Premium
The induction of cardiac ornithine decarboxylase by β 2 ‐adrenergic agents is associated with calcium channels and phosphorylation of ERK1/2
Author(s) -
LópezContreras Andrés J.,
de la Morena Maria Eugenia,
RamosMolina Bruno,
Lambertos Ana,
Cremades Asunción,
Peñafiel Rafael
Publication year - 2013
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24540
Subject(s) - ornithine decarboxylase , verapamil , creb , endocrinology , medicine , calcium channel , phosphorylation , stimulation , kinase , calcium , voltage dependent calcium channel , adrenergic , polyamine , biology , chemistry , receptor , microbiology and biotechnology , biochemistry , enzyme , transcription factor , gene
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 β 2 ‐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 β 2 ‐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 β 2 ‐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.