Disclosure statement: The authors have nothing to disclose.
The induction of cardiac ornithine decarboxylase by β2-adrenergic agents is associated with calcium channels and phosphorylation of ERK1/2
Article first published online: 18 JUL 2013
Copyright © 2013 Wiley Periodicals, Inc.
Journal of Cellular Biochemistry
Volume 114, Issue 9, pages 1978–1986, September 2013
How to Cite
López-Contreras, A. J., de la Morena, M. E., Ramos-Molina, B., Lambertos, A., Cremades, A. and Peñafiel, R. (2013), The induction of cardiac ornithine decarboxylase by β2-adrenergic agents is associated with calcium channels and phosphorylation of ERK1/2. J. Cell. Biochem., 114: 1978–1986. doi: 10.1002/jcb.24540
- Issue published online: 18 JUL 2013
- Article first published online: 18 JUL 2013
- Accepted manuscript online: 20 MAR 2013 07:19AM EST
- Manuscript Accepted: 5 MAR 2013
- Manuscript Received: 25 JAN 2013
- Seneca Foundation. Grant Number: 08681/PI/08
- Spanish Ministry of Science and Innovation and FEDER Funds. Grant Numbers: SAF2008-03638, SAF2011-29051
- ORNITHINE DECARBOXYLASE;
- BETA-ADRENERGIC AGENTS;
- L-CALCIUM CHANNELS;
- MAP KINASES;
The role that the induction of cardiac ornithine decarboxylase (ODC), a key enzyme in polyamine biosynthesis, by beta-adrenergic agents may have in heart hypertrophy is a controversial issue. Besides, the signaling pathways related to cardiac ODC regulation have not been fully elucidated. Here we show that in Balb C mice the stimulation of cardiac ODC activity by adrenergic agents was mainly mediated by β2-adrenergic receptors, and that this induction was lower in the hypertrophic heart. Interestingly, this stimulation was abolished by the L-calcium channel antagonists verapamil and nifedipine. In addition, whereas the treatment with β2-adrenergic agents was associated to both the increases in ODC, ODC-antizyme inhibitor 1 (AZIN1), c-fos and c-myc mRNA levels and the phosphorylation of CREB and MAP kinases ERK1 and ERK2 (ERK1/2), the co-treatment with L-calcium channel blockers differentially prevented most of these changes. These results suggest that the stimulation of cardiac ODC by β2-adrenergic agents is associated with the activation of MAP kinases through the participation of L-calcium channels, and that by itself p-CREB does not appear to be sufficient for the transcriptional activation of ODC. In addition, post-translational mechanisms related with the induction of AZIN1 appear to be related to the increase of cardiac ODC activity. J. Cell. Biochem. 114: 1978–1986, 2013. © 2013 Wiley Periodicals, Inc.