Alterations of beta -adrenergic signaling and cardiac hypertrophy in transgenic mice overexpressing TGF-beta 1

• Published in: American journal of physiology. Heart and circulatory physiology 2002-09, Vol.283 (3), p.H1253-H1262
• Main Authors: Rosenkranz, Stephan, Flesch, Markus, Amann, Kerstin, Haeuseler, Claudia, Kilter, Heiko, Seeland, Ute, Schluter, Klaus-Dieter, Bohm, Michael
• Format: Article
• Language: English
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00578.2001

1  Klinik III für Innere Medizin, Universität zu Köln, 50924 Köln; 2  Pathologisches Institut, Universität Erlangen, Erlangen 91054; 3  Medizinische Klinik III, Universität des Saarlandes, Homburg-Saar 66421; and 4  Physiologisches Institut, Justus-Liebig-Universität Giessen, Giessen 35390, Germany Transforming growth factor- 1 (TGF- 1 ) promotes or inhibits cell proliferation and induces fibrotic processes and extracellular matrix production in numerous cell types. Several cardiac diseases are associated with an increased expression of TGF- 1 mRNA, particularly during the transition from stable cardiac hypertrophy to heart failure. In vitro studies suggest a link between TGF- 1 signaling and the -adrenergic system. However, the in vivo effects of this growth factor on myocardial tissue have been poorly identified. In transgenic mice overexpressing TGF- 1 (TGF- ), we investigated the in vivo effects on cardiac morphology, -adrenergic signaling, and contractile function. When compared with nontransgenic controls (NTG), TGF- mice revealed significant cardiac hypertrophy (heart weight, 164 ± 7 vs. 130 ± 3 mg, P