanine incorporation, RNA and protein mass or by an increased expression of atrionatriurectic factor and ODC. The results on cell cultures were compared to those achieved by isoprenaline perfused mice hearts from transgenic mice overexpressing TGF-β1. Results: ODC activity and expression increased within 2 h in TGF-β1 pre-treated cells under isoprenaline. In the presence of ODC inhibitors ({alpha}-methylornithine or difluoromethylornithine) this increase remained absent and the increases in 14C-phenylalanine incorporation, protein and RNA mass under isoprenaline were abolished. In cells not exposed to TGF-β no induction of ODC was observed. Isoprenaline also induced ODC in isolated perfused ventricles from transgenic mice overexpressing TGF-β1, but not in ventricles from their nontransgenic counterparts. Conclusions: This study shows first, a pivotal role for ODC induction in the hypertrophic response of cardiomyocytes to β-adrenoceptor stimulation and second, that ODC induction in vivo and in vitro requires pre-treatment of cardiomyocytes with TGF-β. It is concluded that TGF-β induces a hypertrophic responsiveness to β-adrenoceptor stimulation that is characterized by ODC induction.

KEYWORDS Adrenergic (ant)agonist; Cytokines; Hypertrophy; Myocytes; Signal transduction


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. Biol. Chem.Home page
K.-L. Su, Y.-F. Liao, H.-C. Hung, and G.-Y. Liu
Critical Factors Determining Dimerization of Human Antizyme Inhibitor
J. Biol. Chem., September 25, 2009; 284(39): 26768 - 26777.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
K. Meurrens, S. Ruf, G. Ross, R. Schleef, K. von Holt, and K.-D. Schluter
Smoking accelerates the progression of hypertension-induced myocardial hypertrophy to heart failure in spontaneously hypertensive rats
Cardiovasc Res, November 1, 2007; 76(2): 311 - 322.
[Abstract] [Full Text] [PDF]

Home page
 Eur J Heart FailHome page
v. E. Martin, S. Rolf, P. A. Doevendans, R. Meyer, C. Grohe, and K.-D. Schluter
The influence of oestrogen-deficiency and ACE inhibition on the progression of myocardial hypertrophy in spontaneously hypertensive rats
Eur J Heart Fail, December 1, 2005; 7(7): 1079 - 1084.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
S. Rosenkranz
TGF-{beta}1 and angiotensin networking in cardiac remodeling
Cardiovasc Res, August 15, 2004; 63(3): 423 - 432.
[Abstract] [Full Text] [PDF]

Home page
 Eur J Heart FailHome page
B. Schwarz, E. Percy, X.-M. Gao, A. M. Dart, G. Richardt, and X.-J. Du
Altered calcium transient and development of hypertrophy in {beta}2-adrenoceptor overexpressing mice with and without pressure overload
Eur J Heart Fail, March 1, 2003; 5(2): 131 - 136.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol PatholHome page
H. Roger Brown, Hong Ni, G. Benavides, L. Yoon, K. Hyder, J. Giridhar, G. Gardner, R. D. Tyler, and K. T. Morgan
Correlation of Simultaneous Differential Gene Expression in the Blood and Heart with Known Mechanisms of Adriamycin-Induced Cardiomyopathy in the Rat
Toxicol Pathol, June 1, 2002; 30(4): 452 - 469.
[Abstract] [PDF]

Home page
 Cardiovasc ResHome page
X.-J. Du, X.-M. Gao, B. Wang, G. L Jennings, E. A Woodcock, and A. M Dart
Age-dependent cardiomyopathy and heart failure phenotype in mice overexpressing {beta}2-adrenergic receptors in the heart
Cardiovasc Res, December 1, 2000; 48(3): 448 - 454.
[Abstract] [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.