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- but not 
-adrenergic hypertrophic growth responses in adult cardiomyocytes
1 Physiologisches Institut, Justus-Liebig-University, Giessen, Germany
* To whom correspondence should be addressed. E-mail: Gerhild.Taimor{at}physiologie.med.uni-giessen.de.
In some models of cardiac hypertrophy, activation of AP-1 correlates with growth. However, AP-1 is also activated by stimuli not involved in cardiac growth. This raises the question if AP-1 plays a causal role for cardiomyocyte growth and if this role is model- or stimulus dependent. We now address this question using a single model, i.e. ventricular cardiomyocytes of adult rats, and two growth stimuli, i.e. 
- or 
-adrenoceptor agonists (10µM phenylephrine, PE, and 1 µM isoprenaline, ISO, respectively). After 1 h stimulation with PE, mRNA expression of c-Fos and c-Jun was upregulated to 185 ± 32 % and 132 ± 13 % of control. Fos and Jun proteins formed the AP-1 complex. PE stimulated DNA binding activity of AP-1 to 165 ± 22 % of control within 2 h, increased protein synthesis to 161 ± 27 % and cross sectional area to 126 ± 4 % of control. Inhibition of AP-1 binding activity by CRE-decoy oligonucleotides abolished both of these growth
responses. ISO stimulated AP-1 binding activity to 203 ± 19 % of control within 2 h and stimulated protein synthesis to 145 ± 17 % of control. But the growth effect of ISO was not abolished by CRE-decoys: ISO increased protein synthesis to 158 ± 17 % of control in presence of CRE.
In conclusion, AP-1 is a causal mediator of the -adrenergic but not the -adrenergic growth response of cardiomyocytes.
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